Disclaimer: Step 6 is for educational purposes only. It does not diagnose, treat, or cure any disease, and it creates no physician-patient relationship. Within the SR™ program, Step 6 serves as a referral gate. The Burris Gut Health Checklist identifies when a client should be referred to an MD for testing and supervision. The checklist is completed at intake; when indicated, referral occurs at Step 6, or first for anyone too sick to work through SR™. Do not implement anything in it, including supplements or changes to medications such as antidepressants or PTSD medications, without your MD’s supervision. These statements have not been evaluated by the Food and Drug Administration. SR™ Practitioners provide a support role only and do not give medical advice.

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How To Use This Guide

Gut dysfunction and repair involve many interacting mechanisms, and even with more than 470 peer-reviewed references, this guide cannot cover all of them. It moves from why, to what to measure, to what to do. Statements marked (Author’s Observation) come from my own experience and have not yet been studied in published research.

Mind First, Body Next: When To Begin Step 6

SR™ is sequenced psychological first, physiological second, and for most people that order should hold. But SR™ can override a poor gut, and that is the danger. Through the 2000s, SR™ carried me through symptoms that, looking back, were signs of a failing gut. The gains were real, so I had no reason to look further. The first distinct symptoms appeared in 2009, and by 2013 I had crashed (see Why This Guide Exists: My Story). It took the next decade to trace the cascade to the mechanisms described in this guide. A poor gut can significantly slow progress in SR™ and wear away gains already made (Author’s Observation).

For this reason, we complete the Burris Gut Health Checklist at intake. If any score is 5 or above over the past 30 days, you will begin the SR™ Gut Barrier and Microbiome Restoration under your MD’s supervision.

When Step 6 Comes First: Some people are too sick to work through SR™. This includes people with anorexia and people sickened by medication. For them, Step 6 comes first under their MD’s supervision, and SR™ begins once they are well enough to engage.

For anyone with anorexia or another eating disorder, the fasting components of this protocol, including the Warrior/OMAD eating window in Phase 1 and the extended fasts in Phase 3, are not used. Step 6 must be adapted by an MD experienced in treating eating disorders.

For anyone sickened by medication, do not stop or change any medication on your own. Your MD decides whether and how medications are adjusted.

Quick Start: Complete the Burris Gut Health Checklist at intake, rating how you have felt over the past 30 days. If any score is 5 or above, begin the SR™ Gut Barrier and Microbiome Restoration, under your MD’s supervision. Read Test Do Not Guess to work with your MD on testing, then Assume And Implement before starting Phase 1.

Part 1: The Problem Top

Why This Guide Exists: My Story Top

I tell you this story in the hope that you will comprehend how insidious oxalate poisoning is, and why any noticeable physiological change, no matter how small, must be addressed.

In the late 1990s, I was a single father of a brilliant child who, at 19, after his software engineering training, asked me to help him take over a contract to build NetSyncLive, a program that synchronized television and the internet for live gameplay. I had introduced SR™ into psychiatric care in 1990, and by 1999 I was ready to launch the Burris Institute. I was still working in the film industry as a producer and actor to keep everything funded. 1999 was a hard year. I broke my ankle, and six months later I had major back surgery. During anesthesia I woke up and pulled out the intravenous line delivering the sedative. To say I was hit a lot harder with the sedatives afterward is an understatement. That, in combination with the antibiotics that followed, is what I believe made me vulnerable to oxalate poisoning. Holding multiple leadership positions at once was surely a contributing factor, but I do not believe it would have made me vulnerable on its own (Author’s Observation).

I felt off shortly after the surgery but could not pin it down. A decade later, at graduation ceremonies in 2009, the first distinct symptoms appeared. In November 2011, I passed large oxalate kidney stones. In mid-2012, I had a gallbladder attack. Instead of surgery, I did an olive oil flush and passed a wide variety of debris, including rock-hard emerald stones I could have made jewelry from. In January 2013, after cranking out about 500 sit-ups, I had a catastrophic event: I could not stand upright and had to crawl to the bathroom.

Over the next six years I burned through 30 MDs trying to get to the root of it. In 2016, a urologist who insisted on a cystoscopy gave me an infection so severe that I was sent to the ER six times and hospitalized five, on antibiotics the entire time. The last round came through a PICC line, and it was my last hope. The infection came back again. This time I was prepared with a regimen of therapeutic oregano oil. That was not a risk for me, because the only other option was worse. At that point I turned all of my research skills to gut health and posted a gut health checklist on Burris Connect. In the decade of data collected since, I have seen only one person who did not have gut health issues (Author’s Observation).

It took me another three years, until 2019, to get to the root of the problem, and another six to get ahead of the ongoing damage the oxalate crystals had done. Twenty years passed between the surgery that started it and the day I understood what was happening. Every symptom along the way had an explanation that was wrong. That is what insidious means.

Gut Barrier Dysfunction Top

The Convergence Point In Chronic Disease, Inflammation, Aging, And Emotional Health

Aging, chronic disease, and emotional suffering share a common thread that is only now coming into full scientific focus: the failure of the intestinal barrier. While researchers have long recognized that conditions such as cardiovascular disease, type 2 diabetes, neurodegeneration, autoimmune disorders, and depression involve persistent low-grade inflammation, the question of what drives that inflammation has remained open. A growing body of evidence now points to the intestinal epithelium as the convergence point where multiple upstream insults translate into systemic inflammatory disease.

The intestinal barrier is the body's largest interface with the external environment. Its integrity depends on a complex interplay of epithelial tight junction proteins, the mucus layer, commensal microbiota, short-chain fatty acid (SCFA) production, mucosal immune function, and mitochondrial energy metabolism within epithelial cells [1]. When this system functions properly, it allows selective nutrient absorption while preventing bacteria, endotoxins, and other harmful substances from entering the bloodstream. When it fails, the consequences are far-reaching.

The Mechanism: From Barrier Failure To Systemic Disease

Intestinal barrier dysfunction, commonly referred to as "leaky gut," allows the translocation of microbial components, particularly lipopolysaccharide (LPS), into the bloodstream. This triggers a cascade of immune activation and chronic, low-grade systemic inflammation that has been directly linked to the development and progression of metabolic, autoimmune, and aging-related disorders [2]. A 2024 review published in Internal and Emergency Medicine confirmed that barrier disruption, caused by bacterial infections, oxidative stress, alcohol exposure, and dysbiosis, is highly connected to conditions including obesity, non-alcoholic fatty liver disease, neurodegeneration, cardiovascular disease, and type 1 diabetes [2].

This process does not operate in isolation. The research consistently identifies a self-reinforcing cycle: age-related changes in the microbiome reduce populations of SCFA-producing bacteria (such as Faecalibacterium prausnitzii and Akkermansia muciniphila), which degrade the intestinal barrier, increase LPS translocation, drive systemic inflammation, and in turn worsen dysbiosis in a feed-forward loop [3, 4]. Intestinal permeability increases with age due specifically to microbial dysbiosis.

Inflammaging: An Evolutionarily Conserved Hallmark Of Aging Top

A 2023 review published in Disease Models & Mechanisms characterized intestinal barrier dysfunction as an evolutionarily conserved hallmark of aging [5]. The phenomenon termed "inflammaging," chronic, low-grade inflammation that arises in the absence of overt infection, is now understood to be tightly coupled to this age-related decline in the barrier.

What makes gut barrier dysfunction so central is that nearly every recognized driver of chronic disease and aging either damages the barrier directly or is amplified by its failure. The variables that converge on this single point include the following.

Microbiome Dysbiosis: Age-associated shifts in microbial composition, marked by losses in Clostridiales and Bifidobacterium and enrichment of Proteobacteria and pathobionts, reduce SCFA synthesis, degrade the mucus layer, and increase intestinal permeability [4, 6]. Depleted SCFA-producing bacteria also impair butyrate availability, the primary energy source for colonocytes and a critical regulator of tight junction integrity.

Mitochondrial Dysfunction: Maintenance of the epithelial barrier is energy-dependent. Mitochondrial dysfunction within intestinal epithelial cells, including impaired oxidative phosphorylation and excessive reactive oxygen species (ROS) production, disrupts tight junction proteins and compromises epithelial self-renewal capacity [1, 7]. ROS-induced barrier disruption has been shown to facilitate bacterial translocation even independent of cell death. Emerging research identifies mitochondrial dysfunction as both a consequence and a perpetuator of intestinal inflammation, establishing it as a key amplifier of the cycle [8].

Immune Senescence and Inflammaging: Immunosenescence, the age-related decline of immune function characterized by thymic involution, reduced hematopoietic stem cell output, and impaired adaptive immunity, both contributes to and is worsened by gut barrier failure [3].

Diet, Stress, and Circadian Disruption: The Western diet, psychological stress, alcohol exposure, circadian rhythm disruption, and antibiotic use are all recognized extrinsic disruptors of barrier integrity [2]. Oxidative stress from these exposures compounds the vicious cycle of intestinal permeability, chronic low-grade inflammation, increased pro-inflammatory cytokine production, enhanced ROS generation, and further barrier degradation.

The Gut-Brain Axis: Barrier dysfunction does not merely affect peripheral tissues. When microbial endotoxins enter systemic circulation, they increase blood-brain barrier permeability, activate microglia, and drive neuroinflammation [6, 9]. This mechanism has been linked to anxiety, depression, PTSD, and neurodegenerative diseases, including Alzheimer's disease [10, 11]. The dysregulation of the gut-brain axis through intestinal barrier failure represents a plausible biological substrate for the well-documented comorbidity of chronic physical disease and mental health disorders.

Candida, Oxalates, and Fungal Overgrowth: A weakened intestinal barrier creates conditions favorable for Candida translocation into the bloodstream and systemic infection. Simultaneously, when oxalate-reducing microbes are depleted through dysbiosis, oxalate crystals accumulate in tissue, irritate the intestinal lining, damage mitochondria, and further weaken the barrier, creating yet another self-reinforcing loop of damage and inflammation.

Oxalates, Candida, And Inflammaging: The Overlooked Connection Top

Inflammaging is usually explained by dysbiosis, a leaking barrier, senescent cells, and immune aging [3, 5]. Those are real, but two drivers that run through this entire document, oxalates and Candida, are missing from that list, and they are missing from the clinical workup as well. The connection is not speculative. Both of them trip the same alarm that defines inflammaging in older adults.

• The alarm is the NLRP3 inflammasome. It is a sensor inside immune cells that, when triggered, releases IL-1β, one of the most potent inflammatory signals in the body. In a 10-year study of older adults, the people whose immune cells had this inflammasome pathway switched on were the ones with high blood pressure, arterial stiffness, and higher mortality; the people without it were healthier and longer-lived. The authors identified this signature as a core mechanism of inflammaging [12].
• Oxalate crystals trigger it. Calcium oxalate crystals activate NLRP3 directly and drive IL-1β release; this is how they cause inflammation in kidney tissue [13], and the same crystals deposit in joints, vessels, bone marrow, thyroid, breast, and prostate [14, 15]. Oxalate also damages mitochondria [16], and damaged mitochondria are themselves a second trigger for the same inflammasome [17]. A body that cannot clear oxalate, because the oxalate-degrading bacteria are gone [18], is a body with a standing supply of inflammasome triggers in its tissues.
• Candida triggers it. The NLRP3 inflammasome is the immune system's primary detector of Candida albicans, and it fires specifically when Candida converts to its invasive hyphal form [19]. Candida crossing a weakened barrier into the bloodstream [20, 21] therefore does more than seed infection; it keeps the inflammaging alarm pressed. Candida also forms amyloid in tissue, including in the brain [22].
• They reinforce each other. Oxalate suppresses the gut bacteria that keep Candida in check [18, 23]. The loss of butyrate-producing bacteria that comes with age [3, 4] removes the signal that holds Candida in its harmless yeast form [24]. Candida biofilm and oxalate crystals both damage the barrier, and a damaged barrier lets both through. The result is a loop in which oxalate, Candida, barrier failure, and inflammasome activation each drive the other three.
• Why it is overlooked. The major reviews of inflammaging do not name oxalate or fungal burden as drivers [3, 5], and a bibliometric analysis of 1,800 inflammaging papers published between 2005 and 2024 found eight research clusters, none of which involved oxalate, Candida, or fungi [25]. Standard medical testing does not measure either: there is no urinary oxalate, no fungal antigen, and no gut permeability test in a routine panel, and the tests that do exist produce frequent false negatives (Part 3). A clinician who never looks for oxalate or Candida will never see them, and will attribute the inflammation to age itself. That is the gap this document is written to close (Author's Observation).

The SR™ Chronic 9: Gut Barrier Dysfunction As The Common Denominator

In 2025, the Make America Healthy Again (MAHA) initiative identified eight chronic diseases as the top focus areas for reducing the nation’s disease burden. We have added a ninth, mental health disorders, many of which are chronic and all of which are part of the gut barrier dysfunction equation. Together these form The SR™ Chronic 9. These conditions rarely occur in isolation. About 1 in 3 adults with diabetes has chronic kidney disease [460], and adults with diabetes are nearly twice as likely to have heart disease or stroke as adults without diabetes [461]. Each of these conditions has documented links to intestinal barrier dysfunction and the systemic inflammation it triggers. This is not coincidental. It reflects the central role that gut barrier failure plays in translating environmental and metabolic insults into organ-specific disease.

Mental Health: The intestinal barrier does not merely regulate what enters the bloodstream from the digestive tract. It also serves as a critical gatekeeper for the brain. When this barrier fails, the consequences extend well beyond gastrointestinal symptoms, reaching directly into the neural circuits that govern mood, cognition, stress resilience, and emotional regulation. A growing body of peer-reviewed evidence now identifies gut barrier dysfunction as a mechanistic driver of multiple psychiatric conditions, including major depressive disorder (MDD), generalized anxiety disorder (GAD), bipolar disorder (BD), and post-traumatic stress disorder (PTSD) [6, 10, 26].

Obesity: Disrupted gut permeability represents both a predisposing and an aggravating condition in obesity. The translocation of LPS across a compromised barrier initiates metabolic endotoxemia, driving the chronic low-grade inflammation that underlies insulin resistance, adipose tissue dysfunction, and weight gain [27]. Germ-free mice colonized with microbiota from obese donors develop weight gain and altered glucose tolerance, directly implicating the microbiome-barrier axis in obesity pathogenesis [27].

Cancer: The dynamic interaction between the gut microbiota, the intestinal barrier, the immune system, and SCFA production directly influences cancer development, progression, and treatment response [28]. Barrier disruption promotes dysbiosis that reduces mitochondrial beta-oxidation in epithelial cells, expands non-anaerobic bacteria, and creates a pro-inflammatory, pro-tumorigenic microenvironment [28]. Chemotherapy itself further damages the barrier by killing gut stem cells, increasing endotoxin translocation, and compounding immune suppression [29].

Heart Disease and Stroke: Increased intestinal permeability is observed in patients and mouse models of cardiovascular disease, including hypertension, atherosclerosis, heart failure, and myocardial infarction. This increased permeability enhances systemic inflammation, alters gut immune function, and has been demonstrated as predictive of adverse cardiovascular outcomes [30]. Stroke has been linked to gut dysbiosis and intestinal barrier dysfunction, with bacterial LPS translocation driving vascular inflammation and endothelial damage [30]. Heart failure itself induces gut ischemia and congestion, which further degrades barrier function, creating a bidirectional cycle of gut and cardiac deterioration [31, 32].

Diabetes: Type 2 diabetes has been associated with increased intestinal permeability, enabling bacterial penetration across the gut barrier and resulting in metabolic endotoxemia that drives low-grade systemic inflammation [27]. Hyperglycemia itself increases intestinal permeability via glucotoxicity, altering tight junction integrity and creating a vicious cycle of barrier impairment, inflammation, and insulin resistance [33]. In germ-free mice, resistance to diet-induced obesity and glucose intolerance is observed, confirming the microbiota's role in metabolic disease [27].

Chronic Lung Diseases (COPD): The gut-lung axis connects intestinal barrier dysfunction to pulmonary inflammation. Systemic endotoxemia originating from a permeable gut activates innate immune pathways that amplify airway inflammation and contribute to the progression of chronic obstructive pulmonary disease. Gut dysbiosis and reduced SCFA production impair systemic immune regulation, with downstream effects on pulmonary immune homeostasis [34].

Alzheimer's Disease and Dementia: Intestinal dysbiosis and increased gut barrier permeability enable bacterial LPS translocation systemically, leading to activation of pro-inflammatory immune cells, increased blood-brain barrier permeability, and microglial activation [9]. These inflammation-driven processes contribute to neurodegeneration, amyloid-beta accumulation, and cognitive decline [10, 11]. The gut-brain axis has emerged as a plausible mechanistic pathway connecting intestinal barrier failure to the neuroinflammatory cascade underlying Alzheimer's disease and related dementias.

Arthritis: Elevated serum zonulin levels, bacterial dysbiosis, and a permeable gut barrier have been observed in patients with rheumatoid arthritis, while subclinical intestinal inflammation has been documented in ankylosing spondylitis [34]. Activated immune cells in mucosal tissues with compromised barriers can migrate to joints and other organs, driving the systemic autoimmune inflammation characteristic of these conditions. Treatment with a zonulin antagonist has inhibited the development of arthritis in mouse models, confirming the intestinal-articular axis [34].

Chronic Kidney Disease (CKD): Reduced SCFA-producing taxa in CKD patients increase intestinal permeability, enabling the translocation of endotoxins and bacterial DNA into the systemic circulation. These factors activate TLR4/TLR9 signaling, triggering inflammatory cascades that exacerbate systemic microinflammation and accelerate organ damage. Gut-derived uremic toxins, including TMAO, indoxyl sulfate, and p-cresyl sulfate, further compromise cardiovascular and cerebrovascular health in CKD, establishing the gut-kidney axis as a critical driver of disease progression.

Mental Health: The Chronic Multiplier

Mental health disorders are not only one of The SR™ Chronic 9; they run through the other eight. People with mental disorders face more than twice the risk of death and lose a median of 10 years of life [462]. When a mental health disorder accompanies a chronic disease, healthcare costs rise by 72% [463]. The relationship runs in both directions:

Obesity: Depression raises the odds of developing obesity by 58%, and obesity raises the odds of developing depression by 55% [464].

Cancer: Depression and anxiety raise cancer incidence by 13% and cancer-specific mortality by 21% [465].

Heart Disease And Stroke: Depression raises the risk of coronary heart disease by 30% [466].

Diabetes: Depression raises the risk of type 2 diabetes by 37%, and the two occur together about twice as often as chance would predict [467].

Chronic Lung Disease (COPD): Depression or anxiety raises the risk of COPD onset or flare-ups by 43%, and COPD raises the risk of depression by 69% [468].

Alzheimer’s Disease And Dementia: Late-life depression raises the risk of all-cause dementia by 85% and Alzheimer’s disease by 65% [469].

Arthritis: Major depression affects 16.8% of people with rheumatoid arthritis [470].

Chronic Kidney Disease (CKD): More than one in four people with CKD are depressed, and depression raises their risk of death by 59% [471].

Treating the body while leaving the mind untreated leaves the multiplier in place.

The Vagus Nerve: The Gut’s Direct Line To The Brain Top

The vagus nerve is the main physical connection between the gut and the brain. About 80% of its fibers are afferent, meaning they carry information up from the gut and other organs to the brain, while only about 20% are efferent and carry commands down from the brain to the organs [35]. In other words, the gut does most of the talking. These ascending fibers report on stretch, nutrients, inflammation, and signals from gut bacteria, and they connect to brain regions that regulate fear, mood, reward, and appetite [35]. This is why a damaged gut barrier is not only a digestive problem. When the barrier fails, the signals traveling up the vagus nerve change, and the brain responds to those changes.

PTSD: In veterans and others with PTSD, the fear response stays active long after the danger has passed. In a sham-controlled study of people who had experienced trauma (but did not have a PTSD diagnosis), noninvasive stimulation of the vagus nerve reduced activity in fear-related brain regions while participants listened to recordings of their own trauma stories [36]. In rats, stimulating the vagus nerve during fear extinction training helped the animals unlearn conditioned fear and reduced PTSD-like symptoms [37]. These studies stimulated the nerve directly and did not test gut restoration. However, they show that the vagal pathway is a real lever on the fear circuitry, and the gut is the largest source of the signals that travel along it.

Depression And Suicidality: The vagus nerve also links the gut microbiome to depression [38]. In mice, a Lactobacillus strain reduced anxiety-like and depression-like behavior and changed GABA receptors in the brain, but these effects disappeared when the vagus nerve was cut [39]. Vagus nerve stimulation is FDA-approved for treatment-resistant depression, and a systematic review of neuromodulation treatments concluded that it may reduce suicidality, although the evidence is still limited [40]. If you are a veteran in crisis or having thoughts of suicide, dial 988 and press 1, or text 838255, to reach the Veterans Crisis Line. Anyone else can call or text 988. Gut restoration is meant to support mental health care, not replace it.

Anxiety: In rats, cutting the vagal afferent fibers from the gut reduced innate anxiety and altered how fear was learned [41]. In mice with colitis, gut inflammation signaled through vagal afferents to the amygdala, the brain’s fear center, and produced anxiety-like behavior. Interrupting that pathway reduced the anxiety [42]. An inflamed gut can send signals that drive anxiety.

Addiction: Vagal fibers from the gut feed directly into the brain’s reward system. In mice, stimulating vagal fibers from the upper gut triggered dopamine release and was rewarding enough that the animals worked to receive it [43]. This means the gut helps decide what the brain craves. In a small trial in alcohol-dependent men, ear-based vagus nerve stimulation improved depression and sleep during protracted withdrawal, but it did not reduce alcohol craving [44]. The vagus nerve is part of the craving circuitry, but stimulating it alone is not a treatment for addiction.

Weight Control: The vagus nerve carries fullness signals from the gut to the brain. In diet-induced obesity, vagal afferent neurons become less responsive to these satiety signals, which promotes overeating and weight gain [45]. In mice, removing leptin signaling from vagal afferent neurons caused overeating and obesity [46].

Other Conditions: Ascending vagal signals also contribute to interoception, the brain’s sense of the body’s internal state, and to the perception of gut pain [35]. Disturbed interoception is common in anxiety, depression, and PTSD.

The Anti-Inflammatory Return Path: The 20% of fibers that travel downward also matter. They form the cholinergic anti-inflammatory pathway, through which the brain signals the immune system to reduce inflammation in the gut and the rest of the body [47]. The loop is complete: the gut reports inflammation to the brain, and the brain sends signals back to calm it.

Caution: Most of this evidence comes from animal studies and from studies that stimulate the vagus nerve with devices. No human study has yet shown that repairing the gut barrier improves PTSD, depression, or suicidality through the vagus nerve. My expectation that it can is based on these pathways and my own experience.

How food composition shapes these signals, and why it led to the SR™ Flexible Carnivore design, is covered in Phase 1.

Why The Gut Barrier Is The Therapeutic Target

None of these variables operate in isolation. Mitochondrial decline, cellular senescence, immune aging, psychological stress, dietary insult, and microbial imbalance each contribute independently to the burden of chronic disease. However, the intestinal barrier is where these pathways converge and where their effects are translated into systemic consequences. A 2023 review further confirmed that understanding the interplay among the microbiome, the gut barrier, and the immune system is critical to piecing together mechanisms of age-related chronic disease [7].

This is why the SR™ Gut Barrier and Microbiome Restoration places gut barrier restoration at its center. Rather than treating downstream inflammation in individual organ systems, the protocol targets the barrier itself by rebuilding beneficial microbial populations, restoring SCFA production, supporting mitochondrial function in epithelial cells, managing oxalate burden, and addressing Candida overgrowth. By restoring intestinal epithelial integrity, the protocol aims to interrupt the feed-forward cycle of dysbiosis, translocation, and inflammaging at its source.

The SR™ Gut Barrier and Microbiome Restoration is organized around this principle: while chronic disease and aging involve many interacting variables, gut barrier dysfunction is the central convergence point where those variables become systemic disease; therefore, it is the barrier that must be addressed first.

How Oxalates, Candida, And Leaky Gut Shape Chronic Disease And Mental Health

New research is revealing that gut health may be the missing link between the body’s physical decline and emotional suffering. A 2024 study showed that a common gut yeast, Candida albicans, can cross the intestinal lining by damaging gut cells, a step the host immune response normally limits [20]. In mice, Candida that reached the bloodstream caused brain inflammation and memory deficits [22]. Candida translocation through the intestinal barrier into the bloodstream (leaky gut) is essential for systemic infection and inflammation [21]. Other findings highlight that an unbalanced microbiome, especially one lacking beneficial bacteria, can disrupt communication along the gut–brain axis, influencing mood, focus, and resilience [26]. Chronic diseases like cardiovascular disease, diabetes, arthritis, and cancer often involve persistent inflammation as a key mechanism [48].

An important part of this equation involves oxalates. Oxalates are naturally occurring compounds found in plants that, when the body can’t break them down efficiently, are stored in tissue and bone and become toxic when released. When oxalate-reducing microbes are depleted, these crystals can irritate intestinal tissue, damage energy-producing mitochondria, and further weaken the gut barrier. This allows more toxins and inflammatory signals to enter the bloodstream, intensifying symptoms of both chronic disease and mental distress [49].

The SR™ Gut Barrier and Microbiome Restoration targets these interconnected processes at their root. It helps restore beneficial microbes that metabolize oxalates, strengthen the intestinal lining, and calm the inflammation that drives physical illness and emotional imbalance. Rebuilding the gut ecosystem provides a realistic, science-based path to reversing the cycle of chronic disease and mental health disorders.

The Synergistic Trifecta Of Gut Homeostasis Top

The synergistic trifecta of gut homeostasis comprises gastrointestinal stem cells, the intestinal mucosa, and the gut microbiome. If any of these components is disrupted, it affects the other; therefore, all must be addressed simultaneously.

Gastrointestinal Stem Cells

The gastrointestinal stem cell produces all the adult cell lineages of the gastrointestinal mucosa and is thereby perceived as the most important regulatory element in gastrointestinal function [50]. Stem cell regeneration is the very foundation of recovering normal gut function. The endocannabinoid system (ECS) is a significant part of the stem cell equation because cannabinoid receptors are attached to the stem cells, and cannabinoid signaling regulates cell proliferation, differentiation, and survival [51].

Intestinal Mucosa

Tight junctions are integral molecular components of the intestinal mucosa, specifically within the epithelial cells that form the mucosal barrier [52]. Inflammatory bowel disease is characterized by cycles of mucosal injury and ulceration [53]. My question is, can any bowel disorder that may lead to over one hundred forty autoimmune diseases happen without a mucosal injury? I believe that, in most cases, the answer is no. The medical literature regarding DBS/IBS is unclear. Still, it should be absolutely clear, as one of the basic functions of the mucosal layer is to provide adequate containment of luminal microorganisms and molecules while preserving the ability to absorb nutrients [54]. This is what makes Akkermansia muciniphila a fundamental focal point of the SR™ Microbiome Protocol.

The Microbiota And Gut Microbiome

Microbiota refers to the collection of all the microorganisms, including bacteria, fungi, protozoa, and viruses, that inhabit a specific environment, such as the human gut, skin, mouth, or other body sites. Our primary focus will be on the microbiota, which affects the makeup of the microbiome.

Microbiome refers to the populations of microorganisms in the body’s various ecosystems (for example, the gut and skin microbiome). A comprehensive understanding of the microbes that dominate each system is still being discovered [55].

A breach in the mucosa can exacerbate immune reactions toward the microbiome [54]. This means that the immune system will attack the microbiome once the mucosa is breached. My Genova Comprehensive Stool Analysis indicated a very low bacterial diversity on the first test.

With the importance of this trifecta made clear, I established a protocol to heal the gut and clear the remaining symptoms. Some individuals can heal by modifying their diet, others can heal with probiotics, and still others can heal without intervention, allowing the autonomic regenerative processes of the mucosa to restore them. However, an intervention is mandatory for those who have become ill or chronically ill and cannot escape the disruption of the self-perpetuating cycle of the mucosa and microbiome. This cannot be stated emphatically enough, especially with anorexics who may have gotten to the point of not being able to eat because of severely damaged intestinal mucosa.

Oxalic Acid: A Ubiquitous Potentially Deadly Plant Toxin Top

Oxalic acid is a plant toxin found in virtually every fruit, vegetable, grain, and legume. If the gut microbiota cannot process these toxins, they accumulate in the body. Oxalates physically damage tissues via crystal formation and oxidative stress, disrupt the gut microbiome by suppressing oxalate-degrading bacteria, and contribute to kidney stones and biliary issues. The resulting disruption of the gut microbiome also creates an environment in which opportunistic Candida can overgrow. Through these interconnected mechanisms, oxalates lead to a myriad of disorders and diseases [14, 56]. People often overlook the liver and gallbladder when rebalancing the gut, but they are part of the equation and must be addressed effectively.

Oxalates are the most insidious of all plant toxins, as they are the only plant toxin that accumulates in virtually every tissue of the body, including bone [15, 57]. There are two primary ways to become poisoned by oxalates: endogenously (internally) through metabolism or exogenously (externally) through the diet. Endogenous poisoning is usually from a rare genetic disorder or A. Niger, which is a mold and also referred to as black mold.

Oxalic acid is a plant compound that is ubiquitous in the plant kingdom. It can damage tissue and ultimately slowly kill you if you consume large amounts of superfoods such as spinach, chocolate, Swiss chard, or almonds, among many others. However, several factors other than consuming large amounts of this can make one vulnerable to this toxin, which is embedded in one's bones and tissues. Humans should limit their oxalate intake to less than 150 mg per day. This recommendation is reduced to less than 50 mg per day if you have a history of kidney stones. If you eat more than 150 mg of oxalates per day, the question is not whether you are poisoned but how poisoned you are (Author’s Observation).

Oxalate Poisoning Mechanisms

Escherichia coli are commonly found within the nidus of calcium oxalate kidney stones and may play a pivotal role in stone genesis [58]. Candida albicans and Escherichia coli are also believed to be synergistic pathogens [59]. This is why some, such as Great Plains Labs, believe that Candida causes excess oxalate accumulation. In other studies, a higher-than-usual concentration of oxalate was found to inhibit many gut microbes, including the oxalate-degrading Oxalobacter formigenes, and was associated with dysbiosis and an enrichment of acid-tolerant pathobionts [18]. Candida is an opportunistic pathogen, and oxalate does not create it. However, a disrupted microbiome is one of the conditions that allows Candida to shift from a harmless resident to an opportunistic pathogen [23], so once oxalate disrupts the microbiome, it creates an environment conducive to Candida overgrowth (Author’s Observation). Once initiated, either mechanism becomes self-perpetuating and may eventually kill you unless you have a means of disrupting it. Death may not be directly from oxalate poisoning, but from the resulting disorders and diseases caused by being poisoned. I suspect oxalates when a death is determined to be a natural cause, especially if the person is under the age of 70 (Author’s Observation).

The question is: once either mechanism is initiated, how do you interrupt it and rebalance the microbiome? To be clear, oxalates are not the devil. The liver produces oxalates as part of our metabolic processes [60]. They bind with heavy metals and minerals and carry them out of the body. The issue arises when they accumulate in excess.

What Makes You Vulnerable To Oxalate Poisoning And A Disrupted Microbiome

• Stress
• Antibiotics
• Alcohol-Sugar
• Pharmaceutical or Illicit Drugs
• Ingesting Excessive Amounts of Oxalate-Rich Foods (More than 150 mg per day)
• Inflammation
• Inflammatory Foods

Oxalate Damage

Additionally, elevated plasma urinary oxalate has been associated with several other pathological conditions, including diabetes mellitus, obesity, autism, atherosclerosis, cardiovascular events, and neurological disorders. Patients with primary hyperoxaluria are particularly prone to oxalosis, a condition characterized by the presence of calcium oxalate deposits in various extrarenal tissues, primarily in the heart, smooth muscle cells of vessels, bones, skin, and other organs.

However, oxalate deposition has also been reported in non-primary hyperoxaluria patients, affecting extrarenal tissues such as the breast, lungs, thyroid gland, prostate, synovial fluid, and vascular tissues [14].

Systemic Manifestations of Oxalate Disorders [15]

Joints

• Arthritis
• Chondrocalcinosis of the metacarpophalangeal and metatarsophalangeal joints
• Spinal stenosis
• Synovitis
• Tenosynovitis
• Bursitis

Kidneys

• Acute tubular necrosis
• Interstitial fibrosis
• Nephrocalcinosis
• Kidney stones

Heart

• Arrhythmias
• Diastolic dysfunction
• Valvular abnormalities
• Impaired ejection fraction
• Infiltrative process

Skin

• Livedo reticularis
• Acrocyanosis
• Papules and nodules on the face and digits
• Non-healing ulcers

Eyes

• Retinal oxalate deposition

Nerve And Muscle

• Axon loss and Demyelination
• Polyradiculoneuropathies

Teeth

• Periodontitis
• Jaw bone and root resorption
• Dental mobility

Bone Marrow

• Erythropoietin-stimulating agent-resistant anemia

Bones

• Fractures
• Pseudo fractures
• Sclerosis
• Cystic bone changes
• Dense metaphyseal bands
• Increased bone density

Oxalates, Breast Cancer, And Prostate Health

Breast Cancer and Oxalates: Breast cancer is the most commonly diagnosed cancer worldwide [61]. In 2015, the effect of oxalates was first demonstrated in a human breast cell line. At that time, the mechanism by which oxalate exerts its action on breast cells was still largely unknown [62]. A 2023 study gained a much better understanding of the role of oxalates and microcalcifications in breast tissue [63]. Although a direct connection between breast cancer and oxalates has not been established, it is known that oxalates cause mitochondrial dysfunction [16], and mitochondrial DNA mutations are commonly found in cancer cells, which can promote the rewiring of bioenergetics and regulate tumor metabolism and progression [64].

BPH, Prostate Cancer, and Oxalates: Prostate cancer is the second most commonly diagnosed cancer and the fifth leading cause of cancer death among men worldwide [65]. Oxalates may cause benign prostatic hyperplasia (BPH) and prostate cancer; however, a direct link has not been established [14]. As stated above, however, there is clear evidence of oxalate-induced mitochondrial dysfunction [16, 64].

Lycopene Supplements vs Tomato Paste For Breast And Prostate Cancer

Lycopene consumption can reduce the blood concentration of insulin-like growth factor 1 (IGF-1), a key factor in the development of breast and prostate cancer. Therefore, lycopene’s reduction in this growth factor may reduce the risk of these cancers [66]. Many of these studies use tomato products such as tomato paste, tomato sauce, or tomato juice, but only report lycopene, even though there are many other constituents in the tomato lycopene equation. Grabbing a lycopene supplement in hopes of reducing cancer risk is ill-advised, as lycopene supplements can come with a host of contraindications. This is why, when it comes to lycopene, I only use organic tomato paste. For those concerned about lectins, the skin and seeds of the tomato contain the highest levels, which are removed during processing into tomato paste [66]. Lycopene is also an antifungal that induces apoptosis (cell death) in Candida [67].

Tomato Paste Dosing: Dietary ingestion of 50 g of tomato paste daily for 10 weeks significantly reduced mean plasma PSA levels in patients with benign prostate hyperplasia [68]. Organic tomato paste comes in 6-ounce cans. I took 3 ounces per day (84 grams) for 3 months to bring my PSA back to normal.

The Role of Sulforaphane and Cancer: Glucose (sugar) and glutamine are known to feed cancer cell growth [69, 70]. Sulforaphane triggers apoptosis through caspase activation. In prostate and colon cancer models, it disrupts mitochondrial membranes and elevates ROS selectively in tumor cells [71]. Sulforaphane derepresses tumor suppressors, alters DNA methylation, and targets cancer stem cells in gastric and lung cancers. Sulforaphane also enhances chemotherapy efficacy and immune function [72]. Broccoli sprouts are high in Sulforaphane, and you can also get it in supplement form.

Symptoms I Experienced From Eating High Oxalate Fruits, Vegetables, Grains, And Legumes

• Gallbladder and Liver Stones
• Bile Sludge
• Candida Overgrowth
• Hallucinations
• Paranoia
• Poor Sleep
• Suicidality (Suicidal Thoughts)
• Exhibited symptoms of ALS, Parkinson's, Alzheimer's, Aphasia, and Multiple Sclerosis
• Vertigo
• Neuromyelitis Optica
• Seizures
• Tremors
• Skin Peeling off Lips
• Severe Gait Abnormalities
• Axon Loss and Demyelination
• Arrhythmias
• Periodontitis
• Severe Chronic Fatigue
• Severe Brain Fog
• Plaque Build-Up on Lower Front Teeth
• Itchy Skin
• Large Amounts of Oxalate Crystals in My Eyes
• Excessive Earwax
• Dry Cough
• Itchy Throat
• Constipation
• Diarrhea
• Stiff Neck, Shoulder, Back, and Big Right Toe
• Ringing in the Ears (Tinnitus)
• Dizziness, Poor Balance
• Hypersensitivity to Light, Noise, and Odors
• Interstitial Cystitis (Bladder Pain)
• Enlarged Prostate
• ED

The reason the SR™ Gut Barrier and Microbiome Restoration is essential in mental health and chronic diseases is that consistent physiological processes occur in all chronic diseases and some, but not all, mental health disorders. Unless these processes are effectively addressed, mental health disorders and chronic diseases will remain chronic.

Once the microbiome is disrupted, you become vulnerable to oxalate accumulation and poisoning, regardless of what caused the disruption.

Why Collagen, Bone Broth, And Gelatin Should Not Be Used Top

Collagen, bone broth, and gelatin are among the most widely recommended foods for healing a leaky gut. They were also the first things I started with. At the time, I did not know that oxalates were at the root of my dysbiosis, and I did not know that I was causing more damage.

The Problem Is Hydroxyproline

Hydroxyproline is an amino acid found almost exclusively in collagen, the main protein in bone broth, gelatin, and collagen supplements. When the body breaks down hydroxyproline, the liver and kidneys convert part of it to glyoxylate, which is then converted to oxalate [73]. In other words, these foods contain little oxalate themselves, yet they supply the raw material the body uses to make its own.

This has been measured in people. In a controlled study of healthy adults, urinary oxalate excretion was 43% higher on a gelatin diet than on a whey protein diet, and urinary glycolate, another product of hydroxyproline breakdown, was 5.3 times higher [74]. The effect depends on the amount consumed. Single gelatin loads of 5 and 10 grams raised urinary oxalate, while loads of 1 and 2 grams did not [74]. Daily servings of collagen powder, gelatin, or bone broth fall in the range where the increase appears.

Oxalate made inside the body is not a minor source. A substantial share of the oxalate excreted in urine is produced endogenously rather than absorbed from food [75], and hydroxyproline from collagen-rich foods is one of the recognized dietary contributors to that endogenous load [56].

Glycine Is Not Hydroxyproline

Glycine is the most abundant amino acid in collagen. Roughly one in every three amino acids in collagen is glycine. Because of this, some people assume that glycine is what drives the oxalate increase from collagen, and that glycine taken on its own should be avoided for the same reason. That is not correct.

The 43% increase comes from hydroxyproline, not glycine. The two amino acids are handled very differently by the body. Hydroxyproline is broken down through a dedicated pathway that leads directly to glyoxylate and then to oxalate [73]. Glycine is used mainly to build proteins, glutathione, creatine, and other essential compounds, and only a small fraction of it is ever converted to glyoxylate.

This has also been measured directly. In a human tracer study, glycine infused at a normal physiological rate produced no detectable labeled oxalate in the urine, meaning glycine accounted for less than 5% of urinary oxalate [76]. Only when glycine was infused at a rate ten times higher, enough to raise blood glycine by 29%, did it contribute meaningfully to urinary oxalate. The authors concluded that glycine metabolism makes only a minor contribution to oxalate production under normal conditions [76].

The oxalate problem with collagen is not its glycine. It is the hydroxyproline that comes packaged with it. That is why glycine can be supplied on its own without bringing the oxalate load along with it.

Why This Matters For Recovery

For anyone whose dysbiosis includes oxalate overload, collagen, bone broth, and gelatin move recovery in the wrong direction. A low oxalate diet reduces what comes in from plants, but daily collagen, bone broth, or gelatin quietly adds oxalate back from the inside. A gut and kidneys already struggling to clear oxalate are handed more, and every oxalate dump further disrupts the microbiome (Author’s Observation). This is why collagen, bone broth, and gelatin are excluded from the SR™ Gut Barrier and Microbiome Restoration protocol whenever oxalates are part of the dysbiosis equation.

This does not mean the goal behind these foods is wrong. The gut lining still needs support. In this protocol, that support comes from zinc-carnosine and colostrum, along with the glutamine supplied naturally by meat. Glycine is supplied on its own in the Support Stack, without the hydroxyproline load that comes with collagen. As with every part of this protocol, discuss your choices with your MD and use the Oxalic Acid 24-Hour Urine Test to see where you stand.

The Constants Among All Chronic Diseases Top

The SR™ Chronic 9 combines the eight adult diseases named by the Make America Healthy Again (MAHA) Commission with mental health disorders. The question is, what do all these conditions have in common? They are all linked to a disrupted microbiome, Candida, and leaky gut. In some cases, it is a chicken-and-egg conundrum; nonetheless, there is still a solid link, and addressing the disrupted microbiome makes perfect sense.

1. Heart Disease and Stroke [77]
2. Cancer [78]
3. Diabetes [79]
4. Chronic Lung Diseases (e.g., COPD) [80]
5. Obesity [81-83]
6. Alzheimer’s Disease and Dementia [84, 85]
7. Arthritis [86]
8. Chronic Kidney Disease (CKD) [87]

Thoroughly revised estimates indicate that the typical adult human body comprises approximately 30 trillion human cells and about 38 trillion bacterial cells [88]. I am certain this will continue to be updated. The bottom line is that the human body has many more bacterial cells than human cells, which makes for a complex balancing act when attempting to correct a bacterial (gut microbiome) imbalance.

The symptoms of microbiome disruption are wide and varied, affecting each person differently. If oxalate poisoning is present, it is challenging to determine what is directly caused by oxalate dumping and what results from dysbiosis. Regardless, the damaged microbiome must be repaired, and this requires a systematic, focused effort. This is where the SR™ Gut Barrier and Microbiome Restoration comes in.

Restoring the microbiome involves multiple steps, and a literature review reveals that, although most probiotics are generally considered safe and beneficial for healthy individuals, caution is necessary when selecting and monitoring probiotics for patients with compromised immune systems, leaky gut, or critical illnesses [89]. For this and other variables, especially with extended fasting, you must engage a Functional Medicine MD.

Even if you are not poisoned by oxalates, you will still benefit from the SR™ Gut Barrier and Microbiome Restoration if you have any microbiome disruption, are experiencing any malaise, or are over the age of 40.

Candida: A Primary Driver Of The Chronic Disease Equation Top

Candida overgrowth is an overlooked piece of the chronic disease and mental health equation. When someone becomes inflamed or realizes they are oxalate-poisoned, managing symptoms from inflammation or oxalate dumping becomes the singular focus. However, it is absolutely critical that one understands the foundational mechanism of this inflammation.

Candida is one of the earliest and most common opportunistic organisms to overgrow when gut bacterial balance and host defenses are compromised [23]. The implications of this overgrowth are far-reaching and include all of The SR™ Chronic 9. If Candida is not immediately and effectively addressed, it can translocate to other parts of the body, including the brain, where it has been implicated in dementia. The reason it has been implicated is that Candida can form amyloid in human and animal tissues, significantly influencing biofilm formation, immune evasion, and possibly contributing to plaque-like pathology, including in the CNS [22].

Like oxalates, candida overgrowth is a slow, insidious process that manifests as multiple symptoms.

Why Candida Is Seen In The Majority If Not All Chronic Diseases

• A 2020 high-resolution mycobiota analysis study tracked GI colonizing Candida species expanding and translocating into the bloodstream of patients, confirming intestinal origin of bloodstream infections. The study indicated fungal dysbiosis and loss of anaerobic bacteria promoted this translocation [90].
• A 2024 study dissected fungal and host factors involved in intestinal epithelial translocation. Candida albicans populations in the gut serve as the main source of systemic infections, with translocation events linked to antibiotic use, immune suppression, and epithelial damage [20].
• A 2022 review described the process of Candida translocation through the intestinal barrier into the bloodstream as essential for systemic infection. It discussed three hypotheses for yeast presence in blood: mechanical lesions, "hitchhiking" on immune cells, and hypha-to-yeast transition, noting physical barrier disruption or immune cell transport could enable translocation [21].

Part 2: The Objectives Top

Objectives Of The SR™ Gut Barrier And Microbiome Restoration Top

Because microbiome disruption arises from multiple overlapping mechanisms, SR™ Gut Barrier and Microbiome Restoration is organized around three integrated core objectives, each with specific, actionable subobjectives to guide individualized recovery.

Objective 1: Testing – Build an Individualized Baseline

• Use a “test, don’t guess” strategy to create a data-driven starting point that safely guides intervention.
• Quantify and characterize dysbiosis using stool analysis and related markers to clarify microbial balance, diversity, and potential overgrowth patterns.
• Establish objective baselines for oxalate burden, nutrient status, and microbial balance so that correction strategies are precisely targeted rather than generalized.
• Assess oxalate load and oxalate-handling capacity to determine whether oxalate is amplifying microbiome suppression, mitochondrial stress, tissue irritation, or gut–brain axis symptoms.

Objective 2: Map Primary Mechanisms – Identify What’s Driving Disruption

• Clarify the clinical picture and root-cause model so that treatment aligns with root mechanisms, not just symptoms.
• Define the clinical problem and proposed mechanism: describe how oxalate burden, dysbiosis, Candida, and barrier breakdown (“leaky gut”) can mutually reinforce systemic inflammation and gut–brain axis disruption.
• Identify primary upstream disruptors of the microbiome by screening and prioritizing contributors such as:
  • Candida or fungal overgrowth and leaky gut
  • SIBO risk and FODMAP intolerance dynamics
  • Nutrient deficiencies and broader metabolic imbalances
  • Insulin resistance and metabolic risk, for example, fasting insulin trends
  • Thyroid dysfunction that may be linked to oxalate and intestinal stress
  • Restore the synergistic trifecta of gut homeostasis by supporting GI stem cell function, intestinal mucosal integrity, and microbiome diversity and function as interdependent recovery pillars.
  • Rebuild functional microbial capacity, including oxalate metabolism, to reduce oxalate burden and enhance mucosal resilience over time.

Objective 3: 3-Phase Recovery Implementation

• Apply Structure and Track Outcomes
• Organize the protocol into a clear, stepwise plan that improves tolerance, adherence, and measurable progress.

• Implement a three-phase framework: Assessment > Targeted Action > Stabilization and Maintenance, to sequence interventions logically and reduce the risk of overloading the system.
• Use tools such as the Gut Health Checklist and Food & Fitness Planner to track symptom trends, tolerance shifts, and inspect stools, creating feedback loops that refine the plan over time.
• Emphasize safety and adaptability by monitoring real-world responses and adjusting dosing, pacing, and priorities to prevent excessive microbial, metabolic, or oxalate-related stress.
• Establish and retain focus on mitochondrial health.

Part 3: Testing Top

Absence Of Evidence Is Not Evidence Of Absence Top

Diagnostic testing has measurable false-negative rates, and a negative or absent result does not prove that a condition is absent. Diagnostic error affects an estimated one in twenty US adults in outpatient care each year, roughly 12 million people, and about half of those errors have the potential to cause harm [91]. The National Academies of Sciences, Engineering, and Medicine concluded that most people will experience at least one diagnostic error in their lifetime [92]. The same logic applies to research: the failure of a study to detect an effect is not proof that no effect exists [93].

For anyone living with persistent gut and mood symptoms, this distinction matters. Standard workups are designed to rule out acute and structural disease. They are not designed to measure intestinal permeability, microbial imbalance, nutrient insufficiency, or oxalate burden. Behavioral health assessment that relies solely on the absence of positive findings may therefore underestimate need, and interventions targeting such presentations warrant evaluation on their outcomes rather than exclusion on the basis of negative workups. This is the foundation of the SR™ principle that follows: when symptoms persist, test, do not guess, and track the results over time.

Another major issue with Candida overgrowth is the inaccuracy of testing. I was tested multiple times over a decade via blood, urine, and stool, and only tested positive once. This can give one a false sense that the memory, gait, neurological, and cognitive issues may be caused by something else, and enable exponential proliferation of Candida, which is what happened to me. This is why the SR™ Gut Barrier and Microbiome Restoration begins with addressing Candida overgrowth. This assures a foundational approach that is not dependent on false negatives.

Why MDs Do Not Inform Patients Of Candida Tests' Inaccuracies

Public awareness of fungal disease is low; a 2019 national survey found that most adults in the United States had little familiarity with invasive fungal infections [94]. The lack of patient awareness around Candida and leaky gut test inaccuracies is likely influenced by a combination of technical challenges, limited provider education and awareness, clinical decision-making priorities, and communication barriers within healthcare settings (Author's Observation). A recommendation for all MDs who treat Candida and leaky gut is to tell their patients that the tests are unreliable.

Why So Many False Negatives For Candida And Leaky Gut

Candida Tests

Blood cultures miss ~50% of invasive candidiasis cases due to low fungal loads in blood, uneven distribution, and small sample volumes, delaying or preventing detection. Non-culture tests like PCR show pooled sensitivity of 73% but vary by sample type (whole blood performs better than serum), target genes, and detection limits (≤10 CFU/ml needed), with lower performance for certain species, such as C. parapsilosis or C. glabrata. Antigen assays (mannan, CAGTA, BDG) have sensitivities from 42-96% but often fail in uncomplicated candidemia or colonized patients without deep infection [95].

Leaky Gut Tests

Zonulin assays, a common marker, suffer from poor correlation with functional permeability tests like lactulose-mannitol due to commercial ELISA kits detecting unrelated proteins rather than true zonulin/prehaptoglobin-2, leading to unreliable negatives. Antibody tests for zonulin or occludin can yield false negatives in pediatrics (lacking norms) or under steroid suppression, while direct zonulin fluctuates naturally. Functional sugar tests remain the gold standard but still miss subtle permeability changes [96].

Test Do Not Guess: The Top 7 Top

If any score on your intake Burris Gut Health Checklist is 5 or above over the past 30 days, find a Functional Medicine MD who can order the following tests. After getting these tests, you will have enough data to order more tests if necessary, remodel the microbiome, and correct your dysbiosis

*Links to the following tests, tools, etc., are available at BurrisConnect.com.

1. NutrEval: NutrEval® is a blood and urine profile that evaluates over 125 biomarkers and assesses the body's functional need for 40 antioxidants, vitamins, minerals, essential fatty acids, amino acids, digestive support, and other select nutrients. SR™ Practitioners are not allowed to recommend vitamins or minerals, which makes this test a necessity. Once tested, you can see what you need and get approval from your MD.

Kelly Burris: NutrEval

2. Comprehensive Stool Sample: Several labs will do this, but Genova has refined its testing over the last few years, and most insurance companies will cover it. You will want to discuss this with your MD. The bottom line is that you need to comprehensively evaluate your microbiome. My before-and-after is listed below. Note that on the 9-22 test, I was not taking any probiotics. The improvement was from fasting and B vitamins only, and although there was a significant improvement, it was not remotely close to being enough.

Kelly Burris: Comprehensive Stool Test: 9-20

Kelly Burris: Comprehensive Stool Test: 9-22

3. Oxalic Acid 24-Hour Urine Test: Although results for oxalates are available in the NutrEval test, this one is considered the gold standard and my preferred option. The test below was administered after a 33-month low-oxalate diet. As you will see, the Reference Range is 3.6 to 38 mg, and my score was 70.1. Oxalate dumping is, at best, erratic, so it is possible to get a false negative, but all three tests I took were out of range. Before taking a test, I recommend going on a low-oxalate diet for at least 30 days. Low oxalate means less than 50 mg of oxalate daily. This will ensure a reasonably accurate test.

Kelly Burris: Oxalic Acid 24-Hour Urine Test

4. Vitamin D Test: I did this test through Quest because it is oddly not included in the NutrEval Test. The test below was done when I took 20 to 40,000 IU of D3 daily. I reduced it to 10,000 IU daily and got retested, and it was still high, so I reduced it again to 5,000 IU daily.

Kelly Burris: Vitamin D Test

5. SIBO Testing: Small Intestinal Bacterial Overgrowth (SIBO) occurs when fecal bacteria from the large intestine ascend into the small intestine. A reaction to FODMAPS may or may not be linked to SIBO, and it is critical to be able to tolerate FODMAPS to remodel the gut.

A SIBO test was one of the first things I did when I initiated my research on the gut over a decade ago, but there have been considerable advancements since then. Dr. William Davis, author of Super Gut, claims that a device called the FoodMarble Aire and FoodMarble Aire 2 is better than the clunky and hard-to-get SIBO test. I cannot attest to this because I have not tried it, so you will need to do your own research. The Aire device is also much less expensive than conventional testing.

6. Fasting Insulin Test: A Fasting Insulin test assists in determining insulin resistance, which is associated with cardiovascular or all-cause mortality in non-diabetic adults [97]. A fasting insulin test is also important because elevated insulin (hyperinsulinemia) is an early indicator of metabolic dysfunction and is strongly associated with type 2 diabetes [98].
7. Thyroid Test: Calcium oxalate crystals are commonly found in thyroid tissue, including in Graves’ disease, nodular thyroid disease [99, 100], and thyroid disorders can affect the quality of your voice [101]. I brought my tests into a normal range with seaweed (iodine) and started to get my voice back. People with hypothyroidism also have slow peristalsis, causing chronic constipation that may result in weight gain. This weight gain is mainly due to water retention and is unrelated to an increase in fat mass [102].

Your functional medicine practitioner can determine what other tests you may need based on these tests.

Stool Inspector

If you rated yourself a 5 or above on any question on your intake Burris Gut Health Checklist, you will need to inspect your stool regularly for bile sludge, which will show up as emerald green chunks or stone-shaped, and Candida, which is solid white, not to be confused with mucus, which is translucent (Author’s Observation). There is no literature on oxalates in stool, but I have found a correlation between tiny black specks in stool and other oxalate symptoms; however, many other explanations exist for this phenomenon. You will need an LED flashlight and 2.25 power reading glasses or stronger to do a thorough examination.

Oxalate, Nutrition, Glycemic Index, Food Intolerances, And Measuring Tools

• Oxalate.org: It is critical that everyone has a full understanding of oxalates and measures their intake. This site will enable you to calculate your oxalate intake, which should not be more than 150 mg per day. I have found Perplexity.AI and other AI sites helpful in calculating oxalate intake as well.
• MyFoodData.com: This site has several useful tools other than the stock nutritional tools. One I use is the Nutrient Ranking Tool. This tool enables you to select a nutrient and a food category to find the largest amount of that nutrient in the chosen food. You can also simply select all. This is very useful when attempting to lower histidine. Histidine can be decarboxylated to histamine by histidine decarboxylase [103].
• USDA: Considered the gold standard for food data, but I prefer how MyFoodData.com is laid out.
• GlycemicIndex.com: The Glycemic Index enables you to determine how fast a food is turned into glucose. This is also important to determine possible inflammatory foods.
• HowMany.wiki: The primary tool I use on this site is the Volume to Weight Converter. This is an important tool when detoxing from oxalate.
• Food Intolerances: This App covers FODMAPs, Histamine, Lactose intolerance, Fructose intolerance, Sorbitol intolerance, Salicylate intolerance (or aspirin intolerance), Gluten intolerance, celiac disease, and Multiple Allergy Profiles.
• Monash FODMAP App: The Monash app is FODMAP-only, but they do this very well.
• High Lectin Foods: This is a list by Dr. Gundry. There is no information on how he compiled this list, but Dr. Gundry is the super geek on lectins.
• Bristol Stool Form Scale: This scale establishes the guidelines for how your stool should look.

Part 4: The Probiotics Top

The Top 10 Probiotics

Increased Beneficial Microbes: Intermittent fasting (IF) regimens, such as Warrior/OMAD or ADF fasting, consistently enrich key probiotic taxa; This is why we call them The Top 10 Probiotics. However, they require consistency. You will also see how these 10 probiotics affect disease processes.

Key Genera/Species Enriched

1. Akkermansia muciniphila – increased (mucin-degrader) [104]
2. Lactobacillus spp. – significantly increased [104, 105]
3. Bifidobacterium spp. – significantly increased [104]
4. Coprococcus spp. – increased (SCFA-producer) [104]
5. Ruminococcus spp. – increased (SCFA-producer) [105]
6. Roseburia spp. – increased (butyrate-producer) [104]
7. Faecalibacterium prausnitzii – increased (butyrate-producer) [104]
8. Bacteroides fragilis – increased [104]
9. Parabacteroides distasonis – increased (human study) [106]
10. Bacteroides thetaiotaomicron – increased (human study) [106]

Gut Health Improvements

• Microbial Diversity: IF regimens tend to boost overall gut microbiome richness and diversity. A recent review noted that intermittent fasting often increases alpha diversity (species richness) and alters community composition in humans [107].
• SCFA Production: Fasting markedly increases SCFA-producing bacteria and SCFA levels. In animal models, intermittent fasting (time-restricted or alternate-day fasting) enriched SCFA-producers (e.g., Lactobacillus, Coprococcus, Ruminococcus) and raised fecal acetate, butyrate, and related SCFAs [105, 108]. Enhanced SCFA synthesis improves gut barrier function and anti-inflammatory effects.
• Gut Barrier & Inflammation: Extended IF improved intestinal barrier integrity and reduced gut inflammation. In mice with chemically induced colitis, time-restricted feeding and intermittent energy restriction, but not alternate-day fasting, repaired the leaky gut and suppressed colonic inflammatory markers [108]. Specifically, TRF reduced pro-inflammatory taxa (Escherichia coli, Shigella) and boosted anti-inflammatory microbes [105, 108], thereby protecting the mucosa and systemic immunity.
• Pathogen Reduction: IF reduced gut pathogens. In the above studies, colitis-associated bacteria (Enterobacteriaceae, including E. coli/Shigella) were inhibited by TRF, while beneficial strains rose [105, 108]. This dysbiosis correction correlates with reduced endotoxin and inflammation.
• Gastrointestinal Symptoms: In human trials, IF protocols eased gut symptoms. One 4-week IF study found significantly lower GI symptom scores (bloating, pain) in the twice-per-week fasting group (60 h total fasts) [109], suggesting better tolerance or reduced gut distress on IF.
• Metabolic/Gut Health Link: Improved metabolic outcomes accompanied by microbiome shifts. A 3-week IF program (five normal days + two 500–600 kcal “fast” days) produced ~3.7 kg weight loss and better cardiometabolic markers [106]. These benefits paralleled increases in P. distasonis and B. thetaiotaomicron, both inversely correlated with obesity/ASCVD risk factors [106]. Thus, IF-driven microbiome changes likely underlie broader gut and metabolic health gains.

In summary, Warrior/OMAD every day and 24 to 36-hour fasts every 2–3 days (or comparable IF schedules) enrich probiotics, such as Lactobacillus and Bifidobacterium, as well as other SCFA-producing genera, while increasing microbiome diversity [107]. These shifts coincide with higher SCFA output, a more substantial gut barrier, lower pathogen levels, and reduced gastrointestinal inflammation, which are hallmarks of improved gut health [105, 108].

Toxicity

The literature acknowledges the death of pathogens but overlooks the possibility that it may induce the release of toxins that can cause severe malaise. This is indicative of how much more research needs to be done on gut health. In my opinion, the feeling of being poisoned during a 16 to 36-hour fast, or any other form of fasting, will be the primary reason for ending a fasting protocol, not hunger.

How The Top 10 Probiotics Are Linked To The SR™ Chronic 9 Top

While it is critical to address environmental toxins, food additives, oxalates, and a myriad of other factors that disrupt the microbiome, it is equally crucial to understand how to reverse that disruption for individuals currently suffering. The probiotics listed below may not be commercially available, but they are free and effective for anyone who follows the SR™ Gut Barrier and Microbiome Restoration.

1. Heart Disease and Stroke

Akkermansia muciniphila

• Administration is linked to reduced aortic lesions and atherosclerosis [110]
• Linked to a decline in cardiovascular risk factors such as dyslipidemia and metabolic endotoxemia [110]
• Helps maintain gut barrier integrity, preventing bacterial toxins from entering circulation and causing vascular inflammation [110]

Lactobacillus spp. and Bifidobacterium spp.

• Multiple clinical trials demonstrate that specific strains of Lactobacillus and Bifidobacterium can significantly reduce cardiovascular risk factors, including cholesterol levels, blood pressure, and inflammatory markers [111]
• Consistently shown to reduce total cholesterol, LDL-C, and improve lipid ratios, particularly in hypercholesterolemic patients [112]
• A meta-analysis revealed probiotics can lower the risk of cardiovascular disease by improving lipid profiles and modulating inflammatory responses [113]
• Specific mechanisms of cardiovascular protection include: deconjugation of bile salts, cholesterol assimilation, production of short-chain fatty acids, inhibition of cholesterol synthesis, and improvement of gut barrier function [114]
• Bifidobacterium lactis Probio-M8 administered to patients with coronary artery disease showed synergistic benefits with conventional treatments, improving clinical efficacy, reducing inflammation, and lowering LDL-C levels [115]

Faecalibacterium prausnitzii

• Lower abundance is associated with increased cardiovascular risk factors such as hypertension, obesity, and inflammation [116]
• Produces butyrate, a short-chain fatty acid that protects vascular function and reduces inflammation [117]

2. Cancer

Akkermansia muciniphila

A large study reports that primary resistance to PD-1/PD-L1 (PD-1/PD-L1 inhibitors are anticancer drugs that allow the immune system to better attack cancer) is linked to gut microbiome composition, and that [118]:

• Antibiotics inhibited the clinical benefit of checkpoint inhibitors in advanced cancer patients.
• Relative abundance of Akkermansia muciniphila correlated with clinical response to ICIs.
• In mice, FMT from responders improved PD-1 blockade efficacy, while FMT from non-responders did not.
• Oral supplementation with A. muciniphila restored PD-1 blockade efficacy after non-responder FMT, via an IL-12–dependent mechanism and increased recruitment of specific T cells into tumor beds.

Roseburia spp.

• Acts as a protective marker for gastric cancer, particularly against peritoneal metastasis [119]
• Higher abundance is associated with a lower likelihood of gastric cancer peritoneal metastasis [119]
• Produces short-chain fatty acids, especially butyrate, which regulate inflammation and energy metabolism involved in cancer development [119]
• Lower abundance observed in breast cancer patients compared to healthy controls [120]

Ruminococcus spp.

• Higher abundance associated with reduced risk of peritoneal metastasis in gastric cancer [119]
• Significantly more abundant in non-metastatic gastric cancer patients [119]

Faecalibacterium prausnitzii

• Reduced abundance observed in various types of cancer, including colorectal cancer [121]
• Anti-inflammatory properties may help prevent tumor-promoting inflammation [121]

Parabacteroides distasonis

• Shown to attenuate tumorigenesis in experimental colorectal cancer models [122]
• Promotes intestinal barrier integrity, which may prevent tumor development [123]
• Inverse association with intestinal tumor burden [122]

3. Diabetes

Akkermansia muciniphila

• Consistently shown to help manage type 2 diabetes by improving glucose metabolism and insulin sensitivity [110]
• Animal and human studies demonstrate that A. muciniphila controls essential regulatory systems of glucose metabolism [110]
• Negatively correlated with fasting blood glucose, insulin resistance, and HbA1c levels [110]
• Pasteurized A. muciniphila has been shown to reduce insulin resistance and dyslipidemia in mouse models [124]
• Supplementation in overweight and obese individuals improves insulin sensitivity and metabolic parameters [125]

Bifidobacterium spp. and Lactobacillus spp.

• Meta-analysis of 15 randomized controlled trials showed that probiotic supplementation significantly decreased HbA1c, fasting blood glucose, and insulin resistance (HOMA-IR) in type 2 diabetes patients [126]
• Specific strains improve glycemic control and reduce diabetes-related complications [126]

Faecalibacterium prausnitzii

• Reduced abundance observed in diabetic patients [127]
• Higher levels associated with improved insulin sensitivity and better glycemic control [127]

4. Chronic Lung Diseases (COPD)

Lactobacillus spp. and Bifidobacterium spp.

• Development of COPD is associated with a reduction of Lactobacillus species in the gut microbiome [128]
• A Lactobacillus combination (L. reuteri GMNL-89 and L. paracasei GMNL-133) reduced lung inflammation and emphysema in a mouse model of COPD [129]
• Combined treatment of budesonide with Bifidobacteria and Lactobacilli effectively improves lung function and clinical symptoms in COPD patients [130]
• Meta-analysis of randomized controlled trials showed probiotics improved %FEV1 in COPD patients (MD = 3.02, 95%CI: 1.10, 4.93) [131]
• Lactobacillus rhamnosus and Bifidobacterium breve reduce inflammation in cigarette smoke-activated human macrophages, suggesting a protective effect against COPD development [132]

Parabacteroides distasonis

• Reduced in patients with COPD, suggesting a potential protective role [133]

5. Obesity

Akkermansia muciniphila

• Consistently shown to be inversely associated with obesity and weight gain [110]
• Mechanistically reduces fat mass development, metabolic endotoxemia, adipose tissue inflammation, and improves insulin sensitivity [110]
• Pasteurized A. muciniphila enhances its capacity to reduce fat mass development in mice [124]
• Human studies demonstrate a negative correlation between A. muciniphila abundance and obesity, BMI, and waist-to-hip ratio [125]

Bifidobacterium spp. and Lactobacillus spp.

• Meta-analyses support the potential of these probiotics to reduce obesity markers and BMI [134]
• Specific strains like L. gasseri have been shown to reduce abdominal visceral and subcutaneous fat areas [135]

Faecalibacterium prausnitzii

• Reduced abundance observed in obese individuals [127]
• Administration can ameliorate obesity through the production of butyrate and immunomodulatory effects [127]

6. Alzheimer's Disease and Dementia

Bacteroides thetaiotaomicron

• Administration in Alzheimer's disease mouse models (APP/PS1 transgenic mice) decreased amyloid-beta (Aβ) levels in the hippocampus and significantly improved memory function [136]
• Acts on the gut-brain axis to modulate neuroinflammation and amyloid pathology [136]

Coprococcus spp.

• Reduced abundance observed in Alzheimer's disease patients [136]
• Identified as a short-chain fatty acid producer that may have protective effects on brain health [136]
• Depletion is associated with increased neuroinflammation and cognitive decline [136]

Bifidobacterium spp. and Lactobacillus spp.

• Multiple studies show administration helps ameliorate cognitive impairment in Alzheimer's disease models [137]
• Reduces neuroinflammation and amyloid-beta deposition in animal models [137]

7. Arthritis

Faecalibacterium prausnitzii

• Oral administration in collagen-induced arthritis mouse model reduces disease severity and joint tissue damage [138]
• Decreases abundance of systemic immune cells producing IL-17, a key pro-inflammatory cytokine in rheumatoid arthritis [138]
• Modulates short-chain fatty acid profiles, increasing butyrate and decreasing lactate and acetate [138]
• Lower abundance observed in rheumatoid arthritis patients compared to healthy controls [139]

Roseburia spp.

• Significantly lower in rheumatoid arthritis patients compared to healthy controls [140]
• Associated with reduced occurrence of seropositive rheumatoid arthritis [141]
• As a butyrate-producer, it may have anti-inflammatory effects in joint tissues [140]

Ruminococcus spp.

• Alterations in abundance observed in rheumatoid arthritis patients [142]
• May play a role in modulating immune responses in arthritis [142]

8. Chronic Kidney Disease (CKD)

Akkermansia muciniphila

In a 5/6 nephrectomy rat model of CKD, supplementation with A. muciniphila (2×10^8 CFU/0.2 mL for 8 weeks) was reported to [143]:

• Suppress epithelial–mesenchymal transition (EMT) (a pro-fibrotic process)
• Restore disordered intestinal microecology (16S rRNA findings)
• Enhance intestinal mucosal barrier function
• Reduce renal interstitial fibrosis (anti-fibrotic effect)

Bacteroides fragilis

• Shown to ameliorate renal fibrosis in mouse models via decreasing lipopolysaccharide (LPS) levels and increasing 1,5-anhydroglucitol (1,5-AG) levels [144]
• May have protective effects against kidney disease progression [144]

Parabacteroides distasonis

• Alterations observed in CKD patients, suggesting a potential relationship with kidney function [123]
• Can modulate systemic inflammation and metabolic parameters that affect kidney health [145]

Bifidobacterium spp. and Lactobacillus spp.

• Shown to reduce uremic toxins in CKD patients, particularly p-cresol and indoxyl sulfate [145]
• May improve intestinal barrier function, reducing bacterial translocation and systemic inflammation in CKD [145]

9. Mental Health

The links between the Top 10 Probiotics and anxiety, depression, and sleep are covered in the next section, Effects Of The Top 10 Probiotics On Anxiety, Depression, And Sleep.

Conclusion

The evidence demonstrates that these specific probiotic bacteria play significant roles in the prevention and management of various chronic diseases. Their mechanisms of action include modulating inflammation, improving gut barrier function, producing beneficial metabolites like short-chain fatty acids, and regulating immune responses. While the evidence is strongest for certain bacteria in specific conditions (like Akkermansia muciniphila in metabolic disorders and Faecalibacterium prausnitzii in inflammatory conditions), research continues to expand our understanding of these complex microbe-host interactions in chronic disease.

Effects Of The Top 10 Probiotics On Anxiety, Depression, And Sleep Top

The Gut-Brain Axis: An Overview

The bidirectional communication network between the central nervous system and gut microbiome, known as the gut-brain axis, provides the foundation for understanding how probiotics may influence mental health. This complex system involves neural, immune, endocrine, and metabolic pathways that allow gut bacteria to impact brain function and behavior, including mood regulation and sleep patterns.

1. Lactobacillus spp.

Lactobacillus species have been extensively studied for their psychobiotic properties:

• Depression: In an 8-week open trial in patients with major depressive disorder, Lactobacillus plantarum PS128 significantly reduced depression scores [146].
• GABA Modulation: Lactobacillus rhamnosus JB-1 reduced anxiety-like behavior through modulation of GABA receptors and vagus nerve signaling in preclinical models [39, 147].
• Clinical Efficacy: In a randomized pilot trial, Lactobacillus casei strain Shirota reduced anxiety symptoms in patients with chronic fatigue syndrome [148].

2. Bifidobacterium spp.

Bifidobacterium species demonstrate significant effects on mood regulation and sleep:

• Brain Activation Patterns: Bifidobacterium longum NCC3001 reduced depression scores and altered brain activation patterns in patients with irritable bowel syndrome and comorbid anxiety [149].
• Cognitive Reactivity: A combination of Bifidobacterium bifidum W23, Bifidobacterium lactis W52, and other strains significantly reduced cognitive reactivity to sad mood, including rumination and aggressive thoughts [150].

3. Coprococcus spp.

• Population Studies: Large-scale microbiome analyses revealed that Coprococcus species were consistently depleted in individuals with depression, with their abundance positively correlating with quality of life scores [151].
• Dopamine Metabolism: Coprococcus was linked to the gut’s capacity to produce a dopamine metabolite, which correlated with better mental quality of life [151].

4. Ruminococcus spp.

• Abundance in Depression: Changes in Ruminococcus abundance have been reported in major depressive disorder, although findings differ between studies [152].

5. Roseburia spp.

• Butyrate Production: Roseburia species, as important butyrate producers, were found to be reduced in patients with depression [152].
• Sleep Quality: In healthy adults, greater gut microbiome diversity was associated with better sleep efficiency and longer total sleep time [153].

6. Faecalibacterium prausnitzii

• Major Depression: F. prausnitzii, one of the most abundant butyrate-producing bacteria in the human gut, was significantly reduced in patients with major depression [154].

7. Akkermansia muciniphila

• Mood: Evidence linking A. muciniphila to mood comes mainly from animal studies; human data are still limited.

8. Bacteroides fragilis

• Anxiety Behaviors: In a mouse model of autism-like behavior, B. fragilis reduced anxiety-like behavior and corrected gut permeability [155].

9. Parabacteroides distasonis

• Mood: Human evidence linking P. distasonis to mood is limited and inconsistent.

10. Bacteroides thetaiotaomicron

• Mood And Sleep: Evidence linking B. thetaiotaomicron to mood or sleep in humans is not yet available.

How The Top 10 Probiotics Are Affected By Candida Overgrowth Top

Beneficial Bacteria That Help Keep Candida in Check

Candida overgrowth and gut dysbiosis feed each other. Laboratory and animal research shows that several groups of beneficial bacteria antagonize Candida, and that losing them, for example after antibiotics, makes it easier for Candida to colonize the gut [156, 157]. Whether each of these groups is consistently depleted during Candida infections in people has not been established, so the list below is based on what each group does against Candida.

Key Beneficial Bacteria

1. Lactobacillus spp.

Lactobacillus species directly antagonize Candida [158]. Under normal conditions, these beneficial bacteria:

• Produce lactic acid that maintains an acidic environment inhospitable to Candida
• Generate hydrogen peroxide with antifungal properties
• Compete with Candida for adhesion sites on epithelial surfaces
• Produce specific anti-Candida compounds

Their loss creates a more favorable environment for Candida, and their interactions with Candida have been documented in both the gut and the vagina [156]. Multiple studies demonstrate that Lactobacillus species can inhibit Candida growth and biofilm formation [159], suggesting a reciprocal antagonistic relationship.

2. Bifidobacterium spp.

Bifidobacterium species also antagonize Candida [160]. These beneficial bacteria normally:

• Produce acetic and lactic acids that inhibit Candida growth
• Compete with Candida for nutrients and adhesion sites
• Support immune function through interaction with gut-associated lymphoid tissue
• Maintain gut barrier integrity

Loss of Bifidobacteria contributes to dysbiosis and weakens gut defenses. In laboratory studies, bifidobacteria produced compounds that act against Candida and its biofilms [160].

3. Faecalibacterium prausnitzii

In mice, F. prausnitzii inhibited Candida colonization and reduced Candida-aggravated colitis [161]. This keystone species:

• Is a major butyrate producer in the human gut
• Has significant anti-inflammatory properties
• Supports intestinal barrier function
• Regulates immune responses

Its loss may contribute to increased inflammation and compromised gut barrier function, creating conditions that further promote Candida colonization and invasion [161]. The anti-inflammatory properties of F. prausnitzii appear particularly important, as inflammation can further disrupt microbial balance and enhance conditions favorable to Candida.

4. Roseburia spp.

Roseburia species are butyrate producers whose loss is associated with several diseases [162], and Candida colonization alters how the gut bacterial community recovers after antibiotics [157]. These bacteria:

• Produce butyrate that nourishes colonocytes
• Support gut barrier integrity
• Have anti-inflammatory effects
• Contribute to colonization resistance against pathogens

Their depletion may facilitate Candida adhesion and invasion of the intestinal epithelium by reducing butyrate production and increasing intestinal permeability [162]. Like F. prausnitzii, Roseburia species contribute to maintaining a healthy gut environment that naturally restricts Candida overgrowth.

5. Ruminococcus spp.

Ruminococcus species are among the commensal bacteria that interact with Candida in the gut [156]. These bacteria:

• Ferment complex carbohydrates
• Produce short-chain fatty acids
• Participate in cross-feeding relationships with other beneficial bacteria
• Contribute to overall microbial community stability

Their loss impairs gut metabolism and may contribute to a dysbiotic environment that favors Candida proliferation [156]. The metabolic activities of Ruminococcus help maintain a diverse and stable gut ecosystem that is more resistant to pathogen overgrowth.

Additional Considerations

An important question in understanding the relationship between Candida and gut bacteria is whether bacterial depletion precedes Candida overgrowth or results from it. Evidence suggests both mechanisms may occur [156, 163]:

• Pre-existing dysbiosis (often from antibiotic use) can create conditions favorable for Candida proliferation
• Once established, Candida can further suppress beneficial bacteria through various mechanisms, including pH alteration, toxin production, and competition for resources
• This creates a potential cycle where initial dysbiosis enables Candida growth, which further exacerbates microbial imbalance

Variations By Infection Type

The pattern of bacterial depletion may vary depending on [163]:

• Location of infection (oral, vaginal, intestinal, systemic)
• Candida species involved (C. albicans vs. non-albicans species)
• Host immune status and underlying conditions
• Severity and chronicity of infection

Research focusing specifically on gut microbiome changes provides the most direct evidence for the patterns described above, while systemic infections may have more complex and widespread effects.

Conclusion:

Based on NIH-published research, the beneficial bacteria with the clearest activity against Candida are:

• Lactobacillus spp. [158, 159]
• Bifidobacterium spp. [160]
• Faecalibacterium prausnitzii [161]
• Roseburia spp. [157, 162]
• Ruminococcus spp. [156]

Loss of these beneficial bacteria creates a favorable environment for Candida by reducing competition, altering the gut environment, and compromising barrier function. In mice, commensal anaerobes, including clostridial Firmicutes and Bacteroides, are also critical for resisting Candida colonization [164], and antibiotics combined with mucosal damage and low immunity allow Candida to spread [163]. The roles of Coprococcus spp. [156] and Akkermansia muciniphila are less clear.

Understanding these microbial dynamics offers potential therapeutic approaches, including targeted probiotic supplementation to restore these bacteria and create conditions less favorable for Candida overgrowth. Future research should further clarify the temporal relationships and mechanistic interactions between Candida and specific bacterial species.

I could go on with many more disorders and diseases caused by a microbiome disruption, but that would require another book. For now, I hope this drives home how important a balanced microbiome is.

Part 5: The Protocol Top

Assume And Implement Top

I am a big believer in the Test-Do-Not-Guess approach, which works well regarding vitamins, minerals, amino acids, and heavy metals, among others. However, testing for conditions like Candida and intestinal permeability (leaky gut) is highly inaccurate, which can exacerbate damage. I am not saying do not get tested for Candida and leaky gut (Zonulin and LPS tests), what I am saying is that if you have been suffering with the myriad of symptoms or even just one symptom, it is better to assume and implement foods and supplements, Not Medications, that will begin addressing these processes, regardless of attempted diagnosis. No one discusses the issue of false negatives in Candida and leaky gut testing, and I am unable to explain it.

Candida can cause or exacerbate leaky gut syndrome by damaging intestinal barrier integrity and promoting increased permeability [165]. One of the many reasons we initiate the SR™ Gut Barrier and Microbiome Restoration with the eradication of Candida, along with dietary adjustments and supplements, is to heal the intestinal mucosa and tight junctions so that only what is meant to get through actually does, and nothing else.

Candida Eradication: More Than Just Killing It

There are several components to consider when eradicating Candida overgrowth.

• Break down Candida Biofilm
• Inhibit Candida growth primarily through the production of lactic acid
• Use Natural antimicrobial compounds that directly damage Candida cells, leading to loss of metabolic activity and cell death.
• Inhibit Candida growth and damage fungal cell walls
• Use natural compounds that can stimulate epithelial cells to secrete immune mediators (e.g., IL-8 and IP-10) that enhance clearance of Candida infections.
• Use probiotics that exhibit aggregation abilities that help them outcompete Candida and impede its growth.

*We Use Foods, Not Meds, That Can Accomplish This

Multiple meta-analyses demonstrate that probiotic supplementation improves cognitive function in patients with AD and Mild Cognitive Impairment (MCI). Treatment with probiotics improved Mini-Mental State Examination (MMSE) scores in AD patients and reduced inflammatory markers. These effects likely occur through restoration of gut microbiota balance, reduction of systemic inflammation, and modulation of the gut-brain axis [166].

Candida albicans is the most common Candida species and cannot be controlled until the body's oxalate levels are within a safe range (Author’s Observation). There is, however, some question as to whether Candida contributes to oxalate crystal formation. Nonetheless, Candida and oxalates are self-perpetuating mechanisms. This is one of the primary reasons so many people report that it keeps coming back. One can have a Candida flare-up without oxalates, but it is highly unlikely that it is not part of the equation. Candida is classified as a yeast and fungus, and its fungal form is the most aggressive and tenacious when restoring the microbiome [167].

For Women: Recurrent Vaginal Candidiasis

If C. albicans were cultured from the vagina, it was always found in the stool. Conversely, if it was not isolated from the stool, it was never found in the vagina. These data are presented as an explanation for the recurrent nature of Candida vaginitis. Thus, a cure for vaginitis would not be possible without prior eradication of C. albicans from the gut [168]. This mechanism is one of the many reasons that Lactobacillus rhamnosus GR-1 and L. reuteri RC-14 rank first on our extended fermentation list.

It is estimated that 75% of females will have a yeast infection at some point in their lives. This completely discredits the notion that yeast overgrowth is primarily found in immunocompromised people.

Candida Overgrowth Home Test

Among the foods I have used to target Candida overgrowth, Nori seaweed stands out as particularly effective. However, its impact may vary from person to person, and it is important to proceed cautiously and monitor your response.

How To Use Nori Seaweed For Candida Testing

1. Start Slowly: If you have never eaten roasted seaweed, begin by testing a single sheet. Observe your body’s response for any adverse reactions.
2. Prepare the Test Meal: After confirming tolerance, tear 4 full sheets of Nori seaweed into small pieces and mix them into ½ to 1 cup of Bulgarian yogurt. Stir thoroughly and consume.
3. Inspect Stool: Use a high-intensity flashlight to examine your stool. If you notice solid white discharge, scoop it out, place it in a freezer bag, and freeze it for possible lab testing.
4. Repeat and Escalate: On day 2, repeat the process with 6 sheets of seaweed. On day 3, use 8 sheets. Continue to monitor your stool for changes.

Yogurt And Alternatives

Bulgarian yogurt is generally well tolerated because its longer fermentation reduces lactose, and A2 varieties should be chosen whenever possible (see Why A2 Half And Half Only). If yogurt is not suitable for you, you can use the seaweed sheets to roll up your regular meals.

Important Considerations

• Monitor for Die-Off: Candida die-off can cause temporary discomfort. Adjust the dose if symptoms become severe.
• Lab Testing: If you suspect Candida overgrowth, consult a healthcare provider for comprehensive testing. The home test can help guide your approach, but should not replace professional evaluation.

Bringing The Microbiome Back Into Balance

Candida is very good at adapting. However, there are 3 things Candida cannot adapt to: starvation via fasting, extended-fermentation yogurt, and seaweed (Author’s Observation). After trying every form of fasting, I came to realize that the two most effective fasting protocols are ones you can do consistently: the Warrior (4-hour eating window) and OMAD (one meal a day).

SR™ 3 Phase Gut Barrier And Microbiome Restoration

Of everything in this protocol, CoreBiome tributyrin in Phase 2 produced the most significant change I experienced. I believe that is because Phase 1 had already prepared the ground; it is the last piece, not a shortcut (Author's Observation).

I started slowly with all of it. Every component of this protocol produced Candida die-off for me, and the combination produced a lot of it. I added one component at a time, began at the lowest amount, held it for several days, and increased only as my symptoms allowed. I kept a daily note of stool, sleep, energy, and any flu-like symptoms. When a component caused symptoms I could not tolerate, I dropped back to the previous amount rather than stopping.

Phase 1: Warrior/OMAD Flexible Carnivore Diet

Glycine, Extended Fermentation Yogurt, Nori Seaweed, And Walnuts

Phase 2: CoreBiome Tributyrin

Oregano Oil, Black Seed Oil, Or Nystatin As Backups

Phase 3: Mitochondrial Restoration

24 To 44 Hour Fast And Olive Oil Flush

The Support Stack used during all three phases is described in its own section, immediately after Phase 3.

Phase 1: Warrior/OMAD Flexible Carnivore Diet Top

Glycine, Extended Fermentation Yogurt, Nori Seaweed, And Walnuts

What The Gut Tells The Brain: The Case For Flexible Carnivore

Every meal sends a message to the brain. Specialized cells in the gut lining, called neuropod cells, form direct connections with vagal neurons and relay information about nutrients, such as sugar, to the brain within milliseconds [169]. What you eat shapes what the vagus nerve reports, and that in turn shapes appetite, mood, and cravings. The SR™ Flexible Carnivore design is built around this.

Protein: Digested protein releases peptides and triggers gut hormones, such as CCK, GLP-1, and PYY, that signal fullness through the vagus nerve [170]. This is one reason a protein-centered meal satisfies longer than a carbohydrate-centered one.

Fat And Sugar: In mice, fat and sugar activate separate gut-to-brain vagal circuits. When they are eaten together, the two circuits combine to drive overeating beyond what either causes alone [171]. Removing added sugar breaks this pairing. This is a central reason the SR™ Flexible Carnivore approach eliminates sugar while keeping natural animal fats.

Removing Irritants: Processed food additives, such as emulsifiers, promote low-grade intestinal inflammation [172], which alters the signals traveling up the vagus nerve. Eliminating processed foods removes these irritants.

Fiber, Protein, And Short-Chain Fatty Acids: The approach is flexible, not strictly carnivore, because fiber matters too. When gut bacteria ferment fiber, they produce short-chain fatty acids, which activate vagal afferent neurons and suppress food intake [173]. Without fiber, bacteria can still make some short-chain fatty acids from protein and from the gut’s own mucus [472, 473], but neither is a substitute when the gut is damaged. Protein fermentation also produces ammonia, p-cresol, and hydrogen sulfide, which promote inflammation and gut permeability [474], and an all-animal diet shifts the microbiome away from butyrate producers toward inflammation-linked species such as Bilophila wadsworthia [475]. In mice, even intermittent fiber deprivation led gut bacteria to feed on the protective mucus layer and erode it [476]. Fiber lowers the toxic byproducts of protein fermentation [477] and keeps bacteria fed without consuming the mucus barrier. If there is gut damage, fiber is not optional.

Walnuts And Seaweed: Walnuts are the protocol’s most proven fiber source for the microbiome. In a controlled feeding trial, 42 grams of walnuts daily for three weeks increased the butyrate-producing bacteria Faecalibacterium and Roseburia and lowered proinflammatory secondary bile acids [478]. Nori contributes differently. Its fiber, porphyran, is digested by gut bacteria carrying genes that are common in Japanese populations, who eat seaweed daily, but absent in North American gut data [479]. For most Western guts, nori’s value in this protocol is its anti-Candida effect alongside extended fermentation yogurt (Author’s Observation), not short-chain fatty acid production. Along with inulin and pumpkin, these foods keep the gut fed through Phase 1, and tributyrin is added in Phase 2 to deliver butyrate directly.

Serotonin: Approximately 90% of the body’s serotonin is made in the gut, mainly by enterochromaffin cells [174]. Gut serotonin does not cross into the brain. Instead, it activates vagal nerve endings that relay signals to the brain [174]. A healthier gut lining supports healthier serotonin signaling.

Is Fat Satiating?

When fat reaches the small intestine, it triggers the release of cholecystokinin (CCK), a hormone that activates vagal afferents and signals fullness to the brain [175]. In my experience, as with other carnivores, fat is highly satiating, and a meal of fatty meat keeps me full for many hours. Some mouse studies seem to contradict this. In mice fed high-fat diets, vagal satiety signaling became blunted, and the animals overate [45, 176]. However, these were refined, obesogenic laboratory diets that typically combine fat with sugar or starch, not whole animal fat eaten without sugar. No human study has yet tested whether whole-food animal fat, eaten without sugar, blunts vagal satiety signaling. The flexible design accounts for this: fat comes from whole foods, sugar is removed, and fiber is added back.

In a survey of 2,029 adults following a carnivore diet, participants reported few adverse effects, high satisfaction, and improvements in health and well-being [177]. However, the results were self-reported, the participants chose to respond, and there was no control group, so the findings cannot prove that the diet caused the improvements.

SR™ Fasting And Flexible Carnivore Considerations

• Oxalate Dumping
• Candida Die-Off
• Bile Sludge
• Fat to Protein Ratio
• Mineral Balance
• Supplements
• Glycine Balance
• Water

Note: Bone broth, a staple of many carnivore diets, is excluded from this protocol whenever oxalates are a factor. See Why Collagen, Bone Broth, And Gelatin Should Not Be Used in the oxalate section.

Fat To Protein Ratio

Even though this diet contains some carbs, I still found it necessary to pay attention to how much fat I ate. If constipation is an issue, then I was not eating enough fat. I did not eat just any fat. Vegetable oils (grain oils) or seed oils were not a consideration. If you are cooking with it, the smoke point is also a consideration. Ghee, for instance, has a much higher smoke point than butter, so I do not use butter or olive oil for cooking.

Top 6 Fats

• First, Cold-Pressed Organic Extra Virgin Olive Oil DPO/PDO Designation and low phthalates
• Organic Ghee from Grass-Fed Cows with low phthalates (Ghee is higher in SCFAs than Butter)
• Organic Butter from Grass-Fed Cows, if tolerated, with low phthalates
• Organic Tallow from Grass-Fed Cows with low phthalates
• Organic Virgin Coconut Oil with low phthalates

There are many more good ones; these just happen to be the ones I use.

Flexible carnivore, in its most simplistic terms, is meat, fat, water, and salt.

The Warrior designation means it is a 20-hour fast with a 4-hour eating window. The Flexible designation of this diet is because it is not purely carnivore. This is because when the body detects low or no oxalate intake, it begins purging the oxalates stored in the body (Author’s Observation). This is why it is important to come off them slowly; oxalates are toxic and abrasive to the gut's mucosal lining. Additionally, the introduction of Candida die-off and bile sludge, which can be caused in part by oxalate dumping, can make the process extremely unpleasant.

Working up to this must be implemented slowly because if you are severely infected with oxalates, Candida, and bile sludge, the malaise from this combination can be catastrophic.

Acclimation To Fasting And The Flush

Phase 1 is where I prepared my body for Phase 3.

• The eating window. I did not jump straight to Warrior. I closed my eating window a little at a time until I reached a 4-hour window. That got my body used to going longer without food before I attempted the 24 to 44 hour fasts.
• Olive oil. I took 1 to 2 ounces of olive oil before my first meal. That got my gallbladder and digestion used to a concentrated dose of olive oil before the full flush (Author's Observation).

Phase 1 Implementation Top

I prefer the OMAD protocol, but I do Warrior because of the timing needed for the Phase 2 backups and the scheduling of colostrum. I choose my 4-hour window from 10 AM to 2 PM and fit all my food and two doses of colostrum and zinc carnosine at the beginning and end of this window. I take 10 grams of colostrum, mixed with water, and take zinc carnosine one hour before I eat and again an hour after I eat. I sometimes mix colostrum into extended-fermentation yogurt, as colostrum works synergistically with yogurt. Any 4-hour window that works for you will work. The colostrum did not seem to elicit any improvement after 30 days.

Glycine

Glycine is taken throughout all three phases. Its role in gut barrier and Candida support is covered under Support 3: Glycine, and its broader benefits are covered under Glycine in Amino Acid Uses, Toxicity And Side Effects.

Why Glycine Repairs The Gut And Rebalances The Microbiome

Restoring the gut barrier and microbiome requires multiple mechanisms working together, including diet, fasting, probiotics, colostrum, zinc-carnosine, and the rest of the Support Stack. Based on my results, glycine is the foundation the other mechanisms build on (Author’s Observation). It supplies the raw material for the gut wall, the antioxidant that protects it, and the signals that calm inflammation and favor beneficial bacteria. The six effects below explain why.

1. It Rebuilds The Structure Of The Gut Wall. Roughly one in every three amino acids in collagen is glycine, and collagen forms the supporting framework beneath the intestinal lining. The body makes about 3 grams of glycine a day and gets 1.5 to 3 grams from food. That may fall about 10 grams a day short of what collagen synthesis alone requires [178]. A gut repairing itself on a glycine shortfall is building without enough material.
2. It Seals The Barrier. Under cellular stress, glycine preserved the tight junction proteins that hold intestinal cells together and reduced cell death in the intestinal lining [179]. Human intestinal cells take up glycine through a dedicated transporter, GLYT1, and that uptake is what protects them from oxidative damage [180].
3. It Supplies The Gut’s Antioxidant Defense. Glycine is one of the three building blocks of glutathione. In older adults, glutathione deficiency was corrected by supplementing glycine with cysteine [181]. The intestinal lining relies on glutathione to withstand the oxidative stress of inflammation, toxins, and die-off.
4. It Calms The Immune Cells In The Gut Wall. Immune cells carry glycine-gated chloride channels, and when glycine activates them, the cells react less to bacterial toxins [182]. In piglets given bacterial endotoxin (LPS), glycine improved the structure of the intestinal lining and suppressed the TLR4 and NOD inflammatory pathways that bacterial toxins switch on [183]. In rats, a glycine-enriched diet protected against two chemically induced forms of colitis, reducing diarrhea, weight loss, ulceration, and inflammatory cytokines in the colon [184].
5. It Strengthens The Mucus Layer And Local Immunity. In weaned piglets, a diet containing 2% glycine increased intestinal mucins, the protective proteins of the mucus layer, along with secretory IgA and the antimicrobial peptides beta-defensin 2 and 3. At the same time, it lowered the inflammatory cytokines TNF-alpha, IL-1 beta, and IL-6 [185].
6. It Shifts The Microbiome Toward Beneficial Bacteria. In the same study, glycine reduced potentially harmful bacteria, including Escherichia-Shigella and Clostridium, and increased short-chain fatty acid producers, including Blautia, Lachnospiraceae, Anaerostipes, and Prevotella [185]. Short-chain fatty acids are the main fuel for colon cells and help keep the barrier sealed. Glycine also interferes with how bacteria build their cell walls [186], which may help explain its effect on bacterial biofilms.

Warning: Taking glycine in therapeutic amounts (above 15 grams per day) before bed can cause hypersensitivity to morning light, so that normal morning sunlight or indoor lighting feels harsh, and your sleep and wake times can shift further than expected (Author’s Observation). This has not been tested directly in humans, but the mechanism is plausible. Glycine promotes sleep and lowers core body temperature by acting on NMDA receptors in the suprachiasmatic nucleus, the brain’s master clock [187]. Those same NMDA receptors are the main pathway through which light resets the master clock [188]. In mouse brain tissue, glycine applied directly to the master clock shifted its rhythm, and the direction of the shift depended on the time of day it was applied [189]. In humans, 3 grams of L-serine, the amino acid the body uses to make most of its glycine, taken before bed enhanced the shift in the body clock produced by bright light the next morning [190]. If you notice this sensitivity, move more of your daily glycine earlier in the day, reduce the bedtime portion, and ease into morning light rather than going straight into bright sunlight. Discuss any dosing changes with your MD.

Oxalate And Vitamin B6: Glycine is not hydroxyproline, and its contribution to oxalate is far smaller, but it is not zero. In a human tracer study, glycine accounted for less than 5% of urinary oxalate at normal blood levels, but it contributed meaningfully when infused at ten times that rate [76]. At therapeutic doses, a small percentage of a large intake can still add to your oxalate load. Vitamin B6 helps counteract this. The liver enzyme that converts glyoxylate, the immediate precursor of oxalate, back into glycine is alanine:glyoxylate aminotransferase (AGT), and it requires P-5-P, the active form of vitamin B6, as its cofactor [191, 192]. When AGT works efficiently, glyoxylate is recycled into glycine instead of being oxidized to oxalate. In cell studies, adding vitamin B6 made AGT more effective and lowered oxalate and glyoxylate output [191]. In a clinical trial in primary hyperoxaluria type 1, a genetic disorder of AGT, vitamin B6 lowered urinary oxalate by an average of 25.5% [192]. Because that trial used high doses in a genetic disorder, the size of the benefit in people without it has not been established. Test your B6 status (Test, Do Not Guess), use the P-5-P form rather than pyridoxine HCl, and see the warning under B6 (Pyridoxine).

Glycine Dosing

In a single-patient case report on refractory obsessive-compulsive disorder and body dysmorphic disorder, glycine at 0.6 to 0.8 grams per kilogram per day was used over 5 years, with marked improvement in both disorders and no reported adverse effects [193]. In my experience, 15 grams per day is a good maintenance dose, and above 15 grams is a therapeutic dose (Author’s Observation). I saw a noticeable improvement in gait and balance at 10.5 grams (1 tablespoon) of Microingredients glycine twice daily and never past 3 PM. I mix the glycine into my extended fermentation yogurt. When starting any new therapeutic, begin slowly with one teaspoon once per day, then increase from there. Everyone's optimal therapeutic dose will be different, so working closely with your functional medicine practitioner is imperative.

Why I Do Not Use Glutamine Powder

Glutamine is one of the most commonly recommended supplements for repairing the gut lining, and it was part of my original protocol. I removed it. The glutamine powder was inflammatory for me, and I do not need it because I get my glutamine from meat.

This is also one of the reasons I believe so many people recover when they switch to a carnivore diet. Glutamine is the primary fuel for the cells that line the small intestine, and it helps maintain the tight junctions that seal the gut barrier [194]. Meat is a rich natural source of glutamine, so a carnivore diet provides more of it daily through food, without a powder. If you are considering glutamine supplementation for a specific reason, discuss it with your MD.

My meals consist primarily of grass-fed, grass-finished beef with wild-caught salmon, shrimp, or scallops twice a week and two to six organic pastured egg yolks at every meal. For dessert, I have one cup of extended fermented yogurt with four to six full sheets of Nori seaweed and two teaspoons of glycine. Other seaweeds can be used, but Nori is low in iodine, and it would be difficult to overdose on it. Iodine is a mineral that very few people get enough of, but no worries when you are eating six sheets of Nori seaweed per day.

I use vitamins and minerals that showed up as deficient on my tests. Minerals and B vitamins took the biggest hit from the oxalate poisoning. I do not randomly take vitamins and minerals, nor do I follow recommendations from anyone. I go by the test data only.

What is the objective of this food? You must ask this question about any food you eat outside the carnivore diet. The following are the non-carnivore foods I kept, along with my reasoning.

• Lemon Juice: I kept the lemon juice because it contains citrate, which binds calcium in the urine and helps prevent calcium oxalate crystals from forming, and I use it to take shots of olive and avocado oil.
• Seaweed: My metabolic test indicated low thyroid hormone levels, and my voice quality was poor. Seaweed is rich in iodine. Nori seaweed is low in iodine, but others can be high, so you may need to calculate how much you eat if not using Nori.
• Organic Unsweetened Shredded Coconut: I avoid the reduced-fat versions of this. Shredded coconut is the most potent parasite killer I have found and goes great with pumpkin pie (Author’s Observation).
• Crustless Unsweetened Pumpkin Pie: A good Candida killer; however, Candida can adapt (Author’s Observation).

Temporary Oxalate Foods For Reduction Of Oxalate Dumping Symptoms

• Organic Walnuts: Organic walnuts are relatively low in oxalates and lectins, with 62 to 74 mg of oxalates per 100 grams. The target is 42 grams daily, the amount shown in a controlled feeding trial to increase the butyrate-producing bacteria Faecalibacterium and Roseburia [478]. At 42 grams, walnuts contribute roughly 26 to 31 mg of oxalate, more than half of a 50 mg low-oxalate day, so account for them in your daily total and reduce the amount during heavy oxalate dumping. Walnut consumption increases urolithin A levels, which is a metabolite of ellagitannins that are converted by gut microbiota; however, you do need a population of the right microbes for the conversion to take place. Walnuts are associated with favorable shifts in gut microbiome composition, enhanced short-chain fatty acid production, and reduced systemic inflammation, along with supporting mitophagy and enhancing mitochondrial respiration, ATP production, and energy metabolism, which supports muscle endurance, recovery, and general cellular energy demands [195, 196]. Urolithin A also protects against calcium oxalate-induced crystal formation and kidney injury, restoring mitophagy function in kidney stone disease [197]. In a mouse model, a walnut-enriched diet slowed the growth of human prostate cancer xenografts, which suggests a possible role for walnuts in a cancer-preventive diet [198].
• Blanched Almonds: I only recommend almonds for oxalate dumping because they are extraordinarily high in oxalates (just over 6 mg of oxalate per nut).
• Sesame Seeds: White sesame seeds contain about 12 mg of oxalate per tablespoon. I do not use black sesame seeds because they are very high in heavy metals.
• Raw Organic Cacao: I used this to increase my oxalate intake to significantly lower symptoms. I only used this when necessary, as virtually all cacao contains high concentrations of lead, cadmium, and oxalates. Consumer Reports wrote an article titled “Lead and Cadmium Could Be in Your Dark Chocolate,” outlining chocolate bars with the least and most lead and cadmium. I used a powdered form of cacao and found Navitas to have the lowest cadmium and lead at 0.13mcg/g and 0.07mcg/g, respectively.

Acclimating to this diet can take days, and you could very well heal yourself while doing so. Unfortunately, this was not the case for me, but I do not expect everyone to be as severely infected as I was.

Implementation of the SR™ Warrior/OMAD Flexible Carnivore Diet requires starting slowly with intermittent fasting. This means choosing an eating window of 6 or 8 hours, then slowly narrowing it until you reach a 4-hour window. I prefer OMAD, but this was not possible in Phase 2 because the oregano oil had to be separated from the extended-fermentation yogurt for at least a couple of hours.

Changing The Microbiome Baseline

The reason it is critical to be consistent with your fasting protocol is that, especially if you are chronically ill, the microbiome has been disrupted, and a new baseline has been established, so it must be brought back to a new healthy baseline. The question is, how long will it take on the SR™ Warrior/OMAD Protocol? The literature is all over the map on this due to the range of variables, including diet, genetics, the degree of microbiome disruption, and, in my opinion, the most significant variable of all: the level of oxalate infection. Every time the body dumps oxalate, it disrupts the microbiome (Author’s Observation). This does not even consider the effects of drug or alcohol consumption, poor food choices, and stress.

The estimate to establish a new microbiome baseline is weeks to months. In my case, it may be years, as I have already been on the SR™ for months with good results, but I am still dumping oxalates, which I have little control over.

Fasting can be challenging if you are poisoned by oxalates and have a Candida overgrowth, as it accelerates oxalate elimination and causes Candida to die off (Author’s Observation). The malaise can be extreme, so it's essential to listen to your body and continually adjust your approach. I discovered that Candida die-off and bile sludge symptoms were much more severe than oxalate toxicity, so I stayed focused on fasting and restoring the microbiome to improve the body's ability to process oxalate dumping.

Extended Fermentation Yogurt And Nori Seaweed Top

Extended Fermentation Yogurt With GR-1 And RC-14. This is my daily ferment: four 5-billion CFU capsules (20 billion CFU) per batch, fermented 36 hours at 100°F, rotated with the other three Fantastic 4 cultures as described under Probiotics: The Fantastic 4. I mix my glycine into it, tear seven sheets of nori into it at serving every other day, and add 42 grams of walnuts. On days I do not use the yogurt, the nori goes into a seaweed burrito wrapped around my regular meal. Start with a quarter cup of yogurt and one sheet of nori; the yogurt and nori together are the strongest anti-Candida combination in Phase 1, and the die-off reflects that (Author's Observation).

A Word About Akkermansia Muciniphila

Akkermansia is at the top of the probiotics list, but is not part of the Fantastic Four because we do not buy it or ferment it. It was just discovered in 2004, and as of late, everyone who manufactures probiotics has jumped on the Akkermansia bandwagon, but only one manufacturer, as of this writing, has proven that its probiotic reaches the mucosal layer. I do not recommend this probiotic unless you are unable to fast for at least 17 hours for whatever reason.

Akkermansia increases during fasting even without an extended fast. Nine subjects studied during Ramadan, who fasted 17 h/day for 29 days, showed a significant increase in Akkermansia [199].

Akkermansia muciniphila is a next-generation probiotic bacterium that plays crucial roles in maintaining gut health and influencing systemic metabolic and immune functions. Its key functions and mechanisms include:

• Akkermansia remodels gut microbiota structure and modulates immune responses to confer metabolic benefits [200].
• It promotes the degradation and turnover of mucin in the gut mucosal layer, which thickens and reinforces the intestinal barrier, reducing gut permeability to harmful microbial products. It also induces the production of antimicrobial peptides by Paneth cells, further strengthening the barrier [201].
• Metabolizing mucin proteins to generate short-chain fatty acids (SCFAs) that serve as energy for intestinal epithelial cells and promote mucin synthesis. SCFAs have anti-inflammatory effects and support the induction of regulatory T cells, thereby modulating immune homeostasis [202].
• Enhancing intestinal stem cell proliferation and goblet and Paneth cell numbers, which improves epithelial regeneration capacity. It activates the AMPK signaling pathway and inhibits the TLR2-mediated NF-κB pathway, helping maintain mucosal immune balance [202].
• Stimulating intestinal L cells to secrete glucagon-like peptide-1 (GLP-1), improving peripheral insulin sensitivity, lipid metabolism, and hippocampal function via central insulin signaling [202].
• Increasing central nervous system nicotinamide levels through regulation of tryptophan–nicotinamide metabolism, which can improve mitochondrial function and motor neuron health in neurological disease models [202].
• Modulating neurotransmitters like GABA, influencing neurological conditions such as depression and anxiety, through metabolic activities [203].
• Upregulating genes critical for intestinal barrier function via the ALPK1/TIFA pathway and interacting with mucus barrier components [203].
• Providing a significant energy supply to the liver via SCFAs and reducing oxidative stress and inflammation in the gut-liver axis [204].

Overall, Akkermansia muciniphila functions as a microbial guardian by maintaining the intestinal barrier, regulating metabolism, shaping the immune system, producing beneficial metabolites, and potentially impacting neurological health through multiple interconnected pathways.

Nori Seaweed

Nori seaweed on its own can be effective in eradicating Candida overgrowth, but in combination with extended fermentation L. rhamnosus GR-1 and L. reuteri RC-14, it is absolutely lethal, so much so that during the heaviest die-off I had to regulate the seaweed down to 2 sheets per day and limit the probiotics to one-half cup of extended fermentation yogurt or less. I am now at seven sheets every other day (Author’s Observation). Thus far, C. albicans has not been able to adapt to this seaweed probiotic combination. Seaweed is so effective that one would want to start slowly and work up to a dose that works.

Nori’s value in this protocol is its anti-Candida effect, not fiber. Its fiber, porphyran, is digested by gut bacteria carrying genes that are common in Japanese populations, who eat seaweed daily, but absent in North American gut data [479]. For most Western guts, the protocol’s fiber comes from walnuts, inulin, and pumpkin.

Nori is the lowest-iodine of the common seaweeds, far below kelp or kombu, but iodine content varies by brand. Choose a brand that prints iodine on the label, and if you have a thyroid condition, keep your total under the 1,100 microgram adult upper limit [205] and recheck TSH (see Thyroid Test). Body size does not change this limit.

One virulence factor of C. albicans is its ability to form biofilms. The ability to create biofilm makes C. albicans more tolerant to commercial antifungal agents. The published evidence comes from a laboratory study of a related red seaweed, Gracilaria verrucosa, rather than nori itself. In that study, the highest inhibitory effect was observed in a fungal culture treated with a 25% seaweed extract concentration for 24 hours. The G. verrucosa extract contained steroids, terpenoids, and tannins that effectively inhibited biofilm formation by C. albicans at a concentration of 25% after exposure for 24 hours [206]. L. rhamnosus GR-1 and L. reuteri RC-14 also break down biofilm.

Warning: Brown Seaweed inhibits the formation of oxalate crystals [207]. This is significant because what I found is that it also significantly increases oxalate dumping. There is no literature on this, but I tested this multiple times, and it increases oxalate dumping every time I use it.

I was on Phase 1 for 12 weeks before the Candida die-off calmed down enough to go to Phase 2. This will be different for everyone.

Probiotics

We are now in the age of choosing a probiotic based on what you want to fix or change in your body and mind, and L. reuteri is a good example of this. However, this choice goes far beyond bacterial species. One must also select the strain of the species, which most manufacturers do not disclose on their labels. BioGaia, for instance, is one of the few that lists the strains it uses. This, along with being the most researched among human sources, is one of the many reasons L. reuteri remains at the top of my list after using it for over a decade.

Probiotic Species Compatibility

L. reuteri strains lacked the robust inhibitory antimicrobial effects of bacterial pathogens when combined with other probiotic Lactobacillus species, such as L. acidophilus, L. gasseri, and L. johnsonii. By contrast, L. reuteri potently inhibited L. casei, which highlights the importance of species compatibility considerations when creating mixed-species probiotic formulations [208]. What this means is that you must know your objectives. If you want to maximize the effectiveness of L. reuteri, you must confirm that it does not conflict with any other probiotic in your probiotic formula. The same goes for Dr. Davis’s SIBO formula. L. reuteri should be made and taken separately from L. gasseri.

In other cases, probiotics can work synergistically. L. acidophilus (strains NK1, K3III24, 100 ash), Bifidobacterium adolescentis MC 42, B. bifidum, and B. gallinarum GB synergistically produce lectins with antimicrobial activity against clinical strains of nystatin-resistant Candida albicans, S. aureus, and their biofilms [160]. After significant research, I confirmed that Lactobacillus reuteri 6475 and 17938 and Bifidobacterium longum 1714 could be mixed in the same batch. This is also true with Lactobacillus gasseri BNR17 and Lactobacillus acidophilus La-14. This enables me to prepare The Fantastic Four simultaneously in two separate bowls.

Bacteriocins

Bacteriocins are ribosomally synthesized antimicrobial peptides produced by bacteria or, for our purposes, probiotics. They can kill or inhibit bacterial strains closely related or non-related to the bacteria themselves, but will not harm the bacteria themselves through specific immunity proteins. Bacteriocins may become a potential drug Candidate for replacing antibiotics to treat multiple drug-resistant pathogens in the future [209]. 99% of all bacteria probably produce at least one bacteriocin, most of which have not yet been identified because few researchers have looked for them [210]. We will, therefore, not attempt to give you the number of Bacteriocins per probiotic listed in The Fantastic 4 Probiotics.

Probiotics For Oxalate Degradation

In vitro, oxalate degradation does not reflect the ability of bacteria to metabolize oxalate in vivo after intestinal colonization [211]. This statement was made during an extensive study on probiotics and various disease states, including oxalate degradation. However, oxalate degradation by Lactobacillus indicates that out of 60 strains tested from 12 different species, strains L. acidophilus, and L. gasseri were most efficient in their ability to degrade oxalate in vitro [212]. In other words, science is not yet definitive, and one must experiment to find what works for each species and strain, as I do. The in vitro, however, does at least point one in the right direction.

On my first comprehensive stool test, I scored a 10 out of 10 on Dysbiosis and Metabolic imbalance and a 7 on inflammation. If you have ever wondered what suicidality looks like in the gut, this first test is it. On my second comprehensive stool test, I brought those scores down to 0, 2, and 2, respectively. On the first test, all primary gut bacteria were deficient with Euryarchaeota phylum, so low that it did not register. More on this below. Oxalobacter formigenes, which is a well-established gut bacterium that uses oxalates as fuel, was intact when tested. Because of the severity of my infection, this was not enough, and even taking up to 1.7 trillion CFU of the best probiotic I could find was not sufficient either. This was because the purging of oxalates consistently disrupted bacteria, far beyond what was tested. A study published as I was finishing this paper confirmed the need for a broader spectrum of gut bacteria or effective bacteriotherapy to address oxalate breakdown [213].

Inulin: Pure Fiber Top

Warning: Inulin is a high FODMAP food (explained below), which means it can cause gastrointestinal distress if used in excess. Inulin is a fructan-type oligosaccharide that's found in many plants, which represents the O in FODMAP. This is a dichotomy because this high FODMAP fiber is instrumental in restoring the gut. Yet, if you have gastrointestinal issues, you will immediately be told to avoid high FODMAP foods. Slowly introducing inulin is critical. This is one of many cases where you absolutely do NOT want the whole food, as you will see below.

Benefits Of Inulin

• Consuming inulin alters the colon epithelium by increasing the proliferation of intestinal stem cells, leading to deeper crypts and longer colons. Inulin affects the activity of intestinal stem cells and drives a homeostatic restoration of the colon epithelium [214].
• In a rat model, 24-hour urinary oxalate excretion significantly decreased in the inulin group compared with the control [215].
• The gut microbiome responds to inulin treatment and exhibits significant structural alterations [216].
• The concentration of inulin increases the rate of oxalate degradation [217].
• Inulin use inhibits harmful bacteria or opportunistic pathogens by promoting the proliferation of beneficial bacteria. In addition, pathogenic bacteria tend to colonize the intestine in an alkaline environment. Inulin lowers intestinal pH after enterobacterial fermentation, which also contributes to the inhibition of pathogenic bacteria [216].
• Dietary supplementation with inulin can restore the integrity and function of the intestinal barrier by promoting the expression of zonula occludens [216].
• Inulin treatment promotes the growth of certain beneficial bacteria and bacteria that promote the production of SCFAs (short-chain fatty acids), such as Bifidobacterium [216].
• SCFAs can act locally in the intestine and be used as energy sources by intestinal mucosal cells to promote barrier function, maintain mucosal immunity, and provide energy substrate for colonic cells. SCFAs can also enter the circulation through the hepatic portal vein and act as signaling molecules, thereby regulating systemic immune function [216].
• Inulin supplementation decreased the relative abundance of Bacteroidetes and increased levels of Bifidobacterium spp., Anaerostipes spp., Enterococcus Faecalis, and Lactobacillus. Inulin also promotes an increase in the abundance of bacteria of the genera Phascolarctobacterium, Blautia, Akkermansia, Ruminococcus, and the family Lachnospiraceae, which are also responsible for SCFA production [216].
• Inulin can regulate the metabolism of glucose, lipids, and amino acids in addition to intestinal immune and systemic immunomodulatory effects.
• Inulin can improve the symptoms of many diseases, such as metabolic syndrome, IBD, and chronic kidney disease (CKD), associated with intestinal inflammation and intestinal dysbiosis, as well as allergic diseases and tumors related to immune imbalance [216].
• Inulin intake modulates ecological dysbiosis, reduces the level of fasting glucose, attenuates insulin resistance, and improves lipid disorders [216].

Inulin-Responsive Bacteria In The Gut Microbiome

This is the probiotic information you need after someone tells you to eat more fiber. I will drill down on Faecalibacterium and what I consider to be the Fantastic 4 probiotics, with a comprehensive overview of L. reuteri, L. gasseri, L. acidophilus, and B. longum at the bottom. These are all oxalate degraders and will drive home the importance of Inulin. The following are inulin-responsive probiotics and are listed in order of responsiveness to inulin [218]. I personally have not found a probiotic that is not responsive to inulin. This is why it is also used in our yogurt-making process.

1. Phocaeicola (Bacteroidaceae)
2. Faecalibacterium (Ruminococcaceae)
3. Hydrophilic
4. Hydrophobic
5. Agathobacter (Lachnospiraceae)
6. Streptococcus (Streptococcaceae)
7. Bacteroides (Bacteroidaceae)
8. Prevotella (Prevotellaceae)
9. Blautia (Lachnospiraceae)
10. Fusicatenibacter (Lachnospiraceae)
11. Ruminococcus (Ruminococcaceae)
12. Lachnospiraceae spp.
13. Roseburia (Lachnospiraceae)
14. Bifidobacterium (Bifidobacteriaceae)
15. Lachnospira (Lachnospiraceae)
16. Dialister (Veillonellaceae)
17. Dorea (Lachnospiraceae)
18. Alistipes (Rikenellaceae)
19. Faecalibacillus (Erysipelotrichaceae)
20. Gemmiger (Ruminococcaceae)
21. Mediterraneibacter (Lachnospiraceae)
22. Kineothrix (Lachnospiraceae)
23. Coprococcus (Lachnospiraceae)
24. Parasutterella (Sutterellaceae)
25. Lactococcus (Streptococcaceae)
26. Ruminococcaceae spp.
27. Parabacteroides (Porphyromonadaceae)
28. Ruminococcus spp.
29. Collinsella (Coriobacteriaceae)
30. Clostridium_XIVa (Lachnospiraceae)
31. Mitsuokella (Selenomonadaceae)
32. Agathobaculum (Ruminococcaceae)
33. Paraprevotella (Prevotellaceae)
34. Anaerostipes (Lachnospiraceae)
35. Dysosmobacter (Ruminococcaceae)
36. Lactobacillus (Lactobacillaceae)
37. Raoultibacter (Eggerthellaceae)

Faecalibacterium

• Obese or T2D (type 2 diabetes) patients have lower microbiome diversity, and Faecalibacterium is one of the community members that has been found to differ. In other research, Faecalibacterium was enriched in T2D patients following weight loss. The same study found that samples from lean patients contained higher numbers of Faecalibacterium genes than did samples from obese and T2D patients [121].
• Faecalibacterium is diminished in MDD (Major Depressive Disorder) patients, while an increase in Faecalibacterium improved MDD symptoms. This concludes that Faecalibacterium may be used as an important species for an effective response to depression treatment [219].
• Numerous studies have underscored that low levels of Faecalibacterium are correlated with inflammatory conditions, with inflammatory bowel disease (IBD) in the forefront. Its representation is also diminished in the case of several diseases, including colorectal cancer (CRC), dermatitis, and depression. Additionally, the relative presence of this genus is considered to reflect, at least in part, intestinal health status because Faecalibacterium is frequently present at reduced levels in individuals with gastrointestinal diseases or disorders [121].

Faecalibacterium is just one of 37 species listed here. The bottom line is the use of inulin is a critical factor in restoring the gut microbiome and overall emotional and physical health.

Inulin Safety: Under 40 grams daily is safe for healthy adults [216]. I currently only use inulin to make extended-fermentation yogurt, and even then I am careful about how much I use.

Guar Gum: A Fiber To Stay Away From

Until a study in 2024, it was thought that guar gum was beneficial for the gut. In a mouse model, a Guar gum-containing diet (GuD) increased the susceptibility to colonic inflammation. Unfavorable changes in gut microbiome activity leading to compromised gut barrier function following guar gum feeding contributed to increased colitis susceptibility [220].

Oxalate-Degrading Bacteria in Bifidobacterium and Lactobacillus [217]

• Lactiplantibacillus plantarum
• Lactobacillus brevis
• Lactobacillus acidophilus
• Bifidobacterium infantis
• Bifidobacterium animalis
• Bifidobacterium breve
• Bifidobacterium longum
• Bifidobacterium adolescentis
• Lacticaseibacillus casei
• Lactobacillus gasseri
• Lacticaseibacillus rhamnosus
• Ligiactobacillus salivarius

What Makes The Fantastic 4 So Fantastic?

It is more than just selecting the right probiotic species and strains; it is also about the dose or colony-forming units (CFUs) being accurate. We do this by extending the fermentation of yogurt or whatever you are fermenting, usually for up to 36 hours. Dr. William Davis has done the most experimentation with this and found that extending it to 48 hours killed many of the bacteria. This may not be the case with all probiotics, but it was with L. reuteri 6475 and 17938. Dr. Davis was able to take 2 billion CFUs of 6475 and 17938 and turn them into 200 to 260 billion CFUs per half cup of yogurt. He measured this with flow cytometry. Flow cytometry is a lab test that uses lasers to analyze the physical and chemical characteristics of cells and particles. Without extended fermentation, the effects of these probiotics may not even be noticeable.

The Fantastic 4 probiotics cover a broad range of issues, and I have tested them all. However, this science is still in its infancy, so expect even better results as it becomes more refined.

What The Fantastic 4 Have In Common

• All 4 are human strains
• All 4 are colonizing probiotics as opposed to transient ones
• All 4 populate the upper and lower intestines
• All 4 survive stomach acid

Displacement Of Possible Pathogens

Displacement of possible pathogens is one of the many reasons why I believe I felt better with all the Fantastic 4. Attachment to the intestinal mucosa displaces Candida and makes it difficult to return. This is an essential factor for probiotics in the context of intestinal inflammation. Some probiotic microbes also share binding sites with enteropathogens and can hinder their attachment to host cells by binding to the same sites [160].

Stimulation Of Bowel Microbiome

The gastrointestinal tract (GIT) is home to an organized microbial community (microbiota), which participates in metabolic, nutritional, biochemical, and immunological processes within the body. Hence, cell-to-cell interactions regulate microbial multiplication and maintain intestinal homeostasis, leading to a range of host responses against commensal and pathogenic organisms. The microbiome is an active ecosystem influenced by factors such as genetics, metabolism, nutrition, geographical location, stress, and antimicrobial treatment [160].

Stimulation Of The Digestive Enzymes

Some probiotics aid in the breakdown of complex macronutrients and provide the host with digestive enzymes and vitamins, thereby enhancing nutrient absorption. The ability of probiotics to promote lactose fermentation has made them useful in treating lactose intolerance in humans. Probiotic Bifidobacterium strains, such as B. longum, participate in the metabolism of oligosaccharides [160].

Aging

During aging, the gut microbiome undergoes alterations, and its mediated increase in intestinal permeability leads to chronic inflammation, decreased DNA repair efficiency, stem cell depletion, and cellular senescence in the organism. Altogether, these processes contribute to aging [5].

The decline of brain function in the elderly is linked to conditions such as delirium and dementia, and age-related changes in the gut microbiome may contribute to them [221]. Only by fully understanding the gut microbiome can we uncover more profound mysteries, with the aim of gaining a deeper understanding of its complex relationship with host aging. Unfortunately, we are not there yet, but I believe the Fantastic 4, along with the SR™ Gut Barrier and Microbiome Restoration, represents a foundational approach to living a disease-free life at any age.

Probiotics: The Fantastic 4 Top

1. L. rhamnosus GR-1 and L. reuteri RC-14

Primary Objective: Eradicate Candida, Modulate Bladder Function

Attention, Men: Although the vast majority of studies on these synergistic probiotics have been conducted with women for the treatment of vaginitis, vulvovaginal candidiasis, and modulation and prevention of bladder infections, this powerful combination is also effective for the male bladder and gut. How do I know this? After reading the studies, I tried it on myself, and it worked exceptionally well for both bladder function and Candida eradication when combined with Nori Seaweed. The fascinating thing about these probiotics for women is that when taken orally, they will translocate to the vagina and kill Candida overgrowth, along with modulating the microbial environment of the vagina [158]. The same translocation, however, does not occur with the bladder. It manages to modulate this environment from the gut.

Clinical Evidence Supporting This Combination

Clinical Outcomes

• Higher cure rates for bacterial vaginosis when added to antibiotic treatment [222].
• In postmenopausal women with recurrent urinary tract infections, slightly less effective than antibiotics at preventing recurrences, but without increasing antibiotic resistance [223].
• Improved symptom relief in vulvovaginal candidiasis when combined with antifungals [224].

Safety Profile

• No safety concerns in a feasibility trial combining these probiotics with vaginal estrogen [225].
• Well-tolerated across multiple population studies [226].

Where to purchase: Amazon.com

Tested: Yes

Administration: Extended Fermentation Yogurt

Probiotic Amount: This comes in one billion CFU capsules. There is another brand that comes in 2 billion CFU capsules. I started out with a 2 billion CFU starter. I am now using a 10 billion CFU starter.

A2 Half and Half: 24 ounces per 32-ounce bowl or 48 ounces per 8 yogurt jars

Inulin: 1 rounded tablespoon per 24 ounces or 2 rounded tablespoons per 48 ounces for 8 yogurt jars.

Fermentation Time: 36 Hours

Optimal Temperature: 100°F

Actual Temperature: 100°F

Recommended Amount: Half a Cup Daily

Therapeutic Amount: Self-determined.

Results: I did not see any noticeable results from using the capsules only. However, with extended fermentation, I saw significant results for bladder function and Candida die-off when I used it with nori seaweed within 48 hours.

2. Lactobacillus reuteri ATCC PTA 6475 and DSM 17938

Primary Objective: Microbiome Balance

L. reuteri ATCC PTA 6475, which is an isolate from Finnish mother’s milk, and L. reuteri DSM 17938, which is the daughter strain of Lactobacillus reuteri ATCC 55730, are bacteria originally isolated from the breast milk of a Peruvian mother. These are the two most researched L. reuteri strains on the market. This does not imply they are the best, just the most researched. These two strains are sold as BioGaia Gastrus on Amazon. I ultimately switched to using BioGaia Osfortis, which is just the 6475, because I like making my yogurt with the starter every time as opposed to using yogurt from a previous batch.

Oxytocin: The Love And Empathy Hormone

L. reuteri stimulates the cells lining the intestine to release oxytocin [227]. Oxytocin is normally produced in the hypothalamus, the area of the brain that controls body temperature, hunger, and thirst. However, L. reuteri is believed to inhabit the small intestine predominantly in humans and appears to have co-evolved with its other hosts. Oxytocin is a multifunctional hormone that affects not only social behavior, bone, and skin but also gut motility, inflammation, and the intestinal epithelial barrier. Therefore, L. reuteri signaling through oxytocin could potentially explain many of the systemic effects of this microbe [227].

In humans, intranasal administration of oxytocin was found to increase bonding-related behavior, including gaze-to-eye region, interpersonal trust, empathy, and social cognition. Oxytocin has also been shown to play a role in human parenting, and peripheral levels of oxytocin have been associated with reciprocal parent-infant interactions in both mothers and fathers [228].

The full effects of oxytocin are yet to be fully realized, and the fact that gut microbes can trigger oxytocin release raises more questions about the physiological and emotional systems it affects. In mice, the effects of L. reuteri on oxytocin and wound healing disappeared when the vagus nerve was cut, which suggests the gut signals the brain through this nerve [229].

• L. reuteri 6475 counteracts a degradation of gut microbiome in older women with low bone mineral density [230].
• L. reuteri 6475 prevented abdominal fat pathology and age-associated weight gain in mice regardless of their baseline diet [231].
• In a mouse model, L. reuteri increased testosterone, testicular mass, and other indicators typical of old age were similarly restored to youthful levels [232].
• L. reuteri 6475 has a beneficial effect on sperm concentration and sperm activity in 12-month-old outbred Swiss mice [232].
• L. reuteri 6475 exhibited broad-spectrum antimicrobial activity [208].
• L. reuteri 6475-derived histamine can suppress gut inflammation [233].
• L. reuteri 6475 has anti-inflammatory and anti-infectious capacities [233].
• L. reuteri 6475 can reduce the number and size of colon tumors [233].
• L. reuteri DSM 17938 supplement improved bacterial diversity along with enriched Firmicutes (good bacteria) and reduced abundance of Bacteroidetes [234]. Bacteroidetes increase as obese mice lose weight. Furthermore, when the microbiome of obese mice are transferred to germ-free mice, these mice gain more fat than a control group that received microbiome from lean mice [27, 235].
• L. reuteri DSM 17938 protected the mucosal barrier and reduced inflammatory factors [233].
• L. reuteri DSM 17938 In both children and adults, shortens the duration of acute infectious diarrhea and improves abdominal pain in patients with colitis or inflammatory bowel disease [236].
• L. reuteri DSM 17938 had beneficial effects on people suffering from chronic constipation [237].
• In mice, a lysate of L. reuteri raised oxytocin levels [238].
• L. reuteri restores gut microbiome balance, produces antimicrobial metabolites, regulates intestinal immunity, and mediates mucosal homeostasis, thereby exhibiting protective effects on digestive system diseases [234].
• The symbiotic intervention of Lactobacillus reuteri and inulin protected gut barrier integrity and altered the gut microbiome composition, enhancing the abundance of butyrate-producing Bifidobacterium [239].
• A symbiotic formulation of Lactobacillus reuteri and inulin alleviated Autism Spectrum Disorder-like behaviors in a mouse model [239].
• Four weeks of Lactobacillus reuteri and inulin attenuated inflammatory cytokine expressions in the brain in a mouse model [239].
• L. reuteri significantly reduces chronic functional abdominal pain in children [240]
• High-fat-diet-induced obesity is associated with decreased anti-inflammatory L. reuteri [241].
• L. reuteri reduces hepatic cancer cell proliferation, muscle wasting, and morbidity and prolongs survival [242].
• L. reuteri attenuates stressor-enhanced infectious colitis [243].
• L. reuteri has antifungal effects on oral Candida species in vitro [244].

Where to purchase: Amazon.com

Tested: Yes

Administration: Extended Fermentation Yogurt

Probiotic Amount: Ground up 10 tablets into a powder to equal 2 billion CFUs for 24 ounces of A2 half and half.

A2 Half and Half: 24 ounces per 32-ounce bowl or 48 ounces per 8 yogurt jars

Inulin: 1 rounded tablespoon per 24 ounces or 2 rounded tablespoons per 48 ounces for 8 yogurt jars

Fermentation Time: 36 Hours

Optimal Temperature: 100°F

Actual Temperature: 100°F

Recommended Amount: Half Cup Daily

Therapeutic Amount: Self-determined.

Results: Even though there is no literature on the ability of L. reuteri Strain 6475 and 17938 to degrade oxalates, I did notice a considerable reduction in my oxalate dumping and a lessening of symptoms. There is evidence of oxalate degradation in other L. reuteri strains.

3. Lactobacillus Acidophilus La-14 and NCFM

Primary Objective: Oxalate Degradation

• L. acidophilus La-14, along with many other L. acidophilus strains, has been shown to degrade oxalates up to 100% in vitro [245].
• L. acidophilus La-14 exhibited not only the ability to break down oxalate but also may modulate the release of inflammation mediators associated with oxalate accumulation in the human gastrointestinal tract [211].
• L. acidophilus exhibits an antifungal effect against Candida if harvested after prolonged incubation of 24 to 36 hours [246].
• L. acidophilus restrains the development of S. aureus and P. aeruginosa enteric infections [247].
• Exopolysaccharides (EPS) from Lactobacillus acidophilus have antioxidative properties [248].
• Surface layer protein A (SlpA) from Lactobacillus acidophilus NCFM potentially represents a feasible therapeutic approach to restore intestinal homeostasis [249].

Where to Purchase LA-14: Amazon.com

Tested: Yes

Administration: Extended Fermentation Yogurt

Probiotic Mix Amount: One Capsule to equal 2 billion CFUs per 24 ounces of A2 half and half.

A2 Half and Half: 24 ounces per 32-ounce bowl or 48 ounces per 8 yogurt jars

Inulin: 1 rounded tablespoon per 24 ounces or 2 rounded tablespoons per 48 ounces for 8 yogurt jars

Fermentation Time: 36 Hours

Recommended Temperature Range: 98.6°F to 107.6°F

Actual Temperature: 100°F

Recommended Amount: Half Cup Daily

Therapeutic Amount: Self-determined.

Results: Mixed outcomes.

4. Bifidobacterium Longum 1714

Primary Objective: Sleep

The term psychobiotic is used more often with B. longum 1714 because of its effectiveness with depression and anxiety than any other probiotic listed here.

• B. longum 1714 has been shown to influence stress responses, modulate neural responses during social stress, and influence sleep quality during examination stress in healthy adults [250].
• B. longum 1714 modulated neural activity, which correlated with enhanced vitality/reduced mental fatigue [250].
• B. longum 1714 significantly improved the PSQI (Pittsburgh Sleep Quality Index) component of sleep quality [250].
• B. longum assists in the regulation of the microbiome and helps to prevent IBD [251].
• Preclinical studies have identified the B. longum 1714 strain as a putative psychobiotic with an impact on stress-related behaviors, physiology, and cognitive performance [252].
• B. longum 1714 strain, which has shown anti-stress and procognitive effects in healthy mice, can also ameliorate both the physiological and psychological response to an acute stressor, as well as longer-term daily self-reported psychological stress, in healthy human adults [252].
• B. longum decreases the excitability of enteric (gut) neurons [253].
• B. longum has anti-allergy effects, reducing harmful bacteria, improving intestinal environment, defecation frequency, and improved stool characteristics [254].
• B. longum supplementation prevents bone loss and increases bone formation [255].

Where to Purchase 1714: Amazon

When using it to make yogurt, one capsule is used to make the first batch, and a couple of tablespoons of the current batch are used to make future batches.

Tested: Yes

Administration: Extended Fermentation Yogurt

Probiotic Amount: One Capsule to equal 3 billion cells per 24 ounces of A2 half and half.

A2 Half and Half: 24 ounces per 32-ounce bowl or 48 ounces per 8 yogurt jars

Inulin: 1 rounded tablespoon per 24 ounces or 2 rounded tablespoons per 48 ounces for 8 yogurt jars

Fermentation Time: 36 Hours

Recommended Temperature Range: 96.8°F – 100.4

Actual Temperature: 100°F

Recommended Amount: Half a Cup Daily

Therapeutic Amount: Self-determined.

Results: I initially combined 1714 with LA-14, and it pushed the lids off the yogurt jars. I then fermented just 1714, and it did not push the lids off, but it did push the center of the lid up on the one-quart jars. 1714 is the only probiotic that did this. I also tried coconut milk, and it did not work; it remained liquid, and the cream separated, but there were chunks of coconut floating around, which is not recommended. Even with two ruined batches, I did notice a difference in sleep quality within 7 days.

1714 Sleep: Into the second batch, I took a nap and had the deepest sleep I have had in a long while. There is a question as to how long I will need to use this or any of these probiotics to achieve a permanent effect, or if that is even possible. I split a batch, so I will make 1714 and La-14 to address sleep and oxalate degradation simultaneously. Both oxalate dumping and Candida die-off disrupt sleep, and I was hoping this probiotic would override this, but it ultimately did not.

Other Probiotics To Consider

5. Lactobacillus Gasseri BNR17

Objective: Body Composition

• L. gasseri BNR17 Reduces Visceral Fat Accumulation and Waist Circumference in Obese Adults [135].
• L. gasseri BNR17 was confirmed to have probiotic properties by reducing IBS symptom severity scores, especially in relieving abdominal pain [256].
• In a 21-day mouse model, L. gasseri BNR17 showed a significant increase in lean body mass and a decrease in fat mass [257].

6. Lactobacillus Rhamnosus

• L. rhamnosus exhibits an antifungal effect against Candida if harvested after prolonged incubation of 24 to 36 hours [246].
• Evaluation of L. rhamnosus confirmed that the oxalate degradation is more significant in the presence of glucose [258].
• Lactobacillus rhamnosus GG has been suggested to increase bone formation by stimulating the production of microbial metabolite butyrate, which induced T cell-produced Wnt10b in eugonadic young mice [259].
• L. rhamnosus provides protective effects on alcoholic liver injury by reducing oxidative stress and restoring the intestinal flora [260].
• L. rhamnosus diminishes oxidative markers in the brain [261].
• L. rhamnosus protects against tissue damage mediated through free radicals and inflammatory cytokines [262].

7. Lactobacillus Plantarum

• In a rat model, L. plantarum exhibited oxalate degrading abilities in vitro [263].
• L. plantarum could ameliorate anxiety and depression-like behaviors and modulate neurochemicals related to affective disorders [264].
• L. plantarum potentially enhances the immunity of the small intestine [265]
• L. plantarum positively affects the immune system and acts as an antiviral [266].

8. Lactobacillus Brevis

• L. brevis synthesizes gamma-aminobutyric acid (GABA) [267]. GABA is the primary inhibitory neurotransmitter in the human brain, and oral GABA has been reported to reduce stress and improve sleep in human studies [268].
• L. brevis may prevent some metabolic disturbances [269].

9. Lactobacillus Casei

• L. casei exhibits an antifungal effect against Candida if harvested after prolonged incubation of 24 to 36 hours [246].

10. Bifidobacterium Lactis

• B. lactis improves the intestinal microbiome more effectively than non-proliferating bifidobacteria and lactic acid bacteria [270].
• B. lactis improves defecation frequency [271].
• As part of a multispecies probiotic blend, B. lactis reduced cognitive reactivity to sad mood, which was largely accounted for by reduced rumination and aggressive thoughts [150].

SIBO Yogurt

If you are suffering from SIBO, Dr. Davis recommends ATCC PTA 6475 and DSM 17938, L. gasseri BNR17, and Bacillus coagulans gbi-30 6086. Bacillus coagulans is not included on this list because it is not considered a natural part of the human gut flora, and I am simply not impressed with it. I highly recommend you purchase Super Gut if you want to go beyond The Fantastic 4 or if you need to ferment other foods because of dairy sensitivity.

Yogurt Making: What I Use

Ultimate Yogurt Maker: This is the only one with a lifetime guarantee, which is a good thing since I run it around the clock. I do, however, recommend doing your research. You can buy this yogurt maker with eight 6-ounce jars or two one-quart bowls. It will be 48 ounces for either one, because you cannot fill the one-quart bowls to the brim without making a major mess.

2 Quart Measuring Cup: I use a large measuring cup as a mixing bowl so I can pour it directly into the 6-ounce jars when I am using those.

Extra Yogurt Bowls: I have one set of 6-ounce jars and two sets of one-quart Pyrex bowls. I got different colored silicone lids to decipher which bowl had what strain. I also bought two-cup Pyrex bowls to freeze the excess, as the 6-ounce jars are not freezer-compatible.

Why A2 Half And Half Only

Every extended-fermentation yogurt recipe in this protocol calls for A2 half and half only. This is not a brand preference. It is a requirement for anyone engaged in restoring the gut barrier and microbiome.

Conventional cow’s milk contains two main forms of beta-casein, A1 and A2. They differ by a single amino acid, but that difference changes how the protein is digested. When A1 beta-casein is broken down in the gut, it releases an opioid peptide called beta-casomorphin-7 (BCM-7). A2 beta-casein releases little to none. A systematic review of the animal and human evidence found that A1 beta-casein, acting through opioid receptors in the gut, can slow intestinal transit and promote gastrointestinal inflammation, whereas A2 beta-casein does not [272].

Human trials point in the same direction. In a double-blind, randomized crossover trial, adults who drank conventional milk containing A1 beta-casein had more digestive discomfort, slower transit, higher inflammation-related markers, and lower fecal short-chain fatty acids than when they drank milk containing only A2 beta-casein [273]. Short-chain fatty acids are the primary fuel for the cells that line the colon and are central to barrier repair. An earlier blinded crossover study likewise linked A1 beta-casein to looser stools and to abdominal pain [274].

Animal studies show the mechanism at the tissue level. In mice, A1 beta-casein increased intestinal inflammatory markers, including myeloperoxidase, interleukin-4, and immunoglobulins, and provoked a Th2-type immune response in the gut that A2 beta-casein did not [275]. In rats, A1 beta-casein slowed gastrointestinal transit through an opioid-dependent pathway and increased colonic myeloperoxidase, a marker of neutrophil-driven inflammation [276].

The point is simple. Extended-fermentation yogurt is eaten daily throughout this protocol, and its purpose is to calm inflammation, feed the intestinal lining, and rebuild the microbiome. A dairy base that can promote inflammation and slow transit works against all three goals, especially in a gut that is already permeable. Extended fermentation reduces lactose, but it does not convert A1 beta-casein into A2. A2 half and half removes this variable entirely. Most human trials to date have been small, and larger studies are still needed, but the direction of the evidence and the low cost of switching make A2 the only sensible choice during gut restoration. If you cannot find A2 half and half or do not tolerate dairy at all, discuss alternatives with your MD and see SIBO Yogurt above regarding fermenting other foods.

Phase 2: CoreBiome Tributyrin Top

Oregano Oil, Black Seed Oil, Or Nystatin As Backups

Tributyrin

Tributyrin is a butyrate delivery compound. I take Doctor's Best Tributyrin (CoreBiome), 300 mg softgels, and I began it in Phase 2, once the Phase 1 routine was tolerated. The manufacturer states that it supports gut barrier function within 48 hours; that is a product claim, and I did not find a peer-reviewed human trial behind it. My own experience was faster than the claim. Within 24 hours I noticed a clear improvement in my gait and balance, and I passed a massive amount of Candida, the largest die-off I have had in this protocol. I took my first dose at the same time as my daily nori seaweed, so I cannot say which of the two drove the die-off. What I can say is that the combination did more than nori and extended fermentation yogurt had done on their own over a long period of use (Author's Observation).

Dose and duration. This liquid softgel form was released in May 2025, and no published human study has tested it at any dose. The only published research on CoreBiome is the digestion and gut-model work cited below [277]. The 300 mg amount is the manufacturer's recommendation, not a dose established in a published study.

• I started with 300 mg once daily with food. The die-off was strong. When it is severe, taking it every other day until it settles is an option.
• I stay at 300 mg once daily, the manufacturer's recommended starting dose [278]. I tried 300 mg three times daily, about six hours apart with food, for 900 mg a day. My gait and balance kept improving, but I was severely nauseated each morning, so I went back to 300 mg (Author's Observation).
• Timing. I take it with my extended fermentation yogurt rather than with my main cooking-fat meal. In the CoreBiome digestion model, about half the dose reached the colon intact [277]. A large fat load triggers more of the enzymes that split tributyrin early, and my goal is to get as much as possible to the colon intact. This is my reasoning from how tributyrin is digested; it has not been tested (Author's Observation).
• How long. You and your MD set how long you stay on it, not a calendar.
• Backups. If tributyrin had not worked for me, or my die-off had plateaued, I would have gone back to oregano oil with black seed oil, or nystatin through my MD, as described at the end of this phase.

1. What It Is

• Tributyrin is one glycerol molecule with three butyrate molecules attached, the same structure as a dietary fat.
• Butyrate is the short-chain fatty acid (SCFA) that your gut bacteria normally make when they ferment fiber. It is the main fuel for the cells that line the colon.
• Plain butyrate supplements are absorbed high in the gut and smell and taste terrible. Tributyrin has no smell, survives stomach acid, and is split apart by pancreatic lipase in the small intestine, releasing butyrate along the way. In a digestion model, roughly half the dose was released in the small intestine and the other half stayed intact and reached the colon [277].
• The Candida and barrier mechanisms below were shown with butyrate given directly; tributyrin is the form that delivers it to the gut without the absorption and odor problems of plain butyrate.
• CoreBiome is a brand, not a delivery technology. Tributyrin is the molecule; CoreBiome is Compound Solutions' standardized, high-purity version of it, and the one in Doctor's Best softgels. What carries much of it to the colon intact is tributyrin's own structure. In the CoreBiome digestion model, a capsule and a softgel performed about the same, with roughly half of each reaching the colon intact, which shows the delivery comes from the molecule rather than the packaging [277].
• What CoreBiome adds is consistency, so each softgel delivers the same amount, and evidence: it is the only tributyrin supplement with published research on how it is digested and what it does in the gut [277].

2. How It Works

• Fuel: Butyrate powers the colon lining cells directly, so they can repair and replace themselves.
• Barrier: Butyrate drives assembly of the tight junction proteins that seal the gaps between gut cells, through the energy sensor AMPK [279].
• Gene control: Butyrate is a histone deacetylase (HDAC) inhibitor. In plain language, it changes which genes are switched on in gut cells, immune cells, and, as it turns out, in Candida [280].
• Immune programming: Butyrate reprograms macrophages, the immune cells that eat pathogens, to produce more antimicrobial peptides and kill more effectively without increasing inflammation [281].

3. What It Does For The Gut

• Tributyrin raised butyrate levels and increased Bifidobacterium and Akkermansia muciniphila, two of the Top 10 probiotics in this protocol, in a simulated gut model, while protecting the gut lining in a cell model [277].
• Tributyrin prevented the leaky gut, and the liver inflammation that followed it, in mice given alcohol, a known barrier disruptor [282].
• It replaces what antibiotics take away: antibiotics cut gut butyrate by about 75 percent in mice, and that drop tracked directly with Candida overgrowth [24].

4. Why It Hit Candida So Hard

• Butyrate is the most potent of the three short-chain fatty acids against Candida albicans. In the lab, it cut Candida growth by 93 to 98 percent at a moderate concentration and nearly 100 percent at a higher one [24].
• It blocks the yeast-to-hyphae switch. Candida is harmless as a round yeast and invasive as a thread-like hypha. Butyrate reduced germ tube (hyphae) formation by about 70 percent [24, 283], and the HDAC effect in item 2 is part of how it does this [280].
• It stops Candida from sticking: butyrate blocked about 90 percent of hyphal attachment to surfaces [24].
• It arms your immune cells against Candida: butyrate increased macrophage uptake and killing of Candida, with more reactive oxygen species and nitric oxide, the chemicals macrophages use to kill fungi [280].
• Butyrate is the SCFA that antibiotics, a Western diet, and dysbiosis strip out, and it is the one that normally keeps Candida in its yeast form. Tributyrin puts it back directly, rather than waiting for the microbiome to make it, which removes Candida's advantage.

5. Why It Breaks Down Biofilm

• Biofilm is the slime shield Candida builds so antifungals cannot reach it. Butyrate cut the metabolic activity of Candida biofilm by about 90 percent [24] and significantly reduced biofilm formation [280].
• It also makes azole antifungal drugs work better against Candida [280], which is the same synergy I see when combining tributyrin with oregano oil as a backup (Author's Observation).
• Because hyphae are the scaffolding of Candida biofilm, blocking the hyphal switch (item 4) means new biofilm cannot be built while the old biofilm is being stripped.

6. Tributyrin And Inflammaging

• Inflammaging is the slow, low-grade inflammation that rises with age (see Part 1). One driver is the age-related loss of butyrate-producing bacteria such as Faecalibacterium prausnitzii, which weakens the barrier and lets LPS leak into the blood [3, 4].
• Butyrate is the anti-inflammatory signal those bacteria were supplying. It keeps macrophages in an antimicrobial rather than an inflammatory state [281] and seals the barrier [279], which cuts off the LPS leak at its source.
• Tributyrin supplies butyrate without depending on bacteria that aging has already depleted, which is why I consider it a core supplement for anyone over 40 (Author's Observation).

7. Why Four Tablespoons Of Ghee A Day Did Not Do This

When I started tributyrin, I had been eating four tablespoons of ghee a day, used for cooking, for a long time. Ghee has more butyrate than the supplement. Four tablespoons carry about 1.5 grams of butyrate [284]. One 300 mg tributyrin softgel carries about 0.26 grams. I was eating roughly six times as much butyrate from ghee and getting none of the effect (Author's Observation). The reason is where the butyrate ends up, not how much you swallow.

• Ghee and tributyrin are built differently. In ghee, butyrate makes up a small fraction of each fat molecule, attached alongside long-chain fats; a cow's mammary gland builds it that way. Tributyrin is made by bonding butyrate to all three positions of glycerol, so it is essentially all butyrate.
• Ghee's butyrate is released early. It sits where digestive enzymes cut first, so it is freed in the stomach and upper small intestine, absorbed there, and sent to the liver. Butyrate absorbed that high up mostly never reaches the colon [285].
• Much of tributyrin arrives intact. In the CoreBiome digestion model, about half the dose reached the colon intact [277], where Candida, its biofilm, and the damaged gut lining are. Researchers have measured this, but the reasons are not fully understood.
• Ghee feeds the wrong address. Ghee's butyrate goes to the liver. Tributyrin's butyrate goes to the colon wall and to Candida itself.
• Concentration matters. Butyrate's effect on Candida depends on the dose that reaches it [24]. A softgel delivers concentrated butyrate to one stretch of gut. Ghee releases butyrate a little at a time over a meal, and it is absorbed before it gets anywhere useful.
• Cooking is not the reason. Butyrate stays bound to the fat at cooking temperatures. Ghee is still a good cooking fat for this protocol. It just isn't a way to get butyrate to the lower gut.

8. How Tributyrin Fits The Phase 1 Stack

Tributyrin was added to a routine I had been following for a long time: glycine, extended fermentation yogurt, nori seaweed, and walnuts. I took it with the nori, and the die-off that followed was larger than anything that routine had produced without it. I cannot separate the contribution of the two, and nori on its own is already the most potent food against Candida in this protocol (Author's Observation). No study has tested this combination, so I will not call it synergy as a scientific claim. What I can show is that each component attacks a different part of the Candida problem, and that tributyrin covers the one part the others do not.

• Tributyrin (butyrate): blocks the yeast-to-hyphae switch, strips biofilm, and arms macrophages to kill Candida [24, 280, 281, 283].
• Glycine: seals the tight junctions that Candida hyphae pry open [20, 179, 180], restores glutathione [181], calms immune cells through glycine-gated chloride channels [182], and interferes with bacterial cell-wall construction [186].
• Extended fermentation yogurt (GR-1, RC-14, and the others): direct antagonism of Candida, competition for the adhesion sites hyphae need, bacteriocins, and lactic acid, which lowers gut pH; in the laboratory, butyrate's antifungal effect was strongest under acidic conditions [24, 158, 159, 160, 210].
• Nori: the anti-Candida and anti-biofilm effect described under Nori Seaweed, including the Gracilaria biofilm data [206], and in my experience the single most potent food against Candida in this protocol (Author's Observation).
• Walnuts: urolithin A production by the microbiome [195], which drives mitophagy, the clearing of damaged mitochondria [196]. That matters here because oxalate damages mitochondria [16] and damaged mitochondria are an inflammasome trigger [17] (Part 1). At 42 grams daily, walnuts also increase butyrate-producing bacteria [478].

Put together: the yogurt and nori combination kills Candida and keeps it from re-attaching; glycine repairs the wall Candida came through; walnuts clear the mitochondrial damage left behind; and tributyrin removes Candida's last two defenses, the invasive hyphal form and the biofilm that shields it. That is the most plausible explanation for why adding tributyrin to an already effective routine produced a response within 24 hours rather than weeks. Even though I noticed the most significant improvement with tributyrin, I believe that was because I was already on an aggressive gut healing protocol when I added it. Tributyrin was the last piece, and it may have been the most significant, but it worked on ground the rest of the protocol had prepared. The message is: do not skip anything (Author's Observation).

Two cautions. First, do not start all five on the same day. The die-off from this stack is substantial, and starting them together makes it impossible to tell which one is doing what. Build the routine in the order given in Phase 1 Implementation and add tributyrin once the yogurt and nori are tolerated. Second, I did not follow that advice perfectly myself: I took the first tributyrin with nori, which is why I cannot tell you which of the two did more. If you want that information for yourself, add tributyrin on a day you are not eating nori, and hold the rest of the routine constant.

Caution: The lab concentrations above are higher than what 300 mg of tributyrin produces in the gut [24], so the clinical effect likely comes from the combination of direct antifungal action, immune activation, and barrier repair rather than any one of them. Expect die-off. As with nori and the Fantastic 4, start with one capsule per day and increase only as the die-off symptoms allow.

Backups: Oregano Oil, Black Seed Oil, And Nystatin

Oregano oil with black seed oil, and nystatin through your MD, were the original Phase 2 antifungals in this protocol, and they remain available as backups: use them if tributyrin is not tolerated, or if die-off plateaus and your retest is still not clean. Everything below describes how I used them.

As a behavioral microbiome scientist, I have always been uncomfortable with oregano oil because there is no established clinical dose. The only human dosing study I am aware of gave adults with intestinal parasites 600 mg of emulsified oregano oil daily for 6 weeks [286]. It was small and had no control group, so it does not establish a validated dose. Beyond that study, timing guidance comes from clinics that use herbal antimicrobials rather than from research.

In 2016, I developed a severe bladder infection while under a urologist’s care. After five rounds of antibiotics, the last one through a PICC line, I was at the end of my rope. By the time it recurred again, I had thoroughly researched oregano oil and began a regimen of 300 mg of oregano oil containing 225 mg of carvacrol, the primary active compound in oregano oil. This finally resolved what five rounds of powerful antibiotics could not, and without the severe damage (Author’s Observation). This does not mean that oregano oil spares good bacteria; in my experience, the damage is simply not remotely as severe as with antibiotics.

For this microbiome restoration protocol, I doubled the oregano oil dose to 600 mg per day, using a product with a lower carvacrol concentration that supplied 325 mg of carvacrol, 100 mg more than my original regimen. Clinics that use herbal antimicrobials generally consider this a moderate amount and limit use to no more than 4 to 6 weeks (Author’s Observation). The one human dosing study also ran for 6 weeks [286].

Phase 2 Implementation: I purchased Micro Ingredients Oil of Oregano Softgels in a 150-pack. This worked out to 37.5 days at 600 mg/day. I would take four softgels with my main protein meal and keep them at least 2 hours away from when I ate my extended-fermentation yogurt. I took Kyolic Aged Garlic along with this.

Before I completed Phase 2, I had to engage Phase 3 because of a painful gallbladder with a fluttering, spasm-like sensation. I was so toxic that it took six olive oil flushes before the gallbladder pain and spasms calmed down. This will be different for everyone.

Flexibility In Phase 2: Oregano Oil, Black Seed Oil, Nystatin, Or A Combination

Phase 2 is the most aggressive step in this protocol, which is exactly why it must also be the most flexible. The goal is to reduce Candida and pathogenic overgrowth without undoing the beneficial microbial rebuilding achieved in Phase 1. How hard you need to push depends on how severe your overgrowth is, how your body responds, and what your testing shows.

Oregano oil is a powerful, broad-spectrum antimicrobial: it kills bacteria as well as fungi. Origanum oil has demonstrated antifungal activity against Candida albicans [287]. Its breadth raises concern about collateral effects on beneficial bacteria; however, in laboratory testing, carvacrol- and thymol-containing essential oils inhibited pathogens such as Salmonella and E. coli with little inhibition of lactobacilli and bifidobacteria [288]. Whether the same selectivity holds in the human gut has not been established. In a small retrospective study, herbal antimicrobial regimens that include oregano performed comparably to the antibiotic rifaximin for small intestinal bacterial overgrowth, but those regimens were clinician-directed and time-limited [289].

Some people will be able to recover without oregano oil at all. Black seed oil (Nigella sativa) is a much less harsh option and, in my experience, a more selective one. It has a long history of food use, a favorable safety record in human studies, and anti-inflammatory and antioxidant properties alongside its antimicrobial effects [290]. Its primary active compound, thymoquinone, is fungicidal against Candida glabrata in laboratory testing [291]. For those with milder overgrowth, black seed oil combined with the Phase 1 foundation of fasting, extended-fermentation yogurt, and nori seaweed may be enough. Others may use black seed oil alongside a lower dose of oregano oil, or step up to oregano oil only if symptoms and test results fail to improve.

Nystatin: A Narrower Option To Discuss With Your MD. Nystatin is a prescription antifungal, and unlike oregano oil, it is not a broad-spectrum antimicrobial. It binds to sterols in fungal cell membranes, which bacteria do not have, so it targets Candida without directly killing gut bacteria. Taken by mouth, it is not absorbed from the gut, so it acts where the overgrowth is [292]. That makes nystatin the narrower choice when testing and symptoms point to Candida rather than bacterial overgrowth. It does nothing for SIBO or other bacterial overgrowth, which is where oregano oil’s breadth can be an advantage. Clearing Candida can still shift the bacterial community indirectly, so a narrower tool is not the same as no effect on the microbiome.

If Phase 1 is already producing strong die-off symptoms, do not add nystatin, oregano oil, or black seed oil on top of them without your MD. Add one change at a time so you can tell what is causing what (Author’s Observation).

I had to go with oregano oil. My case was severe, with oxalate toxicity, Candida overgrowth, and bile sludge all at once, and it warranted the stronger approach. That does not make it the right choice for you.

All of these options must be discussed with your MD. Black seed oil can lower blood sugar and blood pressure [290], which matters if you take medication for either, and oregano oil carries its own risks with extended use. Nystatin requires a prescription, so your MD decides whether it fits your case. Whether you use oregano oil, black seed oil, nystatin, or a combination, the amount and the timeline must be determined by you and your MD based on your symptoms, your test results, and how your body responds. Use the Burris Gut Health Checklist to track your progress so that every adjustment is based on data rather than guesswork.

Phase 3: Mitochondrial Restoration Top

24 To 44 Hour Fast And Olive Oil Flush

Phases 1 and 2 clear Candida and seal the gut barrier. Phase 3 repairs what they leave behind: damage to the mitochondria, the energy-producing structures inside every cell.

• Oxalates damage mitochondria. Oxalate disrupts mitochondrial function and the cell's antioxidant balance [16].
• Candida damages them too. Its toxin, candidalysin, triggers a burst of mitochondrial reactive oxygen species in epithelial cells. This was shown in the laboratory [293].
• Damaged mitochondria keep inflammation going. They are a direct trigger for the NLRP3 inflammasome, the same alarm behind inflammaging [17]. The gut barrier itself runs on mitochondrial energy, and when the mitochondria in the gut lining fail, the barrier fails with them [1, 7, 8].

The extended fast and the olive oil flush belong here for two reasons:

• The fast helps rebuild. In mice, a 24-hour fast switched the gut lining's stem cells to burning fat in their mitochondria and boosted their ability to regenerate [294].
• The flush depends on the fast. An optimal flush includes a 24-hour fast, so I pair them. If gallbladder symptoms called for a flush earlier, I would not wait for Phase 3 (Author's Observation).

Phase 3 closes with Mitochondrial Regeneration and the Mitochondria Supplement Stack, alongside three tools already in this protocol: walnuts and urolithin A, glycine and glutathione, and red-light therapy.

Phase 3 consists of a 24 to 44-hour fast one to three times a week, followed by an olive oil flush. In mice, a 24-hour fast activates fatty acid oxidation and boosts the regenerative capacity of intestinal stem cells [294], and repeated cycles of prolonged fasting promote regeneration of blood-forming stem cells [295].

The olive oil flush consisted of 3-4 ounces of olive oil with an equal amount of lemon juice, which will be reduced to 1 to 2 ounces once healed. In the early days of doing these flushes, I experimented with 4, 6, 8, 12, and 16 ounces of olive oil, and there was no increased effect past 4 ounces.

Warning: A stone that passes during a flush can become lodged in the common bile duct and cause a blockage, an infection (cholangitis), or pancreatitis, all of which can be life-threatening [296]. Do not do a flush without your MD’s approval, especially if you have known gallstones. Go to an emergency room if you develop fever or chills, yellowing of the skin or eyes, dark urine, abdominal pain that lasts more than a few hours, or persistent vomiting.

Why is this phase critical? The biliary duct network, known as the biliary tree, is a branching system that transports bile from the liver to the gallbladder and the intestine, which is essential for digestion and the elimination of metabolic waste. This sophisticated ductal network is essential for precise bile delivery and overall digestive health [297].

MDs will tell you not to do a liver-gallbladder flush and to let the bile ducts and gallbladder clear on their own. What they do not tell you is that the standard of care for gallstones is the surgical removal of the gallbladder (cholecystectomy). Let's take a look at the data.

Deaths in the US From Gallbladder Surgery: Approximately 2,000 to 3,000 deaths annually

Deaths Worldwide From Olive Oil Flushing: No documented deaths

MDs will also tell you that gallstones cannot pass through the cystic duct. As someone who has passed rock-hard gallstones that you could make jewelry out of, I can definitely say this is false. It is true, however, that stones can get stuck in the cystic duct. This happened to me twice, and I had to do another flush the following morning. This was in 2012, when I initiated this process, and it has not happened since, primarily because I do liver gallbladder flushes on the regular.

Bile sludge is thought to be a precursor to gallstones and liver stones. I have experienced both, and I can tell you that this is indeed accurate. Advanced spectroscopic techniques have greatly improved the analysis of gallstone composition [298], and in one chemical analysis of 40 gallstones, 25 contained oxalate [299]. There are many types of gallstones, and oxalate is a common component.

Olive Oil Dosing

• 1-2 ounces for maintenance
• 3-4 ounces for flushing the liver and gallbladder
• 3-4 ounces for prevention of constipation up to 2 times daily. If you are using inulin, this may be enough to avoid constipation.

Any time I take olive oil, I always use an equal amount of lemon juice. If constipation is an issue, I will do 2-3 ounces in the morning and 2- 3 ounces at night before bed. After 2 months of 24-hour fasting, constipation became less of an issue, so I lowered the dose.

Bile Sludge And Gallstone Symptoms

The most common symptomatic manifestation of gallstones is episodic upper abdominal pain. Characteristically, this pain is severe and located in the epigastrium and/or the right upper quadrant. The onset is relatively abrupt and often awakens the patient from sleep. The pain is steady in intensity, may radiate to the upper back, be associated with nausea, and lasts for hours to up to a day. Dyspeptic symptoms of indigestion, belching, bloating, abdominal discomfort, heartburn, and specific food intolerance are common in persons with gallstones but are probably unrelated to the stones and frequently persist after surgery [300]. This is only one of the many reasons surgery does not make sense for most people.

Effects Of Bile Acids On Neurological Function

Bile acids are synthesized from cholesterol and are known to be involved with the emulsification and digestion of dietary lipids and fat-soluble vitamins. Outside of this role, bile acids can act as cell signaling effectors. Bile acids are the end products of cholesterol metabolism and can contribute to hepatic, intestinal, and metabolic disorders [301].

Neuromyelitis Optica

Neuromyelitis Optica [302] is one of the neurological autoimmune conditions in which altered bile acid levels have been found [303, 304]. This was one of the multitude of symptoms I had and recovered from. Another theory is that oxalate crystals travel down the optic nerve from the brain (Author’s Observation). This is why I am still flushing oxalate crystals from my eyes with water up to 10 times a day. The medical literature does not make the connection between oxalate and this condition, nor does it explain how to reduce bile sludge effectively.

The Nerve Repair Stack

• B1: Benfotiamine
• R-Lipoic Acid
• B6: Pyridoxal-5-Phosphate
• B9: Folate
• B12: Methylcobalamin
• L-Citrulline
• Carnitine: I do not supplement this as I believe I get enough from meat.

Check with your Functional Medicine MD to determine the dosage of each supplement.

Mitochondrial Regeneration Top

The Key To Energy, Healthspan, And Longevity

Mitochondria are engaged in the pathogenesis of human diseases and aging directly or indirectly through a broad range of signaling pathways. They are the cell's primary source of ATP (Adenosine triphosphate) and play a pivotal role in cell life and death. ATP is the energy source for use and storage at the cellular level [305]. This is why most in the medical community refer to the mitochondria as the cell's powerhouse.

Due to their central role in cell life and death, mitochondria are also involved in the pathogenesis and progression of numerous human diseases, including, among others, cancer, neurodegenerative and cardiovascular disorders, diabetes, traumatic brain injury, and inflammation [305].

Mitochondria And Emotional Fitness (Mental Health)

The mitochondrial response to stress is communicated both locally within the cell and systemically throughout the body. Exposure to stress mediators precipitates the mitochondrial release of signaling molecules, collectively called mitokines. Mitokines serve as signals that indicate mitochondrial fitness, which is particularly important in environmental stressors. Mitokines include various mitochondrial metabolites, calcium, and reactive oxygen species (ROS). When elevated, ROS overwhelms the cell's antioxidant capacity and promotes oxidative stress, causing cell death and tissue damage. These mechanisms allow mitochondria to influence broad physiological processes throughout the body, including molecular mechanisms of aging and stress-related conditions, psychiatric disorders, cardiovascular disease, obesity, diabetes, and cancer [306].

If you view your body as an electric vehicle, the batteries would be the mitochondria. Unfortunately, over time, the batteries become dysfunctional and slowly die, while your energy slows down until the entire machine dies unless there is consistent maintenance and replacement of the dysfunctional cells. I know this is an oversimplification, but the important thing is to understand the impact and importance of mitochondria. Maintenance and replacement of the mitochondria is a multipronged approach that includes diet, exercise, and supplementation, which we will discuss below.

If you would like to go full geek on mitochondria, especially in terms of the brain and human behavior, you may want to look at a book called Brain Energy. I am not in agreement with this author's assertion that the mitochondria are at the root of mental illness, but he is at least headed in a good direction.

Mitochondria Supplement Stack

PQQ (Pyrroloquinoline Quinone): PQQ is associated with biological processes such as mitochondriogenesis, reproduction, growth, and aging. In addition, PQQ attenuates clinically relevant dysfunctions (e.g., those associated with ischemia, inflammation, and lipotoxicity) [307]. This is the only supplement I am aware of that regrows new mitochondria.

Niacin: Niacin (vitamin B3) comes in two main forms, nicotinamide (also called niacinamide) and nicotinic acid. Nicotinic acid causes flushing, while nicotinamide does not. Both increase NAD+ (nicotinamide adenine dinucleotide), but only nicotinic acid improves your lipid profile [308]. Niacin modulates SIRT1 (sirtuin 1) [309], which is how nicotinic acid inhibits vascular inflammation [309].

NAD+: Nicotinamide adenine dinucleotide (NAD+) is an important coenzyme for redox reactions (electron transport and transfer), making it central to energy metabolism.

The slow, inevitable aging process has been described as a "cascade of robustness breakdown triggered by a decrease in systemic NAD+ biosynthesis and the resultant functional defects in susceptible organs and tissues [310]. Niacin is an efficient NAD+ booster for treating mitochondrial myopathy [311]. In this study, 750 to 1000 mg was used for 4 and 10 months, but I have looked at individual data that showed improvements in NAD+ with much less using nicotinic acid. I take 500 mg of nicotinic acid after eating. Taking it on an empty stomach can cause significant flushing. This is another vitamin that you will want to start slowly. I am currently using niacinamide.

NMN and NR (Nicotinamide Mononucleotide and Nicotinamide Riboside): I do not recommend NMN or NR.

By middle age, our NAD+ levels have plummeted to half that of our youth. Numerous studies have demonstrated that boosting NAD+ levels increases insulin sensitivity, reverses mitochondrial dysfunction, and extends lifespan. NAD+ levels can be increased by activating enzymes that stimulate the synthesis of NAD+, by inhibiting an enzyme (CD38) that degrades NAD+, and by supplementing with NAD precursors, including niacin [310].

Luteolin: CD38 is an enzyme that increases with age via inflammation, and this decreases NAD+. This inflammation is induced by senescent cells (damaged cells that have stopped dividing but do not die). Luteolin and other supplements, such as apigenin, suppress CD38 [312]. This is why autophagy may be even more important as we age because the body consumes senescent cells when in an autophagic state, which, in theory, should also help to lower CD38. I say in theory because there are no studies on this subject at this time.

Urolithin A: Urolithin A (UA) is produced by gut microflora from foods rich in ellagitannins. UA has been shown to improve mitochondrial health preclinically and in humans. Not everyone has a microbiome capable of producing UA, making supplementation with UA an appealing strategy [313]. Urolithin A has been shown to promote mitophagy (clearance of dysfunctional mitochondria), mitochondrial function, and improved muscle function across species in different experimental models and across multiple clinical studies [196]. One cause of the loss of mitochondrial homeostasis during aging is the accumulation of dysfunctional mitochondria [196]. Fasting and exercise also induce mitophagy. Mitophagy must occur to enable mitochondrial biogenesis (generation of new mitochondria).

AKG (Alpha-Ketoglutarate): Recent studies in experimental models have shown that dietary AKG reduces reactive oxygen species (ROS) production and systemic inflammatory cytokine levels, regulates metabolism, extends lifespan, and delays the occurrence of age-related decline [314]. Mechanistically, AKG leads to an energetic state that is reprogrammed toward a mitochondrial metabolism, with increased oxidative phosphorylation and expression of complex mitochondrial enzymes [315].

ALA (R-Alpha Lipoic Acid): The R in Alpha Lipoic Acid indicates it is the natural, more bioavailable form. This supplement must be taken on an empty stomach for maximum bioavailability. ALA is synthesized in the mitochondria and plays an essential role as a cofactor, assisting in the enzymatic nutrient breakdown.

ALA is considered generally safe. A meta-analysis of 71 randomized placebo-controlled trials found that ALA did not increase the risk of side effects, including in studies of children and adolescents [316]. The max I take is 600 mg a day on an empty stomach.

CoQ10 (Coenzyme Q10): In addition to shuttling electrons in the mitochondrial respiratory chain, CoQ10 serves several additional cellular functions, including the transfer of electrons in plasma membranes and lysosomes, modulation of apoptosis (cell death) proton transport of uncoupling proteins, and antioxidant activity including inhibition of lipid peroxidation [317]. My numbers were good for CoQ10, so I do not supplement, but if I did supplement, I would use the freeze-dried beef heart capsules.

L Carnitine: L-carnitine is one of the key nutrients for proper mitochondrial function and is notable for its role in fatty acid oxidation.

L-carnitine also plays a major part in protecting cellular membranes, preventing fatty acid accumulation, modulating ketogenesis and glucogenesis, and in the elimination of toxic metabolites. L-carnitine deficiency has been observed in many diseases, including organic acidurias, inborn errors of metabolism, endocrine imbalances, and liver and kidney disease [318]. I do not supplement with l-carnitine.

Creatine: Creatine monohydrate (CrM) is one of the most widely used nutritional supplements among active individuals and athletes to improve high-intensity exercise performance and training adaptations. However, research suggests that CrM supplementation may also serve as a therapeutic tool in the management of some chronic and traumatic diseases. Creatine supplementation has been reported to improve high-energy phosphate availability as well as have antioxidative, neuroprotective, anti-lactic, and calcium-homoeostatic effects. These characteristics may directly impact mitochondrion survival and health, particularly during stressful conditions such as ischemia and injury [319]. I do not supplement with creatine.

Omega-3 Fatty Acids: Mitochondrial dysfunction represents a common early pathological event in brain aging and in neurodegenerative diseases, e.g., Alzheimer's (AD), Parkinson's (PD), and Huntington's disease (HD), as well as in ischemic stroke. In vivo and ex vivo experiments using animal models of aging and AD, PD, and HD mainly showed improvement in mitochondrial function after treatment with polyunsaturated fatty acids (PUFA), such as docosahexaenoic acid (DHA) [320]. My test showed low omega-3, so I supplement with Total Omega 3 Full Spectrum by Sports Research.

B Complex: Mitochondria are compromised by a deficiency of any B vitamin [321]. More details on this are in the B vitamin section of this paper.

Vitamin D: Skeletal muscle mitochondrial function is the biggest component of whole-body energy output. Mitochondrial energy production during exercise is impaired in vitamin D-deficient subjects. Vitamin D supplementation initiated in older people improved muscle mass and strength [322].

Vitamin C: Vitamin C quenches mitochondrial ROS (reactive oxygen species) and inhibits oxidative mitochondrial DNA damage [323].

Minerals: Mitochondria are particularly rich in minerals, where they function as essential cofactors for mitochondrial physiology and overall cellular health. Eleven of the 12 minerals essential for human health have important roles within mitochondrial metabolism. However, this picture is not yet complete [324]. The bottom line is to make sure that all minerals are well-balanced.

Support Stack Top

Microbiome Restoration And Candida Eradication Support Components Top

When done right, Candida die-off represents multiple mechanisms that cause high levels of toxicity and severe malaise. A primary objective is to break down the biofilm that protects Candida, which releases its own toxins and can cause constipation, one of the most significant issues associated with Candida die-off (Author’s Observation). Then there are all the pathogens that are harbored within this protective layer on top of the Candida itself. This process can then lead to further inflammation and a persistent disruption of the microbiome. To counteract this, several support components are available for all three phases, as listed below.

It is critical to initiate the SR™ Gut Barrier and Microbiome Restoration with the support stack because the toxins from Candida die-off, biofilm, and all the pathogens they harbor can overwhelm the system and may cause you to quit the protocol before completion.

Support Stack For All Phases

1. Organic Extra Virgin Olive Oil
2. Zinc-Carnosine, Colostrum, and Lactoferrin
3. Glycine
4. Niacin (niacinamide)
5. Saccharomyces boulardii in the form of Florastor CNCM I-745
6. Astaxanthin
7. Tryptophan (To get to sleep)
8. L-Theanine in the form of Suntheanine® (To stay asleep)
9. Magnesium Citrate if Oxalate poisoned or Magnesium Glycinate if not poisoned
10. Copper
11. Sunlight or Red-Light Therapy
12. Kyolic Aged Garlic Supplements
13. Hydrogen Rich Water

Support 1: Olive Oil

Olive oil: Although olive oil is the foundation for Phase 3, it is listed first here because it is used to clear the liver, gallbladder, and bile ducts of bile sludge. Even though I followed my own protocol, I had to interrupt it in month four to do an olive oil flush to clear bile sludge, which was characterized by right abdominal pain just below the bottom rib and consistent sleep disruption. Most people will not be able to do a 24-hour fast, then drink 4 ounces of olive oil out of the gate. This is why it is used only as support initially. However, like me, because of the high toxic load and gallbladder pain, one may need to interrupt the protocol and focus on flushing the toxins from the liver and gallbladder.

Olive Oil Components

• Oleuropein constitutes over seventy percent of the phenolic compounds in olive oil and olive leaf. This is why it has gained a reputation as the best anti-inflammatory, antioxidant, antiviral, antimicrobial, anticancer, anti-aging, anti-Candida, antiparasitic, and neuroprotective compound [325].
• Oleocanthal rapidly and selectively induces cancer cell death. As with Oleuropein, Oleocanthal is an effective anti-inflammatory along with several other attributes, including an anti-Alzheimer agent, an anticancer agent, and a cardioprotective agent [326].
• Hydroxytyrosol reduces oxidative stress and inflammation, thus positively altering the key components of metabolic syndrome [327]. Metabolic syndrome is a cluster of conditions that occur together, increasing your risk of heart disease, stroke, and type 2 diabetes. These conditions include increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels.

An in vitro study showed that olive leaf aqueous extracts destroyed 15% of C. albicans within 24 hours [328].

What To Look For When Purchasing Olive Oil

• Organic
• Extra Virgin
• First Cold Pressed
• Sourced From a Single Region
• Use-by Date: 1 Year Out Preferred
• DOP/PDO: DOP stands for "Denominazione di Origine Protetta" in Italy or PDO "Protected Designation of Origin." For a particular area to be awarded the PDO/DOP status, it must produce outstanding olive oil and have a good reputation.
• For olive oil to qualify for the PDO/DOP name and logo, it must be grown, produced, and bottled in the designated area, but it must also meet strict requirements in terms of varietals, method of production, and overall quality. The bottom line is whether you want the best DOP or PDO designation look.
• Type of Olive: There are several olives that produce higher phenolic compounds. The one I use is made from a Greek olive called Koroneiki.
• Counterfeit Olive Oil: If you want a less expensive olive oil and are unsure about the purity of what you are using, go to https://www.aboutoliveoil.org/certified-olive-oil-list to see if it has been tested for purity.
• Phthalates: Phthalates are chemicals used in the production of plastics, such as PVC pipe, and are known endocrine disruptors. In recent testing by a site called mamavation.com, none of the olive oils they tested were found to be free of this endocrine disruptor, so it is worth researching to find a brand with the lowest levels of this chemical.

Support 2: Zinc-Carnosine Colostrum And Lactoferrin

In a small study, heavy exercise increased gut permeability in healthy volunteers, with 70% improvement with both zinc-carnosine and colostrum, and even better results when using both [329]. This, of course, is not the exact mechanism within our context, but it was close enough for me to take myself and recommend.

I used PepZinGI, a patented zinc-carnosine complex with the most research behind it; however, I cannot say definitively that it is the most effective. As for the colostrum, I use Micro Ingredients Bovine Colostrum Powder. This colostrum is freeze-dried and grass-fed, two key factors to consider when purchasing colostrum.

I take colostrum with zinc-carnosine as a 30-day course at the start of Phase 1, one hour before and one hour after my eating window, then stop. The study behind this combination ran 14 days [329]; 30 days is my recommendation, not a study result. Zinc itself continues as a regular supplement after the colostrum course ends, except on days I eat a high-zinc food such as pumpkin seeds. Any time I take zinc I take copper with it, because zinc drives copper down (see Support 10: Copper). Your test results, not this paragraph, should decide your zinc, copper, and other supplement combinations (Author's Observation).

Lactoferrin

Colostrum contains 10 components effective toward candida overgrowth, but lactoferrin is the most effective. Many supplement companies market high IgG (immunoglobulin G), but this can reduce lactoferrin levels. My objective was to balance the microbiome; therefore, the colostrum needed to be balanced. I added 250 mg of lactoferrin twice daily, along with colostrum and zinc-carnosine, and initially experienced a significant die-off and backed off to 250 mg daily. I then picked it back up to 250 mg twice daily and saw improvement every day. This combination represented the most significant for healing the gut. The following is a breakdown of what lactoferrin affects.

Candida

Lactoferrin exhibits broad antifungal activity against several Candida species, including C. albicans, C. glabrata, and C. tropicalis. One of the primary mechanisms involves iron deprivation. The iron-free form of lactoferrin significantly reduces the viability of C. albicans cells depending on time, temperature, and pH, with the most pronounced effect at neutral pH and 37 degrees Celsius. When lactoferrin is saturated with iron, its fungicidal properties are abolished, confirming that iron removal from the environment is a crucial factor limiting the growth of yeast-like fungi [330].

A systematic review and meta-analysis confirmed that bovine lactoferrin and its peptide derivatives can significantly inhibit the growth of C. albicans, both in azole-susceptible and azole-resistant strains [331].

Biofilm

Lactoferrin significantly inhibited biofilm formation in clinical isolates of Pseudomonas aeruginosa, with the most marked effect at 2 mg/ml. Supplementation of lactoferrin to preformed biofilm demonstrated a reduction in biofilm, suggesting that lactoferrin may also have destructive effects on established biofilm [332].

Lactoferrin has also been reported to inhibit biofilm formation by, and to disrupt established biofilms of, Staphylococcus species, including methicillin-resistant strains [333].

The anti-biofilm effects extend to oral pathogens as well. Biofilm formation of P. gingivalis and P. intermedia over 24 hours was effectively inhibited by lower concentrations (at or above 8 micrograms/ml) of various iron-bound forms of bovine and human lactoferrin [334].

In terms of broader mechanisms, lactoferrin inhibits biofilm formation and disrupts existing biofilms either by preventing lectin-dependent bacterial adhesion or by stimulating bacterial motility. Lactoferrin also appears to inhibit bacterial adhesion to epithelial cells and intestinal mucosa [333].

Cancer

Bovine lactoferrin demonstrates high bioavailability after oral administration, high selectivity toward cancer cells, and a broad range of molecular targets that control tumor proliferation, survival, migration, invasion, and metastasis. Notably, lactoferrin can promote or inhibit cell proliferation and migration depending on whether it is acting on normal or cancerous cells, and its administration is well tolerated without significant adverse effects [335].

The mechanisms are multifaceted. In the presence of lactoferrin, different cancer cells suffer significant damage, including cell cycle arrest, cytoskeletal damage, and induction of apoptosis, along with decreased cell migration [336].

Lactoferrin also works through iron metabolism. By chelating free iron ions, lactoferrin reduces oxidative stress and inhibits the mechanisms that promote carcinogenesis, while also exhibiting immunomodulatory and anti-inflammatory effects that may enhance the body's antitumor response [337].

One important caveat: some studies have indicated that high levels of endogenous human lactoferrin expression may be linked to increased carcinogenesis and metastasis, reflecting its context-dependent role in cancer. The distinction between exogenous supplementation and endogenous expression appears to matter considerably [338].

Other Pathogens (Bacterial, Viral, Parasitic)

Lactoferrin's antimicrobial reach is broad. It displays antiviral activity against both DNA and RNA viruses, including rotavirus, respiratory syncytial virus, herpes viruses, and HIV. The antiviral effect lies in the early phase of infection, where lactoferrin prevents viral entry into host cells either by blocking cellular receptors or by directly binding to virus particles [339].

Lactoferrin's antiviral activity has been studied against SARS-CoV-2, Zika, Dengue, Hepatitis, and Influenza viruses in vitro, demonstrating not only competitive binding properties but also potential intracellular impacts on host cells, such as enhancing cellular defenses [340].

Oral supplementation shows practical protective value. Lactoferrin consumption reduced the incidence of noroviral gastroenteritis in children, leading to protection against viral infections [341].

Support 3: Glycine: Gut Barrier And Biofilm Support

Warning: The effects of glycine on cancer are context-dependent, so check with your physician first before implementing this supplement if you have cancer.

Glycine is a precursor of glutathione, and glutathione is needed by the immune cells that clear Candida. In a mouse model, glutathione reductase, the enzyme that recycles glutathione into its active form, promoted fungal clearance and suppressed inflammation during systemic Candida albicans infection [342]. When I took therapeutic amounts of glycine, I passed so much material that appeared to be Candida that I had to cut back several times. Clearing Candida biofilm matters for another reason: the biofilm can shelter viruses. Herpes simplex virus 1, which causes cold sores, showed decreased sensitivity to antiviral drugs and laser treatment when entrapped in Candida albicans biofilm [343].

Glycine Dosing And Toxicity

In a single-patient case report on refractory obsessive-compulsive disorder and body dysmorphic disorder, glycine at 0.6 to 0.8 grams per kilogram per day was used over 5 years, with marked improvement in both disorders and no reported adverse effects [193]. Per my weight, 0.8 grams per kilogram would be 61 grams per day, more than twice my highest dose. My own dosing history follows.

Warning: Glycine is generally well-tolerated at typical doses, although high doses commonly cause digestive side effects such as nausea, vomiting, and diarrhea [344]. When I increased my intake to 27 grams a day, I passed large amounts of what appeared to be Candida and biofilm, the most I have ever experienced. Glycine is not an established antifungal, but several of its known actions could help explain what I observed. In laboratory studies, glycine protects the intestinal barrier by preserving tight junction proteins under cellular stress [179], and it reduces inflammatory activity in immune cells by activating glycine-gated chloride channels [182]. Glycine is also a precursor of glutathione, the body’s primary intracellular antioxidant, which declines with age and can be restored in older adults by supplementing glycine with cysteine [181]. Finally, glycine interferes with the construction of bacterial cell walls [186], which may weaken the bacterial component of mixed bacterial and fungal biofilms in the gut.

I took 6 grams of glycine per day before increasing it, and I did not notice any die-off. Eighteen grams and above caused significant to massive Candida die-offs, so I settled on 9 grams (one tablespoon). I later increased to 18 grams, then at 21 grams I noticed an improvement in my gait and balance, and then at 27 grams I got up in the morning and emptied my bladder for the first time in 15 years. I am now using between 21 and 27 grams per day over a period of 14 hours. Glycine is the most effective amino acid I have used for a multitude of issues, and it has the weakest study data.

For glycine’s additional benefits and side effects, see Glycine under Supplements. For dosing and the morning light and oxalate warning, see Glycine under Phase 1 Implementation.

Support 4: Niacin (Niacinamide)

NAM (niacinamide) exhibited significant antifungal activity against C. albicans, including fluconazole-resistant isolates. NAM could also effectively suppress biofilm formation. In addition, NAM exhibited antifungal activity against non-Candida albicans species and Cryptococcus neoformans. The antifungal activity of NAM was further confirmed in a mouse model of disseminated candidiasis. These findings suggested that NAM might exhibit antifungal activities by affecting cell wall organization [345].

Support 5: Saccharomyces Boulardii CNCM I-745

Anti-toxin Enzyme Activity

S. boulardii CNCM I-745 releases a serine protease capable of digesting pathogenic toxins, such as Clostridium difficile toxin A and similar pro-inflammatory molecules, thereby reducing their binding to intestinal receptors and limiting mucosal damage. This enzymatic detoxification is relevant to Candida die-off because fungal metabolites and endotoxin-like compounds (e.g., acetaldehyde, mannans) can provoke similar inflammatory cascades, although this protection has not been studied in Candida die-off [346] (Author’s Observation).

Restoration Of Immune And Inflammatory Pathways

NIH data show that CNCM I-745 inhibits pro-inflammatory signaling. These pathways are central in immune activation during Candida die-off. Based on this, I use CNCM I-745 to help limit the inflammatory burden of die-off [347] (Author’s Observation).

Enhancement Of Gut Barrier Integrity

The probiotic supports the repair and maintenance of epithelial tight junctions, reducing intestinal permeability caused by microbial toxins and inflammation. By maintaining this barrier [348], CNCM I-745 may limit the passage of Candida-derived toxins into circulation and ease die-off symptoms like fatigue and headaches (Author’s Observation).

Microbiota Restoration And Detoxification Environment

CNCM I-745 fosters restoration of beneficial gut microbiota and promotes short-chain fatty acid production (notably butyrate) that supports mucosal healing and toxin clearance. In my experience, these actions speed recovery after microbial die-off [349] (Author’s Observation).

Support 6: Astaxanthin

In a mouse model, astaxanthin has been shown to be a potent antioxidant and anti-inflammatory compound that positively influences gut microbiota, reduces systemic and local inflammation, and supports gut barrier integrity [350]. I used one bottle of this, but did not experience the effects of S. boulardii, so I stopped taking it.

Support 7: Tryptophan

Tryptophan plays a crucial role in sleep regulation, primarily because it serves as a precursor to serotonin and melatonin, two neurochemicals central to sleep-wake cycles. Increased tryptophan intake, whether by supplementation or tryptophan-rich foods, has been shown in randomized controlled trials and meta-analyses linked from NIH sources to improve sleep quality and duration in individuals with mild insomnia or sleep disorders [351].

For tryptophan’s additional benefits, side effects, and dosing, see Tryptophan (TRP) under Supplements.

Support 8: L-Theanine (in the form of Suntheanine®)

L-Theanine, an amino acid primarily found in tea leaves, supports sleep by modulating neurotransmitter activity, promoting relaxation, and improving sleep quality according to NIH-referenced studies. Research demonstrates that L-Theanine increases brain levels of gamma-aminobutyric acid (GABA), serotonin, and dopamine, neurotransmitters that are closely linked with relaxation and regulation of the sleep-wake cycle [352]. I used Tryptophan to help me fall asleep and L-theanine to stay asleep. This is, at best, difficult when oxalate dumping and experiencing Candida die-off.

Support 9: Magnesium Glycinate And Citrate

Magnesium Citrate if Oxalate poisoned or Magnesium Glycinate if not poisoned. Magnesium glycinate and citrate are among the most bioavailable forms of magnesium, and both assist in over 300 metabolic processes, including mitochondrial function [353]. For our purposes, magnesium glycinate serves as a sleep aid [354], and magnesium citrate helps prevent calcium oxalate crystals from forming.

Support 10: Copper

Conversely, adequate or supplemental dietary copper has been shown to support intestinal barrier integrity, especially in settings such as alcohol-induced intestinal injury. Proper copper supplementation can promote cell growth, reduce oxidative stress (ROS), and restore expression of genes related to the intestinal barrier [355]. The zinc/copper ratio impacts immune, neurological, and hormonal health; maintaining balance is critical [356].

Support 11: Sunlight And Red-Light Therapy

Sunlight (especially UVB) and red/near-infrared light via photobiomodulation (PBM) modulate the gut microbiome by promoting beneficial bacteria, suppressing dysbiosis, and supporting immune and anti-inflammatory pathways. Concurrently, these light therapies enhance mitochondrial energy production and cellular repair mechanisms, fostering a healthier gut environment. This interplay between mitochondrial stimulation and microbiome restoration elucidates potential therapeutic avenues for gut-related diseases and systemic health [357].

A therapeutic effect from sunlight exposure can typically be achieved with about 20 minutes of sunbathing during early morning (7-10 am) or late afternoon (3-5 pm). This timing minimizes harmful ultraviolet radiation exposure while allowing beneficial wavelengths, such as red and near-infrared light, to exert their effects safely [358].

Photobiomodulation (PBM Or Red Light Therapy)

Warning: The outcomes regarding red light therapy and cancer are mixed and context-dependent, so engaging in red light therapy if you have cancer requires MD approval.

PBM specifically utilizes controlled exposure to red (600–700 nm) and near-infrared light (700–900 nm) to stimulate biological effects that are beneficial for mitochondrial function and healing [359]. These wavelengths are a subset of the whole solar spectrum found in sunlight

What To Look For In A PBM Device

While there are over 3,000 studies on PBM, no specific manufacturers were used in these studies; however, standards were set for manufacturers to follow. NovaaLab is one of the manufacturers that follow these standards, and their devices are FDA-cleared as Class II medical devices, which is a primary consideration when purchasing a PBM device. This, among many other issues, makes it a top choice.

There are, however, a couple of issues. The first issue is that you must purchase it directly from the manufacturer, and the second is the cost. I purchased the Novaa Light Pad XL, and it was four times the cost of similar-sized light pads on Amazon. It was an easy rationalization for me, however, because I wanted every assurance that I would recover and function at my absolute peak.

Support 12: Kyolic Aged Garlic Supplements

Aged garlic extract improved gut microbiota, as evidenced by higher microbial richness and diversity, with a marked increase in Lactobacillus and Clostridium species after 3 months of supplementation. It was also effective in reducing blood pressure in patients with uncontrolled hypertension, and has the potential to improve arterial stiffness, inflammation, and gut microbial profile. Aged garlic extract is well tolerated and has a high safety profile as a stand-alone or adjunctive antihypertensive treatment, with multiple benefits for cardiovascular health [360].

Support 13: Hydrogen Rich Water (HRW)

Water: Drinking filtered water is a no-brainer, but mineral and hydrogen water can also have profound effects.

Mineral Water: In a mouse model, kidney crystal formation and fibrosis were attenuated by drinking alkaline mineral water. Furthermore, alkaline mineral water also reduced kidney injury, cell apoptosis, oxidative stress, and inflammation [361]. I put this to the test by drinking mineral water only for three days. After the third day, I had the worst oxalate dump I had ever experienced, and by that time, I was halfway through the fifth year of a low oxalate diet. I now drink only mineral water at least three days a month and at every extended fast.

Hydrogen-Rich Water (HRW)

Warning: While molecular hydrogen can interact with and enhance virtually every cell in the body and assist in restoring the gut, it can also enhance the proliferation of cancer cells [362]. This is why a cancer screening and working closely with your MD are highly recommended before starting a hydrogen water protocol if you suspect you may have cancer.

The research supporting hydrogen-rich water has been moved to Appendix: Hydrogen-Rich Water Research, located just before the References.

Generating HRW: There are several ways to generate HRW. I use an HRW generator, and there are several things you should look for when purchasing one. Here are some attributes of the one I use, the Veemter 3 IN 1 Hydrogen Water Bottle Generator. I highly recommend doing your research before you purchase one. The specs of the one I use are below.

Size: 460 Milliliters (15.5 Ounces)

PPB (Parts Per Billion): The average is 1,500 PPB. The one I use has two modes: Push the button once, and you get 1,500 PPB; push the button twice, and you get 6,000 PPB. This is sometimes measured in PPM (parts per million), but this is an easy conversion: 1,000 PPB is 1 PPM. I could not find any third-party testing for this parameter.

SPE/PEM Technology: SPE and PEM refer to solid phase extraction and proton exchange membrane.

Platinum Titanium Core Electrolytic Sheet: I would not use any less than this.

Base Materials: The body of the hydrogen water bottle is made of high-quality food-grade borosilicate glass, and the lid is made of food-grade stainless steel.

3 Modes: This means you can generate HRW within the container, screw a water bottle to an accessory that is provided or breathe it. I do not use any of the accessories, and I do not drink out of the generator.

Results: I initially tried the single push of the button for 1,500 PPB of hydrogen with no issues, so I then tried the next mode and had a raging case of diarrhea for 24 hours. I returned to the single mode for two days and tried the 6,000 PPB mode again; the diarrhea only lasted a couple of hours. I now generate 2 to 6 15.5-ounce HRW daily in the 6,000 PPB mode. Once I got settled in, I started to feel better.

Optional Support: Coconut Oil

• VCO is an antimicrobial and antifungal [363].
• VCO has antibacterial and skin-protective (emollient) effects [364].
• VCO (virgin coconut oil) significantly reduces plaque and plaque-induced gingivitis [365].

Optional Support: Crustless, Unsweetened Pumpkin Pie

• Pumpkin Puree: Pumpkin has been shown to be antimicrobial, anti-inflammatory, antiparasitic, anticarcinogenic, antioxidant, antidiabetic, hypotensive, and hepatoprotective [366]. There is a concern for high levels of lectins in pumpkins, but these are concentrated in the rind and seeds of the pumpkin and are removed in organic canned pumpkin puree.
• Cinnamon: Cinnamon oil is effective against nearly 50% of the Candida isolates [367].
• Cloves: Clove oil possesses strong antifungal activity against opportunistic fungal pathogens such as Candida albicans, Cryptococcus neoformans, Aspergillus fumigatus, etc. [368].
• Ginger: Ginger extract successfully inhibited biofilm formation by A. baumannii, B. cereus, C. krusei, and C. albicans. The minimum inhibitory biofilm concentrations (MIBCs) of ginger extract for fungi strains (C. krusei and C. albicans) were greater than those of fluconazole and nystatin [369].
• Nutmeg: Nutmeg (Myristica fragrans) was effective against all endodontic pathogens, including C. albicans [370].

Crustless Unsweetened Pumpkin Pie Recipe

• One 15-ounce can of organic pumpkin puree
• One tablespoon of pumpkin spice
• 3 whole eggs or 6 yolks
• ¾ of a cup of heavy cream

Thoroughly mix the first 3 ingredients before adding the heavy cream to keep the spice from clumping, then stir again. I use a 9-inch glass pie pan and rub it down with butter or Ghee, so it is easy to clean. Next, preheat the oven or toaster oven to 350 degrees and bake for 30 minutes. Let it cool for 20 minutes after taking it out of the oven.

Mineral Balance: The Synergistic 4 Top

Magnesium, potassium, sodium, and calcium work synergistically. Oxalic acid binds with heavy metals and minerals. This is why close attention must be paid to this balance. It is difficult to accurately measure calcium and magnesium because the body will pull these two minerals into the bloodstream from bone to keep them in balance. The question regarding magnesium is, do I sleep well, and are my dreams clear and vivid (Author’s Observation)? If the answer is no, sufficient magnesium may be an issue. 'Approximately 50% of Americans consume less than the Estimated Average Requirement (EAR) for magnesium, and some age groups consume substantially less' [371].

Other comments on this diet suggest no issues regarding mineral balance, supplementation, or glycine balance. Everyone seems to agree on the fat-to-protein ratio and water and salt. Nonetheless, I addressed all these issues. I had been battling Candida for over a decade and was suffering from several mineral and vitamin deficiencies. Magnesium and calcium are based on RDA sodium, and potassium is based on AI (adequate intake). You will need to look up your requirements, as the following numbers are based on my gender and age.

• Magnesium: 420 mg per day
• Potassium: 4,700 mg per day
• Sodium: 1,500 mg per day
• Calcium: 1,000 mg per day

Supplements Top

I do not listen to any recommendations regarding supplements because they always come down to Test: Do Not Guess. It is critical, however, to have a basic understanding of supplementation.

Top 10 Gut Health Supplements

1. Glycine: Glycine is a precursor of glutathione, the body’s master antioxidant, and it does much more, including supporting the gut barrier, calming inflammation, and possibly helping to loosen bacterial and fungal biofilms. More on this under Amino Acids: A Complex Picture.
2. Tryptophan: Tryptophan is the sole precursor of peripherally and centrally produced serotonin [372]. A Tryptophan-deficient diet induces gut microbiome dysbiosis and increased systemic inflammation in aged mice (more on this under Amino Acids: A Complex Picture) [373].
3. L-Citrulline: L-Citrulline is a precursor for arginine and nitric oxide. Diminished bioavailability of nitric oxide (NO), the gaseous signaling molecule involved in regulating numerous vital biological functions, contributes to the development of multiple age- and lifestyle-related risk factors and diseases, including hypertension, atherosclerosis, insulin resistance, type 2 diabetes (T2D), and cardiovascular disease [374]. This critical molecule begins to drop off by age 40.
4. Magnesium Citrate: The enzymatic process of vitamin D requires magnesium, along with approximately 300 other enzymatic processes, so I had to increase this mineral intake. Citrate helps prevent calcium oxalate crystals from forming, but there are many forms of magnesium.

The magnesium deception: All magnesium must be bound to something, and most manufacturers include what it is bound to as part of the milligram rating. This can be deceiving, as only about 16% of it is elemental magnesium. The bulk magnesium I recommend clearly states the amount of elemental magnesium you get per serving. If magnesium does not clearly state the amount of elemental magnesium, I would not purchase it.

5. Potassium Citrate: I get this in bulk and take a teaspoon per day, but my potassium was still borderline.
6. R-Alpha Lipoic Acid: ALA represents one of the most convoluted naming conventions for a supplement I have ever seen. The R indicates it is the natural version, which is more bioavailable; however, R-Lipoic Acid is a purer form than R-Alpha Lipoic Acid. The 300 mg R-Lipoic Acid I take states that it is made from 600 mg of R-Alpha Lipoic Acid. I take 300 mg daily based on my NutrEval. ALA and B12 compete for the same pathway, so this takes some adjusting. It is estimated that taking R-Lipoic Acid on an empty stomach increases bioavailability by 40%, so I take this first thing in the morning before any food, along with vitamin C.
7. B Complex: I was low on B1, B2, B3, and B6, so I changed my B vitamin protocol. I am now using B Complex, along with Benfotiamine (B1), B2, and niacinamide, which is a form of B3 and B6.
8. Vitamin C: At the time I took the NutrEval test, I was taking 500 milligrams of vitamin C, and it was still low, so I started taking it on an empty stomach. Caution: The body converts part of supplemental vitamin C into oxalate [375]. In a large prospective study, men who took vitamin C supplements had about twice the risk of kidney stones [376]. If your urinary oxalate is high, discuss vitamin C dosing with your MD.

Ascorbic Acid And Ascorbate: Ascorbic acid is vitamin C, the same molecule found in fruit. Nearly all supplements, whether labeled ascorbic acid or ascorbate, are made synthetically and are chemically identical to the vitamin C in food. Buffered forms such as sodium or calcium ascorbate are gentler on the stomach.

9. Vitamin D3 K2: Sports Research is plant-based, and the best price is at Costco. Just this alone is worth the Costco membership.
10. Krill Oil: Krill oil is more bioavailable than fish oil. Of the two PUFAs within the brain, DHA (docosahexaenoic acid) is the major omega 3, comprising about 10–15% of all fatty acids and over 50% of all brain PUFA (Polyunsaturated fatty acids) [377].

For this reason, DHA was thought to be the most important regarding neurological function, but a recent study found that EPA (eicosapentaenoic acid) was responsible for increased CNS remyelination. The myelin sheath is what protects nerve cells and what becomes damaged in MS [378].

Amino Acids: A Complex Picture

Amino acids (AAs) are organic compounds containing amino and acid groups. Proteinogenic AAs serve as substrates for protein synthesis in animal cells and occur naturally as L-AAs (the molecules used to produce proteins in the human body), except for glycine [379].

Enhanced intake of most amino acid supplements may not be risk-free and can cause a number of detrimental side effects. This is why I have isolated the amino acids I use and no longer use Collagen Peptides.

Collagen peptides also carry a hydroxyproline load that the body converts to oxalate. See Why Collagen, Bone Broth, And Gelatin Should Not Be Used in the oxalate section.

The 22 Amino Acids That Comprise Proteins Include [380]

1. Alanine
2. Arginine
3. Asparagine
4. Aspartic Acid
5. Cysteine
6. Glutamic acid
7. Glutamine
8. Glycine
9. Histidine
10. Isoleucine
11. Leucine
12. Lysine
13. Methionine
14. Phenylalanine
15. Proline
16. Serine
17. Threonine
18. Tryptophan
19. Tyrosine
20. Valine
21. Selenocysteine
22. Pyrrolysine (not used in human protein synthesis)

Of These 22 Amino Acids, Nine Amino Acids Are Essential

1. Phenylalanine
2. Valine
3. Tryptophan
4. Threonine
5. Isoleucine
6. Methionine
7. Histidine
8. Leucine
9. Lysine

Non-essential amino acids, also known as dispensable amino acids, can be excluded from a diet. The human body can synthesize these amino acids using only the essential amino acids. For most physiological states in a healthy adult, the above nine amino acids are the only essential amino acids. However, amino acids like arginine and histidine may be considered conditionally essential because the body cannot synthesize them in sufficient quantities during certain physiological periods of growth, including pregnancy, adolescent growth, or recovery from trauma [380]. Some amino acids may be needed in larger amounts than the body makes, such as glycine, the most important amino acid.

Amino Acid Uses, Toxicity And Side Effects

Glycine

Detailed assessment of all possible sources of glycine shows that synthesis from serine accounts for more than 85% of the total and that the amount of glycine available from synthesis, about 3 g/day, together with that available from the diet, in the range of 1.5-3.0 g/day, may fall significantly short of the amount needed for all metabolic uses, including collagen synthesis by about 10 g per day for a 70 kg human. This result supports earlier suggestions in the literature that glycine is a semi-essential amino acid and that it should be taken as a nutritional supplement to guarantee a healthy metabolism [178].

Glycine has also been suggested as a conditionally essential amino acid. In metabolic disorders associated with obesity, type 2 diabetes (T2DM), and non-alcoholic fatty liver disease (NAFLD), lower circulating glycine levels have been consistently observed, and clinical studies suggest the existence of beneficial effects induced by glycine supplementation.

I consider glycine the most important and versatile amino acid for the following reasons.

1. Data suggest glycine may support mitochondrial function independently of NAC [381].
2. Glycine is a precursor for glutathione [381].
3. Glycine supplies glutathione, and glutathione reductase, the enzyme that keeps glutathione in its active form, promoted fungal clearance and suppressed inflammation during systemic Candida albicans infection in mice [342].
4. Glycine protects human intestinal epithelial cells against oxidative damage [180].
5. Glycine suppresses kidney calcium oxalate crystal depositions [382].
6. Glycine is now recognized as a relevant plasma marker for metabolic diseases associated with obesity [383].
7. Acute glycine supplementation (5 g/day) improved insulin response and glucose tolerance [383].
8. Glycine supplementation was attributed to improved glutathione synthesis and antioxidant protection [383].
9. Oral supplementation with glycine reduces oxidative stress in patients with metabolic syndrome, improving their systolic blood pressure [384].
10. High glycine concentration increases collagen synthesis [385].
11. Acute glycine deficiency could be an important cause of osteoarthritis [385].
12. Glycine extends lifespan in worms, mice, and rats [386].
13. Glycine also improves aspects of health in mammalian models of age-related disease [386].
14. Glycine Regulates Mitochondria-Mediated Autophagy [387].
15. Glycine may prolong life by inducing autophagy and mimicking methionine restriction [386].

Tryptophan (TRP)

Experimental research has shown that L-tryptophan, as the sole precursor of serotonin, plays an important role in brain serotonin synthesis and is involved in mood, behavior, and cognition. Furthermore, clinical trials have provided some initial evidence of L-tryptophan’s efficacy for treating psychiatric disorders, particularly when combined with other therapeutic agents [388].

In the bloodstream, tryptophan competes with other large neutral amino acids such as histidine, isoleucine, leucine, methionine, phenylalanine, threonine, tyrosine, and valine for the BBB transporter [388]. This is why I do not use any other amino acids when I supplement with tryptophan.

I consider tryptophan the second most important amino acid for the following reasons.

1. TRP is an essential proteinogenic amino acid used to treat depression and insomnia [389].
2. TRP increases the synthesis of serotonin (5-hydroxytryptamine), a neurotransmitter known to regulate neuronal circuits that control sleep and mood [389].
3. Next to its role as a neurotransmitter, serotonin is the precursor of melatonin, modulates gut and immune functions, and plays a role in hemostasis [389].
4. TRP supplementation has been employed as a potential treatment for depression and sleep disturbances since the early 1960s [389].
5. There is considerable evidence for the beneficial effects of TRP on mood and social behavior [389].
6. TRP can reduce aggression in schizophrenic patients while increasing agreeableness in people with a tendency to irritability or aggression [389].
7. A Tryptophan-Deficient Diet Induces Gut Microbiome Dysbiosis and Increases Systemic Inflammation in Aged Mice [373].
8. TRP is a constituent of protein synthesis [388].
9. Sole precursor for serotonin synthesis. [388].
10. TRP affects mood, and women may be more vulnerable to the mood-lowering effects of tryptophan depletion than men. [388].
11. Dopamine, norepinephrine, and beta-endorphin have been shown to increase following oral dosing of tryptophan [388].
12. Impairments in a variety of learning and memory skills following tryptophan depletion are well documented [388].
13. In a comparison of adults with and without family histories of bipolar disorder, tryptophan depletion impaired long-term memory consolidation in both groups, and problem-solving was also impaired in those with a family history, while problem-solving improved in those without a family history [388].
14. Tryptophan depletion has also been shown to impair learning on visual discrimination and memory retrieval, episodic memory, stimulus-reward learning, and cognitive flexibility, among other cognitive processes [388].
15. Both animal and human studies have shown that serotonin function is involved in inhibitory control of aggression [388].
16. Tryptophan has been used for a broad spectrum of clinical applications, such as the treatment of pain, insomnia, depression, seasonal affective disorder, bulimia, premenstrual dysphoric disorder, attention-deficit/ hyperactivity disorder, and chronic fatigue [388].
17. Tryptophan has been used for the treatment of sleep disorders and is thought to produce therapeutic effects through melatonin mechanisms [388].

Side Effects

Although TRP has been studied for 6 decades, few side effects, which include tremors, nausea, and dizziness, have been reported. A more common effect of high doses of TRP, which can be expected due to the stimulating effect of TRP on serotonin synthesis, is fatigue or drowsiness. In 1989, an outbreak of eosinophilia-myalgia syndrome, a serious and sometimes fatal condition, was linked to contaminated L-tryptophan from a single manufacturer [390]. Choose tryptophan from manufacturers that provide third-party purity testing.

A potentially life-threatening condition is “serotonin syndrome” (also referred to as serotonin toxicity), which includes neuromuscular abnormalities, autonomic hyperactivity, and mental state changes. Serotonin syndrome is usually precipitated by the simultaneous administration of two or more drugs that enhance serotonin availability, such as serotonin reuptake or MAO inhibitors.

In humans, intestinal cells and gut microbiome play an important role in TRP metabolism. Because TRP is a precursor to serotonin, caution should be exercised when supplementing it with drugs that affect serotonin metabolism [389].

Tryptophan Dosing

Single doses of TRP from 1 g to 15 g were used acutely and chronically for up to 2 years. A commonly used dose is 3 g/day [389]. I started seeing potential contraindications at doses above 2 g.

L-Citrulline (CIT)

Uses: L-Citrulline can be used instead of L-Arginine because it is synthesized into L-Arginine but without the side effects of taking ARG directly, including an increase in Nitric Oxide. Other benefits of short-term therapy include cardiovascular disorders, muscle wasting, intestinal resection, obesity, and insulin resistance. Unlike all other amino acids listed here, which are sourced primarily from meat, the richest source of CIT is watermelon.

Nitric Oxide: Diminished bioavailability of nitric oxide (NO), the gaseous signaling molecule that regulates numerous vital biological functions, contributes to the development and progression of multiple age and lifestyle-related diseases. Supplementation with l-citrulline has shown promise as a blood pressure lowering intervention (both resting and stress-induced) in adults with pre-/hypertension, with pre-clinical (animal) evidence for atherogenic-endothelial protection. Preliminary evidence is also available for l-citrulline-induced benefits to muscle and metabolic health (via vascular and non-vascular pathways) in susceptible/older populations [374].

Side Effects: Because the main mediators of the effects of CIT supplementation are ARG and NO, and long-term studies of the effect of ARG supplementation indicate cardiovascular and renal risks, studies examining the safety of CIT supplementation are necessary [389].

Dosing: I take 1.5 teaspoons daily.

Amino Acids That Can Be Attained Through Diet

I am primarily a carnivore, so I do not supplement with the following amino acids. However, this is not to say you may not benefit from some of these depending on your objectives and dietary needs.

• L-Carnitine
• Creatine
• Glutamine
• Leucine
• BCAA’s

Why D3, K2, Magnesium, B Complex, And Tryptophan Top

Matter For Mood: Discuss Any Medication Changes With Your Prescriber Top

Antidepressants

WARNING: SUICIDAL THOUGHTS AND BEHAVIORS

In October 2004, the FDA required a black box warning for antidepressant drugs of any class that they may increase the risk of suicidality. That warning became effective in January 2005. In 2006, the FDA warning was extended to young adults aged up to 25 years. This is just one of a long list of contraindications, but this is the most significant as it potentially causes what it claims to help.

There is a strong antimicrobial effect of antidepressants from different chemical classes against gut commensal (good) bacteria representative of the predominant species found in the human gut microbiome [391].

As of this writing, the following four antidepressants are used for depression and PTSD in the VA and are widely used in the civilian world. In laboratory testing, antidepressants from several classes, including the SNRI venlafaxine, inhibited beneficial gut bacteria [391], and a screen of more than 1,000 drugs found that many non-antibiotic medications inhibit gut bacteria [392]. The three SSRIs listed here were not tested in [391], so whether they have the same effect in the human gut has not been established.

• Sertraline (Zoloft)
• Paroxetine (Paxil)
• Fluoxetine (Prozac)
• Venlafaxine (Effexor), an SNRI

Suicidal thoughts and behaviors are not the only issues with these antidepressants. The following are several more significant contraindications, but they do not end there. I used Paxil here as an example, but all of the above antidepressants have similar warnings [393].

• Serotonin Syndrome: Increased risk when co-administered with other serotonergic agents (e.g., SSRI, SNRI, triptans), but also when taken alone. If this occurs, discontinue PAXIL CR and initiate supportive measures.
• Embryofetal and Neonatal Toxicity: Can cause fetal and neonatal harm, including increased risk of cardiovascular malformations for exposure during the first trimester. Exposure in late pregnancy may lead to an increased risk of persistent pulmonary hypertension (PPNH) in the newborn.
• Increased Risk of Bleeding: Concomitant use of aspirin, nonsteroidal anti-inflammatory drugs, other antiplatelet drugs, warfarin, and other anticoagulant drugs may increase risk.
• Activation of Mania/Hypomania: Screen patients for bipolar disorder.
• Seizures: Use with caution in patients with seizure disorders.
• Angle-Closure Glaucoma: Angle-closure glaucoma has occurred in patients with untreated anatomically narrow angles treated with antidepressants.
• Sexual Side Effects: Sexual dysfunction is one of the most common side effects of SSRIs and a frequent reason people stop taking them [394].
• Weight Gain: Antidepressants are significantly associated with long-term weight change at two years [395].

Antidepressants And The Placebo Effect

Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory. However, analyses of the published and unpublished data that drug companies hid reveal that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect due to the fact that most patients and doctors in clinical trials successfully break blind.

The serotonin theory is as close as any theory in science's history to being proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability, making people more likely to become depressed in the future [396]. Supplements have side effects too, but they are often milder. Does it make sense, with your prescriber’s guidance, to try supplements that can improve your health in multiple ways? If your answer is yes, read on.

D3, K2 (MK-7), Magnesium, B Complex And Tryptophan Top

Warning: Do not take tryptophan without consulting your physician if you are taking antidepressants.

Vitamin (hormone) D3, K2-7, magnesium, and B Complex work synergistically. K2-7 and magnesium are especially critical when taking high or mega doses of D3. A high dose of D3 is anything up to 100,000 IU. A mega dose of D3 is 100,000 IU and above. I know this sounds like an extraordinary amount, but keep in mind that 40,000 IU of vitamin D is just 1 mg. I will break down all five of these separately, starting with D3.

D3

Anyone who hears about D3 thinks of bone health, but this hormone goes far beyond bone health. Vitamin D receptors (VDR) are found in nearly every cell, and the ability of the cell to produce the active hormone is also widely distributed. Furthermore, the physiological functions with which vitamin D signaling is now associated are as diverse as the tissues in which the vitamin D receptor (VDR) is located [397]. I am going to list just a few attributes of D3 to attempt to drive the point home of how critical D3 is.

1. All-Cause Mortality: A meta-analysis of 32 relevant studies found that concentrations less than or equal to 30 ng/mL were associated with higher all-cause mortality than concentrations greater than 30 ng/mL [398].
2. All-cause, Cardiovascular, Cancer, and Respiratory Disease Mortality: In this large cohort study, vitamin D deficiency concentration <30 nmol/L] was strongly associated with mortality from all causes, cardiovascular diseases, cancer, and respiratory diseases [399].
3. Blood Pressure: Vitamin D Deficiency Is a Potential Risk for Blood Pressure Elevation and the Development of Hypertension [400].
4. Depression: A meta-analysis that included 29 studies with 4,504 participants indicated that the use of vitamin D was beneficial to a decline in the incidence of depression and improvement of depression treatment. Subgroup analysis revealed that people with low vitamin D levels and females could notably benefit from vitamin D in both the prevention and treatment of depression. The effects of vitamin D with a daily supplementary dose of >2,800 IU and intervention duration of ≥8 weeks were considered significant in both prevention and treatment analyses. Intervention duration ≤8 weeks was recognized as effective in the treatment group [401].
5. Sleep, Pain, and Bowel Symptoms: Three months of vitamin D plus B100 improved sleep, reduced pain, and unexpectedly resolved bowel symptoms [402]. The reference to B100 in this study was specific to pantothenic acid (B5). The whole foods B Complex I use happens to have 100 mg of B5.
6. Viruses: A systematic review and meta-analysis of observational studies projected that COVID-19 mortality could theoretically approach zero at blood levels of 50 ng/ml [403]. This was a statistical projection rather than an observed result, and randomized trials of vitamin D supplementation have not shown a reduction in COVID-19 infection or mortality [404, 405].
7. Vitamin D Deficiency Changes the Intestinal Microbiome: This is the single most significant issue with vitamin D because homeostasis can not occur if the microbiome is not in balance. The combination of vitamin D plus B100 creates an intestinal environment that favors the return of four gut bacterial phyla, Actinobacteria, Bacteroidetes, Firmicutes, and Proteobacteria, that comprise the normal human microbiome [402].

These bacteria represent the majority of friendly bacteria in the gut, with Firmicutes and Bacteroidetes representing 90% of gut microbiome [406].

D3 Blood Levels

The recommendations for vitamin D blood levels are all over the map. Low is considered <20 ng/ml, with 30 to 60 in the normal range. I consider 50 ng/ml to be the minimum, with a goal range of 70 to 90 ng/ml (Author’s Observation). This is partly because a systematic review and meta-analysis of observational studies projected that COVID-19 mortality could theoretically approach zero at 50 ng/ml [403], although randomized trials have not confirmed that supplementation prevents COVID-19 deaths [404, 405]. These targets are above current guidelines, so discuss yours with your MD.

D3 Dosing

The current D3 dosing recommendation from NIH is 600 IU for people between the ages of 1 and 70 [407]. This is one of the biggest lies in the medical community. This amount was established in the 1930s to prevent rickets in children and is woefully inadequate for multiple other issues and most people, including children. In 2024, the Endocrine Society recommended against supplementing above the RDA for healthy adults under 75 and against routine vitamin D testing, while suggesting supplementation for adults 75 and older [408]. I believe an acceptable range should be established instead of making up an ultra-conservative number to try and conform to 100% of the population. My position on this is based on the following data.

• Vitamin D can be produced in the skin in amounts estimated up to 25,000 international units (IUs) a day by the action of UVB radiation [409].
• In a hospital setting, 4,700 patients admitted over seven years were administered 5000 to 50,000 IU of D3 per day without any sign of Hypervitaminosis, Hypercalcemia, or any adverse events attributable to vitamin D3 supplementation in any patient [409].

D3 Hypervitaminosis And Hypercalcemia

Vitamin D toxicity is uncommon, but it is well documented and increasing, and it is almost always caused by excessive supplement intake [407, 410]. In one published case, a relative reported the amount and timeline taken [411]. The main danger of too much D3 is hypercalcemia, too much calcium in the blood, which can cause kidney damage, heart rhythm problems, and calcium deposits in the arteries and other soft tissues [407]. K2 helps direct calcium into bone, but it does not lower blood calcium and does not prevent vitamin D toxicity. I take K2 with D3 for its own benefits. The NIH upper limit for adults is 4,000 IU per day [407]; if you take more, have your blood calcium and vitamin D levels monitored by your MD.

Vitamin K2-7

Clinical studies have unequivocally demonstrated the utility of vitamin K2-7 supplementation in ameliorating peripheral neuropathy, reducing bone fracture risk, and improving cardiovascular health. K2-7 accomplishes this with the protein synthesis of osteocalcin and various other proteins [412]. This means that K2-7 delivers calcium where it is supposed to go.

Vitamin K2-7 And Vascular Calcification

Vascular calcification is characterized by mineral depositions on the walls of the vascular system. This is the primary concern when taking high or mega doses of D3. K2 has the potential to inhibit as well as reverse the process of calcification [412]. The benefits of K2 do not stop at simply delivering calcium where it is supposed to go and freeing calcium present in the blood vessels.

• Vitamin K2 suppresses cancer cell growth via apoptosis, autophagy, and cell-cycle arrest [412]
• Vitamin K2 improves sensitivity to insulin in diabetic patients [412]
• Vitamin K2 facilitates the synthesis and repair of the myelin sheath in the peripheral nervous system [412]
• Vitamin K2 has the potential to slow down the progression of Alzheimer's Disease and contribute to its prevention [412]

Contraindications To Vitamin K2-7

There are no severe adverse effects due to the supplementation of vitamin K2-7. However, high doses of vitamin K2 can cause allergic reactions [412]. Warning: Vitamin K counteracts the blood thinner warfarin (Coumadin). If you take warfarin or another vitamin K antagonist, do not start K2 without your prescriber’s approval [413].

Sources Of K2-7

Sources of K2-7 include natto, which is the highest, moderate in chicken, sauerkraut, beef, and a variety of cheeses, and is low in pork, salmon, etc. [412].

K2 Dosing

I do not go beyond the dose that is part of the D3 K2 supplement that I take.

Magnesium

Magnesium assists in activating vitamin D, which helps regulate calcium and phosphate homeostasis to influence the growth and maintenance of bones.

All enzymes that metabolize vitamin D seem to require magnesium, which acts as a cofactor in the enzymatic reactions in the liver and kidneys [414]. This is why you can become deficient in magnesium if high doses of D3 are taken, even if you are taking the daily RDA. As D3 intake increases, magnesium intake must also increase.

B Complex

As mentioned above, three months of B100 or B5 (pantothenic acid) and vitamin D improved sleep, reduced pain, and unexpected resolution of bowel symptoms [402].

This combination also creates an intestinal environment that favors the return of four foundational gut bacterial phyla, Actinobacteria, Bacteroidetes, Firmicutes, and Proteobacteria, that make up the normal human microbiome [402] before and after comprehensive stool tests prove this to be accurate.

Tryptophan

SSRIs do not make new serotonin, but tryptophan does, along with melatonin and NAD, and this is why it is added to this stack again; consult with your MD before taking tryptophan if you are taking antidepressants.

Kelly Burris: Comprehensive Stool Test: 9-20

If you look under Commensal Microbiome Analysis, you will see the four foundational bacteria and a couple of others. All were low, with Euryarchaeota Phylum below detectable levels. MDs, nutritionists, and even Functional Medicine Practitioners recommended probiotics, so I took their advice and researched the top probiotics, taking up to 1.7 trillion CFUs daily. As you can see, it had little to no effect on the commensal bacteria. This is not to say that probiotics do not work because taking the right ones can be very effective. Just do not depend on them to reestablish foundational commensal bacteria.

Kelly Burris: Comprehensive Stool Test: 9-22

Seven weeks before doing this test, I did high doses of vitamin D with 12 days of mega-dosing, which I do not recommend. I was already taking a B Complex that included 100 mg of B5. Another interesting piece is that plant-based diets are recommended to increase Firmicutes Phylum. I had been primarily a carnivore for 33 months when this test was done, yet there were significant increases in all commensal (good) bacteria. Another thing to look at with these two tests is "The Need for Microbiome Support" at the top of the page. Part of this equation is yeast overgrowth (Candida), and this test completely missed it as I was still a 10, as the first one indicated. All tests I had for yeast overgrowth were unreliable. This is after 3 comprehensive tests, 2 standard tests, and several urine tests.

Additional Attributes Of B Complex

B1 (Thiamin And Benfotiamine)

Severe alcoholism can be associated with significant nutritional and vitamin deficiency, especially vitamin B1 (thiamine), associated with neurological deficits impacting mood and cognition. Benfotiamine appears to reduce psychiatric distress and may facilitate recovery in severely affected males with a lifetime alcohol use disorder [415]. Benfotiamine was part of my recovery from Neuromyelitis Optica (Author’s Observation). It is not an established treatment for NMO, a serious autoimmune disease that requires care from a neurologist.

Individuals with thiamin deficiency also require other nutrient supplementation, such as magnesium, vitamin B2 (riboflavin), B3 (nicotinamide), B6 (pyridoxine), B12, vitamin C, potassium, and phosphate. Taking a good B Complex, in my opinion, is the best way to go.

Toxicity

The human body excretes excess thiamin in the urine. There is a lack of evidence of toxicity from high thiamin intake from food or supplements. Food and Nutrition Board (FNB) concluded that excessive consumption of thiamin might cause adverse effects despite a lack of substantial evidence of toxicity. Per the Institute of Medicine, no established upper limit of thiamin intake is reported in the literature to cause any toxicity [416].

B2 (Riboflavin): B2 can be found in a wide variety of foods and natural sources, especially milk and organ meats, mostly in calf liver, egg, fish, nuts, certain fruits and legumes, wild rice, mushrooms, dark green leafy vegetables, yeast, beer, cheese, and dietary products.

Vertebrates poorly store B2 because of its limited absorption in humans. Therefore, orally supplied RF by a healthy diet is required to avoid ariboflavinosis, which causes cheilitis, sore tongue, and a scaly rash on the scrotum or vulva. B2 causes no known toxicity since it is excreted in the urine at higher intakes and not stored. B2 is found in different concentrations in various human body fluids and organs [417].

• B2 reduces reactive oxygen species
• B2 was used for its potent antioxidant and anti-inflammatory effects
• B2 plays an important role in the antioxidant status inside cell systems and is part of the glutathione reductase
• B2 functions as an endogenous antioxidant in different cells
• B2 can attenuate oxidative injuries through its ability to scavenge free radicals and, therefore, decrease re-oxygenation injuries
• B2 is neuroprotective of cerebral ischemia
• B2 intake from food sources was associated with a decrease in the risk of PMS
• B2 with co-treatment with selenium or vitamin E can protect the brain and microsomal membrane.
• B2 contributes to blood cell formation
• B2 was shown to enhance iron absorption

B3 (Niacin): B3 includes two vitamers (nicotinic acid and nicotinamide), giving rise to the coenzymatic forms nicotinamide adenine dinucleotide (NAD+). The two coenzymes are required for oxidative reactions crucial for energy production, but they are also substrates for enzymes involved in non-redox signaling pathways, thus regulating biological functions, including gene expression, cell cycle progression, DNA repair, and cell death. Vitamin B3 has long been recognized as a key mediator of neuronal development and survival in the central nervous system.

Humans obtain niacin from both endogenous and exogenous sources. Only 2% of dietary tryptophan is converted into niacin via a multistep pathway, occurring mainly in the liver. Diet provides vitamins such as nicotinic acid, nicotinamide, and tryptophan, as well as the active coenzymatic forms of niacin. Niacin is found in animal and vegetable foods. In meat and fish, the vitamin is present as nicotinamide, whose amounts are higher in unprepared foods compared to processed foods.

Severe niacin and/or tryptophan deficiency leads to a variety of clinical symptoms, including diarrhea, dermatitis, and dementia, collectively known as "pellagra." Pellagra is common in people who mostly eat maize, as well as in malnourished and alcoholic men. Other risk factors leading to vitamin B3 deficiency are nervous anorexia, AIDS, cancer, and malabsorptive disorders, such as Crohn's disease [418].

Toxicity

Niacin-associated hepatotoxicity is generally related to ingestions of around 3 grams per day. In contrast, the more common symptom of flushing can occur at doses as low as 30 mg per day [419]. The flushing was significant when I took just 250 mg of nicotinic acid on an empty stomach. No flushing occurred at 250 mg after eating.

B5 (Pantothenic Acid): Vitamin B5 is a naturally occurring substance in various plants and animals (i.e., eggs, milk, vegetables, beef, chicken).

An experimental vitamin B5 deficiency study associated the deficiency with symptoms such as fatigue, headache, malaise, personality changes, numbness, muscle cramps, paresthesia, muscle/ abdominal cramps, nausea, and impaired muscle coordination [420].

Toxicity

B5 is considered generally safe. There are currently no upper limits established since there have been no reports of vitamin B5 toxicity in humans with high intakes. However, there are still side effects involved with B5 administration [420].

B6 (Pyridoxine): B6 is involved in the vast majority of changes in the human body because it is a coenzyme involved in over 150 biochemical reactions. It is active in metabolizing carbohydrates, lipids, amino acids, and nucleic acids and participates in cellular signaling. In addition, it is an antioxidant and a compound that can lower the advanced glycation end products (AGE) level [421].

Pyridoxal 5' phosphate (P-5-P) is the active coenzyme form of vitamin B6. P-5-P deficiency leads to immunosuppression, local exacerbation of inflammatory processes, and increased secretion of proinflammatory cytokines. Conversely, replenishing P-5-P may boost immunity and maintain an equilibrium that allows control of viral replication without uncontrolled expression of cytokines [421]. At the time of my first NutrEval test, I was taking 50 mg of B6 in the form of P-5-P per day, and I was deficient. This is a good example of why you always want to test, not guess, because 50 mg should have been more than adequate, but the variable of oxalate poisoning and a disrupted microbiome significantly increased my requirement for B6.

Toxicity

Most studies indicate that an intake below 200 mg of pyridoxine daily does not cause issues [421]. I am taking 100 mg daily of P-5-P.

Warning: Avoid Pyridoxine HCL as it can cause peripheral neuropathy in therapeutic amounts instead of helping peripheral neuropathy [422, 423]. In laboratory studies, pyridoxine, but not the other forms of vitamin B6, caused nerve cell death and blocked vitamin B6 function [424]. Some MDs do not distinguish between P-5-P and pyridoxine HCL, which is a mistake.

B7 (Biotin): Marginal and severe degrees of biotin deficiency lead to various clinical abnormalities, including neurological disorders and dermal abnormalities. Such deficiency/suboptimal levels occur in a variety of conditions, including inflammatory bowel disease (IBD). At the metabolic level, biotin acts as a cofactor for five carboxylases that are critical for fatty acid, glucose, and amino acid metabolism. Essential roles for this vitamin in cellular energy metabolism (i.e., ATP production) and in the regulation of cellular oxidative stress, as well as in gene expression where expression of over 2,000 human genes appears to be affected by biotin status, have also been reported recently. An increase in the levels of proinflammatory cytokines has also been observed in biotin deficiency [425].

Toxicity

Although not impossible, it would be very difficult to overdose on biotin [426].

The most important known risk of high-dose biotin is that it can interfere with laboratory tests, including thyroid tests and troponin (used to diagnose heart attacks), causing falsely high or low results [427]. Tell your MD and the lab if you take biotin, and ask whether to pause it before a blood draw.

B9 (Folate): The decreased folate level of the body, mainly caused by environmental and hereditary factors as well as aging, can lead to genetic, epigenetic, and metabolic changes. It can be related to the development of megaloblastic anemia, various cardiovascular diseases (such as atherosclerosis and stroke), obstetrical complications (such as abruption of the placentae, spontaneous abortion, preterm delivery, neural tube defect), neuropsychiatric diseases (such as Alzheimer's disease, Parkinson's disease, depression) and tumors [428].

Toxicity

Recent folate intervention trials suggest that folate supplementation may increase the risk of the above chronic diseases for individuals at a higher risk [428]. This is why folate does not exceed 200% of the daily value.

B12 (Cobalamin): B12 is a cofactor for enzymes involved in synthesizing deoxyribonucleic acid (DNA), fatty acids, and myelin. B12 deficiency can lead to hematologic and neurological symptoms. Vitamin B12 is stored in excess in the liver, decreasing the likelihood of deficiency. However, hepatic stores are depleted in cases where vitamin B12 cannot be absorbed, such as dietary insufficiency, malabsorption, or lack of intrinsic factor, and deficiency ensues [416, 429, 430].

Sources of B12 are animal products such as red meat, dairy, and eggs.

Toxicity

No toxic effects of vitamin B-12 have been identified, even when it is administered intramuscularly at 300–3000 times the recommended dietary allowance. For this reason, no upper tolerable level for the vitamin has been established [429].

B12: Which Type To Take

Methylcobalamin is the recommended B12.

Avoid cyanocobalamin.

Related Topics Top

Histamine Top

Histamine is an organic nitrogenous compound involved in local immune responses, regulates physiological functions in the gut, and acts as a neurotransmitter for the brain, spinal cord, and uterus.

Oxalate dumping and Candida die-off trigger mast cell histamine release (Author’s Observation). This, in conjunction with eating high-histidine foods, can cause what appears to be histamine intolerance. I say "what appears to be" because virtually no MDs understand the process of oxalate dumping and the results it produces; therefore, they label it histamine intolerance. In my opinion, it is histamine overload if you are dealing with oxalate dumping and Candida die-off. Either way, histamine must be considered an essential piece of the oxalate Candida equation.

The first thing that is prescribed is antihistamines, and this is usually without an accurate diagnosis. Histamine intolerance or overload symptoms are similar to some of the symptoms of oxalate dumping and Candida die-off, so it just adds to the overall malaise.

Diamine oxidase (DAO) is the enzyme responsible for breaking down histamine, and I felt it was better to incorporate a food high in DAO and reduce the amount of histidine I was consuming [431]. Beef kidney is high in DAO, so I took it in freeze-dried capsule form. I was able to tell the difference, which sold me on the idea of freeze-dried animal organs. You do want to be careful about reducing histidine because it has been found to improve mental fatigue, cognitive performance, and sleep disruption [432].

Senescence, Autophagy, And Apoptosis Top

It is important to have a fundamental understanding of senescence, autophagy, and apoptosis, especially as they relate to fasting.

Senescent cells are damaged cells that secrete proinflammatory cytokines, which stimulate the immune system and can cause inflammation, leading to damage to other cells. Senescent cells accumulate in various tissues with aging and at sites of pathogenesis in many chronic diseases and conditions, including metabolic dysregulation, stem cell dysfunction, aging phenotypes, chronic diseases, geriatric syndromes, and loss of resilience. Senescent cells can also stimulate the regeneration of new cells, which creates a double-edged sword [433]. This, in my opinion, is why pharmaceuticals used to kill senescent cells should be closely examined.

Immunosenescence is what it sounds like, which is the slow death of immune cells. Prolonged fasting kills senescent cells, which stimulates the generation of new cells.

Autophagy And Apoptosis

Autophagy means self-eating, and regarding fasting, the body uses old and damaged stem cells and, in theory, senescent cells as fuel. This is why age, disease, and health biomarkers improve. It is impossible to know if autophagy extends one's life, but it can extend one's health. The loss of autophagy is enough to drive cellular, tissue, and organismal dysfunction with detrimental effects on health and lifespan; by contrast, boosting autophagy has the opposite effects [433].

I saw autophagy right before my eyes after suffering a massive oxalate dump, and ended up with a cobweb of floaters in my right eye. I immediately initiated a 72-hour fast, and most of the floaters disappeared. A 48-hour fast had little effect on the floaters in my other eye. This is why I also believe that meaningful autophagy only occurs between 36 and 72 hours (Author’s Observation).

Warning: A sudden shower or cobweb of new floaters, especially with flashes of light or a shadow or curtain across part of your vision, can signal a retinal tear or detachment [434]. This requires a same-day eye exam. Do not wait to see whether fasting helps.

Apoptosis is programmed cell death independent of cell damage [435]. Apoptosis and autophagy are interrelated processes, and nutrient availability influences which path a cell takes [436].

The Inflammatory 8 Top

1. Anti-Nutrients and Plant Toxins: This includes oxalates, lectins, goitrogens, phytoestrogens, phytates, and tannins. Grains, in particular, can also alter the composition of gut microbiome [437].
2. High IgG4 Food Antigens: If over-stimulation of IgG4 is an issue, symptom improvement is confirmed by eliminating beef, pork, lamb, egg whites, and wheat.
3. FODMAPs: The acronym FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) describes poorly absorbed, short-chain carbohydrates. The one FODMAP you do not want to avoid is inulin, but it must be tightly calibrated, and when using it in extended fermentation yogurt, the vast majority is used by the starter bacteria.
4. Alcohol and Sugar:

• In a study of over half a million participants followed for up to 12 years, combined with genetic analyses of 2.4 million people, it was concluded that there is no amount of alcohol that is safe for the brain [438].
• Alcohol increases intestinal permeability by disrupting the microbiome [439].
• The dysbiosis caused by alcohol can perpetuate the habit of drinking [439].
• Alcohol use can lead to more than 200 disorders, including hypertension [440].
• Alcohol makes mitochondria more vulnerable to oxidative damage, which precedes dysfunction [441].
• Brain mitochondria appear to be the principal targets of the oxidative stress generated by ethanol intoxication and withdrawal [441].
• Refined and processed sugars alter the gut microbiome composition [437]. I included sugar here because I refer to alcohol as liquid sugar.

5. NSAIDs: Nonsteroidal anti-inflammatory drugs include aspirin, ibuprofen, and naproxen. These drugs are linked to the onset of IBD [442].
6. Some Polyunsaturated Fats: In mice, diets rich in omega-6 polyunsaturated fats (such as corn oil) promoted inflammatory shifts in the gut microbiome [443, 444].
7. Preservatives: I discovered this one inadvertently while researching Candida antimicrobials. The nearly universal antimicrobial activity attributed to grapefruit seed extract is merely due to the synthetic preservative agents contained within.

Natural products with antimicrobial activity do not appear to be present [445]. The assumption based on this research is that preservatives act as an antimicrobial. If one takes an antibiotic or antimicrobial, they must be accompanied by probiotics to assist in preventing dysbiosis, but I am certain very few people know that preservatives act as an antimicrobial.

8. Caffeine: Cortisol [446] is a stress hormone, and caffeine can cause a robust increase in cortisol [447]. I know how hard it is to quit caffeine, and coffee has many benefits. There should, however, be a consideration of switching to decaf until the dysbiosis is under control.

CBD Top

Reduce Nausea, Improve Sleep, And Lower Toxicity, Inflammation, And Pathogens

CBD (cannabidiol) is the non-psychoactive component of cannabis. With over two thousand full-text articles on PMC, I came to find that CBD had more uses than just as an antipathogen [448]. It was the most industrial-grade anti-inflammatory I had ever used [449].

Studies on models of human diseases support the idea that CBD attenuates inflammation far beyond its antioxidant properties by targeting inflammation-related intracellular signaling events. The details on how it does this remain to be defined.

The use of THC and Candida in a mouse model was deemed ineffective [450]. However, Candida colonization delays the healing of inflammatory lesions, and inflammation promotes colonization. These effects may create a vicious cycle in which low-level inflammation promotes fungal colonization, and fungal colonization promotes further inflammation. High-level Candida colonization is frequently observed in ulcer and IBD patients and is linked to Crohn's disease, ulcerative colitis, and leaky gut [451]. During this vicious cycle, the profound anti-inflammatory processes of CBD became very useful in eradicating pathogenetic Candida (Author’s Observation).

Because cannabinoids are profoundly anti-inflammatory, infections caused by HIV-1 or HSV-1 can worsen. The anti-inflammatory action can impair dependent enzyme systems, which are central to inflammatory and cell-autonomous antiviral responses [452]. This was not the case with me, so the industrial-grade anti-inflammatory nature of CBD worked very well.

Getting Started With CBD

Warning: Even though CBD is difficult to overdose on, it seems good at killing yeast and removing pathogens, making starting with high doses relatively dangerous (Author’s Observation).

The only way to take CBD is in the purest form possible. This is in the form of CBD oil combined with coconut or MCT oil. Some CBD sprays contain Polysorbate 80. In mice, Polysorbate 80 promoted low-grade intestinal inflammation and metabolic syndrome, a group of conditions that increase the risk for type 2 diabetes, heart disease, and stroke [172]. Always ensure that you are taking only oil and CBD. For me, CBD was an important factor in getting through the extreme toxicity brought on by fasting and therapeutic amounts of olive oil.

Where To Purchase CBD

I get mine at CBD Market because I don't particularly appreciate digging for coupons; they have the best prices.

Appendix: Hydrogen-Rich Water Research Top

Hydrogen is produced via gut bacteria (primarily Bacteroides and Firmicutes), and if these bacteria are damaged or lowered, there is a host of physiological issues associated with it [453]. Hundreds of human and animal studies of hydrogen-rich water (HRW) exist. This first group of studies is from a systematic review that looked at human outcomes only. The second group will include animal studies.

HRW Human Studies Only

Benefits Of HRW With Physical Exercise

• HRW has shown antioxidant, anti-apoptotic, cytoprotective, and anti-inflammatory properties [454].
• Hydrogen-rich water before exercising can mitigate the effects of fatigue and build endurance [454].
• HRW administered pre-workout, which showed decreased blood lactic acid levels at a higher intensity and improved ventilatory efficiency [454].
• HRW has been shown to reduce fatigue and improve endurance in the later stages of repeated sprints [454].
• HRW can improve acidosis due to exercise, energy levels, and enhanced muscular performance in athletes [454].

Impact Of HRW On Oxidative Stress

• Hydrogen is effective against oxidative stress and is also known for its anti-inflammatory and anti-allergy benefits [454].
• HRW decreases cellular and mitochondrial injuries [454].
• Even at higher concentrations, hydrogen has no cytotoxicity [454].

Impact Of HRW On Cardiovascular Health

• Molecular hydrogen controls signal transduction and gene expression, suppressing pro-inflammatory cytokines and decreasing reactive oxygen species production [454].
• HRW can potentially decrease LDL-C and apoB (a protein that helps transport lipids, like cholesterol, throughout the blood) levels while improving HDL function [454].
• High-density lipoprotein (HDL) cholesterol increased by 8% [454].
• The use of high-concentration HRW was shown to decrease blood glucose and cholesterol levels, improve serum hemoglobin A1c, and also to improve inflammatory biomarkers. Interestingly, it also led to an improvement in waist-to-hip ratio and body mass index [454].

COVID-19 And HRW

• Molecular hydrogen therapies were also effective in remediating the dangerous consequences of COVID-19 infection [454].
• Hydrogen administration inhibited cytokine cascade and decreased inhalation resistance in patients with mild to moderate disease [454].

Effect Of HRW On Cancer

• HRW has shown anti-cancer properties. With its antioxidant properties and ability to decrease oxidative stress, it could be a potential game changer in the future [454].
• HRW was noted to have potential in treatment, overall prognosis, quality of life, and tumor reduction [454].

Benefits Of HRW On Emotional (Mental) Health

• Subjects who drank HRW for 4 weeks had improved mood and anxiety [454].

HRW And Liver Function

• Liver dysfunction can be caused by inflammation, oxidative stress, and aberrant cellular signaling. It has been shown that the administration of hydrogen-rich water can have beneficial effects on these patients [454].
• Hydrogen-rich water was shown to decrease fat accumulation in the liver and has the potential to be used as an adjuvant treatment for mild to moderate NAFLD (non-alcoholic fatty liver disease) [454].

Effect Of Hydrogen-Rich Water On Aging

• HRW has long-lasting antioxidant and anti-aging effects on vascular endothelial cells through the Nrf2 pathway (a cellular response to oxidative stress), even after transient exposure to H2 [454].

Hydrogen-Rich Water: In Vivo, In Vitro, And Animal Studies

Even though animal studies must be scrutinized much more than human studies, I never immediately discount them, especially if the subject is pertinent to my suffering.

• HRW alleviates cellular senescence in endothelial cells [455].
• Gene sequencing showed that HRW intake induced significant changes in the structure of gut microbiome. HRW intake mainly induced a significant increase in the abundance of Lactobacillus, Ruminococcus, Clostridium XI, and a decrease in Bacteroides [456].
• In a rat model, HRW reduced constipation by modulating the microbiome [457].
• In a laboratory study on mushroom mycelium, HRW decreased malondialdehyde (MDA) and reactive oxygen species (ROS) and significantly increased antioxidant enzyme activity [458]. For me, this was one of the biggest issues because purging oxalates left me incapacitated most of the time from severe poisoning.
• HRW may be involved in the Gut-Brain interaction [453].
• HRW Protects against Neurodegenerative Changes Induced by Traumatic Brain Injury [459].

References