Following is an excerpt from the 2nd edition of “Subconscious Restructuring” and “Reprogramming the Overweight Mind”
Disclaimer: This page is provided for educational and informational purposes only. The information provided on this page should not be used to diagnose or treat a health problem or disease. Always seek the advice of your doctor or another qualified health provider regarding a medical condition. This content or its use creates no physician-patient relationship. For example, stopping an antidepressant or PTSD medication should only be done under the prescriber's supervision. This also applies to supplementation. If under the age of 18, nothing in this article should be implemented without the supervision of a parent or MD.
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 microbiota [35]. The theory is that some people initially feel better because of the antimicrobial effect. Still, there is no discrimination, and all species are affected, which is why the microbiota ultimately becomes disrupted. Given our understanding of the microbiome over the last decade, this should be enough to ban SSRIs.
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. All of these SSRIs will degrade beneficial gut bacterial species [35].
Suicidal thoughts and behaviors are not the only issues with these antidepressants. The following are several more significant contraindicators, but they do not end there. I used Paxil here as an example, but all of the above antidepressants have similar warnings [36].
- 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—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: Overall, 73% of SSRI-treated clients reported adverse sexual side effects [36].
- Weight Gain: Antidepressants are significantly associated with long-term weight change at two years [37].
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 [38]. Does it make sense to use a supplement instead of meds with no side effects and improve your health in multiple ways? If your answer is yes, read on.
D3, K2 (MK-7) Magnesium, B Complex and Tryptophan
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 [39]. I am going to list just a few attributes of D3 to attempt to drive the point home of how critical D3 is.
- 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 [40].
- 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 [41].
- Blood Pressure: Vitamin D Deficiency Is a Potential Risk for Blood Pressure Elevation and the Development of Hypertension [42].
- 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 [44].
- Sleep, Pain, and Bowel Symptoms: Three months of vitamin D plus B100 improved sleep, reduced pain, and unexpectedly resolved bowel symptoms [45]. 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.
- Viruses: A Systematic Review and Meta-Analysis theoretically established that zero mortality could be achieved from COVID-19 with blood levels of 50 ng/ml or greater [45].
- Vitamin D Deficiency Changes the Intestinal Microbiome: This is the single most significant issue with vitamin D because homeostasis cannot 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 species, Actinobacteria, Bacteroidetes, Firmicutes, and Proteobacteria, that comprise the normal human microbiome [45].
These bacteria represent the majority of friendly bacteria in the gut, with Firmicutes and Bacteroidetes representing 90% of gut microbiota [46].
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. This is because a Systematic Review and Meta-Analysis theoretically established that zero mortality could be achieved from COVID-19 with 50 ng/ml [45]. If 50 ng/ml of vitamin D will save your life from the next pandemic, it simply makes sense to look at that as the minimum, NOT 30 ng/ml.
D3 Dosing
The current D3 dosing recommendation from NIH is 600 IU for people between the ages of 1 and 70 [41]. 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. The Endocrine Society has recently increased its recommended amount of D3, but 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 [47].
- 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 [47].
D3 Hypervitaminosis and Hypercalcemia
Getting poisoned from vitamin D3 is extremely rare. I only found one case and a relative reported the amount and timeline it was taken [48]. The big concern with taking too much D3 is hypercalcemia, which is too much calcium in the blood, enabling it to accumulate in the arteries. This can be circumvented with vitamin K2-7, which is why I believe one should always take K2 with D3.
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 [49]. 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 [50]. 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 [50]
- Vitamin K2 improves sensitivity to insulin in diabetic patients [50]
- Vitamin K2 facilitates the synthesis and repair of the myelin sheath in the peripheral nervous system [50]
- Vitamin K2 has the potential to slow down the progression of Alzheimer's Disease and contribute to its prevention [50]
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 [50].
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. [50].
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 [26]. 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 one increases, D3 magnesium must also be increased.
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 [45].
This combination also creates an intestinal environment that favors the return of four foundational gut bacterial species, Actinobacteria, Bacteroidetes, Firmicutes, and Proteobacteria, that make up the normal human microbiome [45] 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
Looking under Commensal Microbiome Analysis, you will see the four foundational bacteria and a few 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. If you have ever wondered what suicidality looks like in the gut, this is it.
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 [142]. I used Benfotiamine to cure my Neuromyelitis Optica.
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 [63].
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 [52].
- 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 [53].
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 [54]. 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 [55].
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 [55].
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 [56].
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 [56]. At the time of my first NutrVal 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 microbiota significantly increased my requirement for B6.
Toxicity
Most studies indicate that an intake below 200 mg of pyridoxine daily does not cause issues [56]. I am taking 150 mg daily of P-5-P.
Warning: Avoid Pyridoxine HCL as it can cause peripheral neuropathy in therapeutic amounts instead of helping peripheral neuropathy [146]. 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 [24], 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 [57].
Toxicity
Although not impossible, it would be very difficult to overdose on biotin.
Since biotin has been documented to play a role in postprandial glucose control, it bears mention that excess would cause signs and symptoms of a person experiencing hyperglycemia (e.g., increased thirst). Diabetic patients should, therefore, be cautious before taking biotin [58].
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 [59].
Toxicity
Recent folate intervention trials suggest that folate supplementation may increase the risk of the above chronic diseases for individuals at a higher risk [60]. 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 [61-62-63].
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 [62].
B12: Which Type to Take
Methylcobalamin is the recommended B12.
Avoid cyanocobalamin.
Kelly Burris has defined 'Normal' in an industry that only defines broken or disordered. He is the developer of the empirically sound Subconscious Restructuring® process and founder of the Burris Institute. With over 250 medical references, Subconscious Restructuring® represents a scientific breakthrough in mental health, and it has done this without meds, labels, or personal history.
As part of the Burris ecosystem, SR™ Practitioners can manage, track, and interact with current and future clients after certification on BurrisConnect.com. This same ecosystem enables corporate, military, and educational entities to supervise and monitor the performance of their internal Subconscious Restructuring® (mental health) infrastructure in the cloud. The “Subconscious Restructuring” and “Reprogramming the Overweight Mind” books are now at Amazon.com.
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