https://pmc.ncbi.nlm.nih.gov/articles/PMC13098529/

Diabetes Primes Neutrophils for Neutrophil Extracellular Trap Formation through Trained Immunity

https://pubmed.ncbi.nlm.nih.gov/38654733/

Decreased Neutrophils Are Associated With Reduced Risk of Type 2 Diabetes Incidence: Results From the CORDIOPREV Study

https://pubmed.ncbi.nlm.nih.gov/39470387/

Transketolase and vitamin B1 influence on ROS-dependent neutrophil extracellular traps (NETs) formation

https://pmc.ncbi.nlm.nih.gov/articles/PMC6695114/

Transketolase and vitamin B1 influence on ROS-dependent neutrophil extracellular traps (NETs) formation     Abstract

https://pubmed.ncbi.nlm.nih.gov/31415630/

Neutrophil CD11b, L-selectin and Fc IgA receptors in patients with dermatitis herpetiformis

https://pubmed.ncbi.nlm.nih.gov/12452859/

Neutrophil CD11b, L-selectin and Fc IgA receptors in patients with dermatitis herpetiformis

https://pubmed.ncbi.nlm.nih.gov/12452859/

While there is greater knowledge of the effects of pharmaceutical therapies for arthritis, there is less knowledge of the effects of many nutrients. And even though there is evidence that physician discussions of diet make a positive influence on patient dietary selections, these conversations are not common in clinical practice. There is a global deficiency of nutrition education in physician training, including the use of nutrients to manage chronic diseases and methods for providing advice to their patients [164, 165]. A recent review highlighted the lack of nutrition knowledge and confidence in counseling among medical students worldwide. Most schools perform less than 25 h of nutrition education over 5 or 6 years of medical training. Trainees often learn about nutrition in biochemistry lectures that are not necessarily relevant to everyday practice [166]. The interest in nutrition among medical students is high. However, it decreases by the time they graduate, since they do not see nutrition substantively incorporated into their curriculum and do not observe clinical mentors incorporating nutritional interventions into their care plans [167]. In fact, a recent study showed that only 36.0% of general practitioners had positive attitudes toward nutrition and nutrition care [168].

This, as well as the data gaps, lack of regulated nutritional supplements with standardized quantities, insufficient or complete lack of insurance coverage for nutritionist or dietician consultations, and lack of dietary programs directed toward arthritis patients result in a lack of confidence in nutrition as a treatment among clinicians. Without adequate nutrition education, it is reasonable to assume that doctors are not able to provide the highest quality care to patients [167]."

Micronutrients: Essential Treatment for Inflammatory Arthritis?

https://pmc.ncbi.nlm.nih.gov/articles/PMC8078476/#R166

Glioblastoma is an aggressive brain cancer.

My mother died from Glioblastoma.  

Can a Common Vitamin Fight the Most Aggressive Brain Cancer?

https://scitechdaily.com/can-a-common-vitamin-fight-the-most-aggressive-brain-cancer/

 And...

A phase I-II study of niacin in patients with newly diagnosed glioblastoma: safety and interim phase II analysis

https://link.springer.com/article/10.1007/s11060-025-05351-z

Thiamine is used in the mitochondria to produce energy (ATP) in the body for cells use as they go about their various functions.  Various chemical reactions take place as the glucose moves through the transport chain in the mitochondria.  Oxygen is needed at the end of the transport chain to pick up electrons leftover from the chemical reactions of ATP production and combines with Hydrogen electrons to form water.  One molecule of glucose results in 32-36 ATP. 

If there is not enough Thiamine for the mitochondria to produce ATP using Oxygen to mop up the spare electrons, the mitochondria switches to anaerobic (without oxygen) production of energy.  Only 2 ATP are produced in this manner from one glucose molecule.  Anaerobic production of ATP leaves lactic acid as a byproduct.  Oxygen delivered to the cell passes through unused or is ignored since it's not capable of being used.  This induces a state of hypoxia.  Thiamine deficiency causes hypoxia.

Hypoxia-Inducible Factor 1 alpha (HIF-1a) is part of a checks and balances system within cells.  HIF-1a is degraded (turned off) by byproducts from aerobic production of energy using thiamine.  However, if the byproducts build up too much, HIF-1a is stimulated.  During low oxygen levels and anaerobic production of ATP, a build up of lactic acid stimulates HIF-1a.  

Hypoxia-Inducible Factor 1α binds to thiamine transporter SLC19A3 and activates it to increase thiamine uptake.

HIF-1a affects genes in the nucleus, entering through micro-pores.  HIF-1α signaling triggers the release of inflammatory cytokines and increases inflammatory cell proliferation.  It can also cause cell death. 

Hypoxia and high levels of HIF-1a are found in many autoimmune diseases and cancer. 

Thiamine attenuates HIF-1a signaling.  Thiamine restores ATP production to aerobic production. 

Here's an excerpt...

"HIF-1α shows its functions through translocating into the nucleus, dimerizing with HIF-1β and binding to hypoxia-responsive elements of the HIF-1α target genes. Recent data have also suggested that HIF-1α plays a role in maintaining intestinal epithelial barrier functions [37,38]. Accumulating evidence has also shown that HIF-1 α plays an essential role in cells via interaction with the NF-kB p65 pathway in the pathogenesis of inflammation [17]. In addition, previous research has further reported that HIF-1α expression is increased in the duodenal tissue of celiac disease patients [19,39]. It has been pointed out that activated HIF-1α is involved in celiac disease pathogenesis.".  

https://pmc.ncbi.nlm.nih.gov/articles/PMC9954839/

References:

Increased Expression of Hypoxia-Inducible Factor 1α in Coeliac Disease

https://www.nature.com/articles/pr2010143

Intestinal parameters of oxidative imbalance in celiac adults with extraintestinal manifestations

https://pmc.ncbi.nlm.nih.gov/articles/PMC5703914/

Emerging role of hypoxia-inducible factor-1α in inflammatory autoimmune diseases: A comprehensive review

https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.1073971/full

Thiamine deficiency activates hypoxia inducible factor-1α to facilitate pro-apoptotic responses in mouse primary astrocytes

https://pmc.ncbi.nlm.nih.gov/articles/PMC5646851/

Stabilization of the hypoxia-inducible transcription Factor-1 alpha (HIF-1α) in thiamine deficiency is mediated by pyruvate accumulation

https://pubmed.ncbi.nlm.nih.gov/30008376/

Thiamine (Vitamin B1)-An Essential Health Regulator

https://pmc.ncbi.nlm.nih.gov/articles/PMC12251314/

https://pubmed.ncbi.nlm.nih.gov/40647310/

Role of HIF-1α in the Hypoxia Inducible Expression of the Thiamine Transporter, SLC19A3

https://pmc.ncbi.nlm.nih.gov/articles/PMC5097002/

https://pubmed.ncbi.nlm.nih.gov/27743994/

Thiamine insufficiency induces Hypoxia Inducible Factor-1α as an upstream mediator for neurotoxicity and AD-like pathology

https://pubmed.ncbi.nlm.nih.gov/36241022/

Mito-Nuclear Communication by Mitochondrial Metabolites and Its Regulation by B-Vitamins

https://pmc.ncbi.nlm.nih.gov/articles/PMC6379835/

The role of hypoxic microenvironment in autoimmune diseases

https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1435306/full

Emerging role of hypoxia-inducible factor-1α in inflammatory autoimmune diseases: A comprehensive review

https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.1073971/full

Increased Expression of Hypoxia-Inducible Factor 1α in Coeliac Disease

https://www.nature.com/articles/pr2010143

Peroxiredoxins and Hypoxia-Inducible Factor-1α in Duodenal Tissue: Emerging Factors in the Pathophysiology of Pediatric Celiac Disease Patients

https://pmc.ncbi.nlm.nih.gov/articles/PMC9954839/

"HIF-1α shows its functions through translocating into the nucleus, dimerizing with HIF-1β and binding to hypoxia-responsive elements of the HIF-1α target genes. Recent data have also suggested that HIF-1α plays a role in maintaining intestinal epithelial barrier functions [37,38]. Accumulating evidence has also shown that HIF-1 α plays an essential role in cells via interaction with the NF-kB p65 pathway in the pathogenesis of inflammation [17]. In addition, previous research has further reported that HIF-1α expression is increased in the duodenal tissue of celiac disease patients [19,39]. It has been pointed out that activated HIF-1α is involved in celiac disease pathogenesis."

Mito-Nuclear Communication by Mitochondrial Metabolites and Its Regulation by B-Vitamins

https://pmc.ncbi.nlm.nih.gov/articles/PMC6379835/

Increased Expression of Hypoxia-Inducible Factor 1α in Coeliac Disease

https://www.nature.com/articles/pr2010143

Intestinal parameters of oxidative imbalance in celiac adults with extraintestinal manifestations

https://pmc.ncbi.nlm.nih.gov/articles/PMC5703914/

Emerging role of hypoxia-inducible factor-1α in inflammatory autoimmune diseases: A comprehensive review

https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.1073971/full

Thiamine deficiency activates hypoxia inducible factor-1α to facilitate pro-apoptotic responses in mouse primary astrocytes

https://pmc.ncbi.nlm.nih.gov/articles/PMC5646851/

Stabilization of the hypoxia-inducible transcription Factor-1 alpha (HIF-1α) in thiamine deficiency is mediated by pyruvate accumulation

https://pubmed.ncbi.nlm.nih.gov/30008376/

Thiamine (Vitamin B1)-An Essential Health Regulator

https://pmc.ncbi.nlm.nih.gov/articles/PMC12251314/

https://pubmed.ncbi.nlm.nih.gov/40647310/

Role of HIF-1α in the Hypoxia Inducible Expression of the Thiamine Transporter, SLC19A3

https://pmc.ncbi.nlm.nih.gov/articles/PMC5097002/

https://pubmed.ncbi.nlm.nih.gov/27743994/

Thiamine insufficiency induces Hypoxia Inducible Factor-1α as an upstream mediator for neurotoxicity and AD-like pathology

https://pubmed.ncbi.nlm.nih.gov/36241022/

Mito-Nuclear Communication by Mitochondrial Metabolites and Its Regulation by B-Vitamins

https://pmc.ncbi.nlm.nih.gov/articles/PMC6379835/

The role of hypoxic microenvironment in autoimmune diseases

https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1435306/full

Emerging role of hypoxia-inducible factor-1α in inflammatory autoimmune diseases: A comprehensive review

https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.1073971/full

Increased Expression of Hypoxia-Inducible Factor 1α in Coeliac Disease

https://www.nature.com/articles/pr2010143

Peroxiredoxins and Hypoxia-Inducible Factor-1α in Duodenal Tissue: Emerging Factors in the Pathophysiology of Pediatric Celiac Disease Patients

https://pmc.ncbi.nlm.nih.gov/articles/PMC9954839/

Human Leukocyte Antigens are coded for in our DNA.  They act like street signs on cells so the body knows that they are "Self".   Tissue typing in organ transplantation looks for donors with "Self" street signs similar to the recipient's in order to prevent rejection of the transplanted organ.  

The HLA DQ genes code for immune cells.  Some immune cells are encoded to recognize certain protein strings when that protein string attaches to the receptor on its cell membrane.  Originally, these protein strings were found in the cell walls of harmful viruses and bacteria.  

I like to think of these immune cells as patrolling police with orders to "be on the lookout for armed and dangerous suspects matching your cell membrane receptor description".  

However, segments of these dangerous protein strings are also found in the carbohydrate storage protein Gluten.  During digestion, Gluten segments bind with Tissue Transglutaminase, an enzyme that builds and repairs structural components of our "Self" cell membranes in our bodies.  

This Gluten-Transglutenaminase globule fits into the receptors on the patrolling police immune cells and sets off an alarm.  Mother immune cells begin producing antibodies (anti-tissue Transglutaminase antibodies ie, tTg antibodies) against the Transglutaminase-Gluten globule.  

Unfortunately, we have tissue Transglutaminase in the structure of all our cell membranes.  The antibodies attack healthy cells in our digestive tract, damaging them, causing them to signal to nearby cells "I'm sick, get away from me so you don't catch it!".  Spaces appear between cells.  The tight junction between cells is lost.  Gastrointestinal permeability is compromised.  This allows for other Transglutaminase-gluten globules to leave the intestinal tract, enter the blood stream, and travel to other organs and cause problems there. 

All the while, more police immune cells are alerted along the way with more mother cells producing more antibodies.  Sort of ends up looking like a "Smokey and the Bandit" movie in my mind, but with more than one "Bandit" driving around.  

So, people with a genetic predisposition (they have HLA DQ genes known to code for Celiac Disease) can go for years without developing Celiac Disease.  There needs to be a trigger that turns the genes on.  Triggers can be physical stressors like having an infection (like the flu or the common cold), or an injury, or an emotional stressor (like losing a loved one or abuse).  

There's some scientific proof that Thiamine insufficiency triggers autoimmune diseases.  During times of illness and emotional stress, the body requires additional Thiamine to provide the energy for the increased metabolic demand that comes with physical and emotional trauma or stresses.  Athletes have higher metabolic demands.   People who work outside in sunshine have higher metabolic demands, too.  This is because light (sunlight or indoor lighting) breaks thiamine down, denatures it, so that it cannot be used.  People who drink alcohol need more thiamine because alcohol will cleave thiamine in half making it useless.  People who eat a diet high in carbohydrates have a higher metabolic demand for thiamine and the other B vitamins needed to turn food into energy.  

Mitochondria are involved in producing energy, ATP, from Thiamine Vitamin B 1.  When there is a thiamine deficiency inside a cell, the mitochondria can no longer make energy ATP.  This is relayed to the DNA.  On the DNA, a switch is thrown to signal there's no thiamine, and another switch is turned on.  This is the switch that turns on the DQ autoimmune genes coded for in that DNA.  Whatever autoimmune genes are on your DNA start turning on. 

Thiamine Vitamin B 1 is needed to turn food into energy for the body along with the seven other B vitamins and minerals. Thiamine and magnesium make life sustaining enzymes.  Thiamine does stuff by itself, too, like regulate the immune response, and prevent mast cells from degranulating histamine. Thiamine influences which bacteria grow in our microbiome.  Thiamine deficiency allows Small Intestinal Bacterial Overgrowth (SIBO).  Immune responses and inflammatory cytokines are higher in thiamine deficiency.  

Thiamine cannot be stored long (18 days).  Thiamine insufficiency or deficiency can occur within three days if stores are depleted due to high metabolic demand and depleted stored thiamine.   

The majority of people with Diabetes have been shown to be deficient in Thiamine.  People with obesity who plan gastric bypass surgery have been found to have insufficient thiamine.  People Hashimoto's (autoimmune thyroid problems) have been found to improve with thiamine supplementation.  People with autoimmune arthritis have been shown to improve with thiamine supplementation.  People with MS have been shown to improve with thiamine supplementation.   

Blood tests are not reliable measures of thiamine level.  The brain controls the amount of thiamine in the blood stream.  The brain will order tissues to release their stored thiamine into the blood stream in order to keep a constant supply going to the brain, heart, and lungs.  So, there can be organs with depleted thiamine stores, while blood levels stay constant.  This results in a localized deficiency within the organ or tissue.  

The best way to tell if there's a deficiency is to take thiamine hydrochloride for several weeks and look for health improvements.  Higher amounts of thiamine are needed to correct thiamine insufficiency or deficiency.  This helps replenish thiamine stores inside cells and tissues as well as meet increased metabolic demands.  

Processed foods containing wheat are required to have vitamins added to them to replace the ones lost with the removal of the germ and bran.  Food manufacturers use Thiamine Mononitrate, a cheap, shelf-stable form of thiamine that is not easily absorbed nor utilized by the body.  

A diet high in ultra processed foods, high in sugar and simple carbohydrates requires additional thiamine to turn the carbs into energy for the body.  Excess carbohydrates and low thiamine encourages SIBO.  For every 1000 kcal of carbohydrates the body needs an additional 500 mg of Thiamine.  The RDA is based on the minimum amount required to prevent disease.  This was set in the 1940's, when people ate very differently.  

Early symptoms of thiamine insufficiency include depression, anxiety, impulsivity, and changes in mood and cognitive function, digestive problems, nausea, abdominal pain, diarrhea, constipation, fatigue, muscle cramps, high blood pressure, tachycardia, blurry vision, insomnia or other sleep disturbances.  All so easily overlooked or attributed to daily stresses.  

Genetic Variants of the Human Thiamine Transporter (SLC19A3, THTR2)—Potential Relevance in Metabolic Diseases

https://pmc.ncbi.nlm.nih.gov/articles/PMC11988879/

Thiamine, gastrointestinal beriberi and acetylcholine signaling

https://pmc.ncbi.nlm.nih.gov/articles/PMC12014454/

Thiamine and METTL14 in Diabetes Management with Intensive Insulin Therapy

https://pmc.ncbi.nlm.nih.gov/articles/PMC12024880/

https://pubmed.ncbi.nlm.nih.gov/19290628/

Gliadin and Casein Metabolism: Synthesis of Gliadomorphin and Casomorphin and Their Biological Consequences

https://www.researchgate.net/publication/397908713_Gliadin_and_Casein_Metabolism_Synthesis_of_Gliadomorphin_and_Casomorphin_and_Their_Biological_Consequences

Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ milk

https://pmc.ncbi.nlm.nih.gov/articles/PMC4818854/#:~:text=Results,lactose tolerant and intolerant subjects.

Casomorphins and Gliadorphins Have Diverse Systemic Effects Spanning Gut, Brain and Internal Organs

https://pmc.ncbi.nlm.nih.gov/articles/PMC8345738/

Brain Opioid Activity and Oxidative Injury: Different Molecular Scenarios Connecting Celiac Disease and Autistic Spectrum Disorder

https://pmc.ncbi.nlm.nih.gov/articles/PMC7407635/

I was eating the Standard American Diet at the time, which is a diet that causes High Calorie Malnutrition.  Consuming large amounts of carbohydrates without a corresponding increase in Thiamine causes a Thiamine deficiency.  For every extra 1000 calories an additional 0.5 g of Thiamine HCl is needed.  Thiamine deficiency can cause a voracious appetite, or conversely, anorexia.  

I developed Type Two Diabetes and was prescribed Metformin, another drug that causes Thiamine deficiency.   The majority of people either type of diabetes are deficient in Thiamine. 

My digestive symptoms were just awful.  Thiamine deficiency causes Gastrointestinal Beriberi.  Symptoms include abdominal pain, gas, and bloating, nausea, vomiting, diarrhea, constipation.  

I broke a leg.  Doctor suggested I increase my calcium consumption.  Thiamine deficiency causes renal calcium leaks.  Years later, I was found to have a severe Vitamin D deficiency.  Thiamine is needed to activate Vitamin D.  Vitamin D and Thiamine are both instrumental in Calcium reabsorption in the kidney.

My blood pressure got too high.  I was prescribed an calcium channel blocker, which is a drug that causes Thiamine deficiency.  Niacin deficiency causes high blood pressure.  Calcium deficiency can affect blood pressure.  

I started retaining water and was prescribed a diuretic, Hydrochlorothiazide.   Thiazide is another drug that causes Thiamine deficiency.  Edema, water retention, especially in the lower legs, is a symptom of Thiamine.  

My gallbladder needed to be removed.  Thiamine deficiency causes gallbladder dysfunction.  

I had menstrual problems.  I had to have surgery.  Vitamin D acts as a hormone.  Vitamin D deficiency affects fertility.  

My health continued to spiral down.  Doctors laughed at me when I asked about being tested for Celiac Disease.  I developed Wernicke's.  The doctors called it "depression".  They had written me off and sent me home.  My family, friends, and fiance all fled like rats abandoning a sinking ship.

I had to beg a doctor to test my Vitamin D level. He agreed after he made sure my insurance would cover it.  Vitamin D helps with depression.  My doctor was surprised by the severely low level.  He prescribed Vitamin D 2, the synthetic form which is not very easy for the body to utilize.  He refused to test for further deficiencies because he "can't make money prescribing vitamins."

I lost sixty pounds in a month.  Thiamine deficiency causes unintentional weight loss.  I could feel myself dying. 

I developed the eye infection.  Thiamine has antibacterial and antiviral properties.  Vitamin A is important to eye and skin health.  

I developed Casal's necklace.  A different doctor sent me out the back door of the clinic to get tested for syphilis.  Casal's necklace is different in Pellagra.  It's on the sun exposed areas of the neck.  In syphilis, it's on the outside of the shoulders, usually under clothing.  I knew this!  The four D's of Pellagra are diarrhea, dermatitis, dementia, death.  

It couldn't be that easy, could it?  It was!  I started feeling better as soon as I started taking Niacin.  

I threw away all the pharmaceuticals.  

I had health improvement within an hour of taking the first high dose of Thiamine HCl required to correct Thiamine Deficiency. 

I started a gluten free diet and continued to supplement with all the essential vitamins and minerals and nutrients my body required.  I follow a Paleo diet.  Meat is an excellent source of Thiamine and B Complex vitamins.

I couldn't do a long gluten challenge because I got so ill, but I was seronegative.  The test showed no tTg IgA antibodies.  Seronegative Celiac Disease happens after one has had long-term malnutrition.  A DNA test shows I have Celiac Disease, one of the worst combinations. 

Subclinical Thiamine deficiency can occur over many years.  Symptoms may wax and wane mysteriously.  A twenty percent increase in dietary thiamine causes an eighty percent increase in brain activity, resulting in periods of better health.

But one doesn't have to have Celiac in order to have Thiamine deficiency.  If given pharmaceutical drugs that cause Thiamine deficiency, Thiamine levels should be monitored.  Thiamine deficiency can result in stroke, heart attack or death.  The Erythrocyte Transketolace Activity Assay is more accurate than a blood test.  Test before supplementing, otherwise the test will pick up on supplements taken prior to the test.  Thiamine is safe and nontoxic even in high doses.  High dose Thiamine is required to correct deficiency.  Doctors can administer Thiamine HCl through an IV.  Diagnosis through elimination.  

I hope this is helpful.  Best wishes.

I wasn't diagnosed with Celiac until midlife. My various health problems for which I sought medical attention were treated as separate entities.  No medical professional looked for the root cause of any one of my various health problems, much less connect the dots to a systemic illness.  They simply treated the immediate symptoms, much like putting a bandaid on.  No medical professional tied them together as being related to Celiac disease and the nutritional deficiencies caused by Celiac disease.  I have already had unnecessary surgeries for health problems that could have easily been resolved by treating the nutritional deficiencies caused by Celiac Disease Malabsorption and a gluten free diet.  

I have suffered permanent damage to the optic nerve caused by vitamin deficiencies.  I have functional eye damage from an eye infection.  Specialists at the Helen Keller Institute did not recognize nutritional deficiencies as part of the problem.  Eye surgery is out of the question because the eye infection would most certainly recur and eye removal would be necessary. 

I do use adaptive devices.  Light from electronic devices, indoor LED lights, outdoor LED lights like street lights and signage, and sunlight over-stimulate my optic nerve permanently damaged by nutritional deficiencies.  This triggers ophthalmic migraines with aura and a type of seizure.  My optic nerve shuts down and I lose my vision completely.  My vision returns after an (increasing) time period, but there's always the chance it won't return at all after such an episode. (Apologies if I don't respond to posts immediately.)

I studied nutrition at university, but earned a degree in Microbiology because I was curious what the vitamins were doing inside the body.  I'm not a doctor, although I have been ridiculed by doctors for even suggesting Celiac Disease and malnutrition were the underlying problems.  Pharmaceutical bandaids, only made nutritional deficiencies worse as many medications are known to block absorption and function of different vitamins.  When I presented with B12 Deficiency Dementia and Wernicke's Encephalopathy,  I was diagnosed with "Depression" and briefly institutionalized.  When I presented with Casal's necklace, I was hurriedly ushered out the backdoor of the clinic, and sent to be tested for Syphilis.  Afterwards, I threw out all my medications.  I started supplementation based on what I had learned at university and started a gluten free diet.  My health miraculously improved. 

I am now here, thanks to the grace of  G*d and @Scott Adams, to help others find their way on this journey.  If I can clear a few stumbling blocks out of their way, my journey has been worthwhile. 

The immune cells that make tTg IgA antibodies which are triggered today are going to live for about two years. During that time, inflammation is heightened.  Those immune cells only replicate when triggered.  If those immune cells don't get triggered again for about two years, they die without leaving any descendents programmed to trigger on gluten and casein.  The immune system forgets gluten and casein need to be attacked.  The Celiac genes turn off.  This is remission.  

Some people in remission report being able to consume gluten again without consequence.  Another triggering event can turn the Celiac genes on again.  

Celiac genes are turned on by a triggering event (physical or emotional stress).  There's some evidence that thiamine insufficiency contributes to the turning on of autoimmune genes.  There is an increased biological need for thiamine when we are physically or emotionally stressed.  Thiamine cannot be stored for more than twenty-one days and may be depleted in as little as three during physical and emotional stresses. Mitochondria without sufficient thiamine become damaged and don't function properly.  This gets relayed to the genes and autoimmune disease genes turn on.  Thiamine and other B vitamins, minerals, and other nutrients are needed to replace the dysfunctional mitochondria and repair the damage to the body.

Avoid B Complex vitamins if they contain Thiamine Mononitrate if possible.  (Read the ingredients listing.)  Thiamine Mononitrate is the "shelf-stable" form of B 1 that the body can't utilize.  B vitamins breakdown when exposed to heat and light, and over time.  So "shelf-stable" forms won't breakdown sitting on a shelf in a bright store waiting to be bought.  (It's also very cheap.)  Thiamine Mononitrate is so shelf-stable that the body only absorbs about thirty percent of it, and less than that is utilized.  It takes thiamine already in the body to turn Thiamine Mononitrate into an active form.  

I take MegaBenfotiamine by Life Extension.  Benfotiamine has been shown to promote intestinal healing, neuropathy, brain function, glycemic control, and athletic performance.  

I take TTFD-B1 Max by Maxlife Naturals, Ecological Formulas Allthiamine (TTFD), or Thiamax by EO Nutrition.  Thiamine Tetrahydrofurfuryl Disulfide (TTFD for short) gets into the brain and makes a huge difference with the anxiety and getting the brain off the hamster wheel.  Especially when taken with Magnesium Threonate.  

Any form of Thiamine needs Magnesium to make life sustaining enzymes and energy.  I like NeuroMag by Life Extension.  It contains Magnesium Threonate, a form of magnesium that easily crosses the blood brain barrier.  My brain felt like it gave a huge sigh of relief and relaxed when I started taking this and still makes a difference daily.  

Other brands of supplements i like are Now Foods, Amazing Formulas, Doctor's Best, Nature's Way, Best Naturals, Thorne, EO Nutrition. Naturewise.  But I do read the ingredients labels all the time just to be sure they are gluten and dairy free.

MegaBenfotiamine by Life Extension, TTFD-B1 Max by Maxlife Naturals, and NeuroMag by Life Extension.  Ecological Formulas Allthiamine (TTFD).

https://pubmed.ncbi.nlm.nih.gov/10919966/

The effects of endurance training and thiamine supplementation on anti-fatigue during exercise

https://pmc.ncbi.nlm.nih.gov/articles/PMC4241913/

Effects of thiamine supplementation on exercise-induced fatigue

https://pubmed.ncbi.nlm.nih.gov/8815395/

Exploring the Relationship between Micronutrients and Athletic Performance: A Comprehensive Scientific Systematic Review of the Literature in Sports Medicine

https://www.mdpi.com/2075-4663/11/6/109

Nutritional Imbalances in Adult Celiac Patients Following a Gluten-Free Diet

https://pmc.ncbi.nlm.nih.gov/articles/PMC8398893/

Clinical trial: B vitamins improve health in patients with coeliac disease living on a gluten-free diet

https://pubmed.ncbi.nlm.nih.gov/19154566/

Nutritional Consequences of Celiac Disease and Gluten-Free Diet

https://www.mdpi.com/2036-7422/15/4/61

Impact of a Gluten-Free Diet in Adults With Celiac Disease: Nutritional Deficiencies and Challenges

https://pmc.ncbi.nlm.nih.gov/articles/PMC11692684/

https://pmc.ncbi.nlm.nih.gov/articles/PMC12014454/#ref3

https://pmc.ncbi.nlm.nih.gov/articles/PMC12014454/#ref3

From Section 3:

"In conclusion, TD limited to the gastrointestinal system may be an overlooked and underdiagnosed cause of the increasingly common gastrointestinal disorders encountered in modern medical settings. Left unattended, it may progress to wet or dry beriberi, most often observed as Wernicke encephalopathy."

https://pmc.ncbi.nlm.nih.gov/articles/PMC12014454/#ref3

References:

Dietary intake of B vitamins and their association with depression, anxiety, and stress symptoms: A cross-sectional, population-based survey

https://pubmed.ncbi.nlm.nih.gov/33848753/

The Role of Vitamins and Minerals in Psychiatry

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3046018/

Thiamine and benfotiamine: Focus on their therapeutic potential

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10682628/

Hiding in Plain Sight: Modern Thiamine Deficiency

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8533683/

Vitamin B6: A new approach to lowering anxiety, and depression?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9577631/

High‐dose Vitamin B6 supplementation reduces anxiety and strengthens visual surround suppression

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9787829/

Higher vitamin B6 intake is associated with lower depression and anxiety risk in women but not in men: A large cross-sectional study

https://pubmed.ncbi.nlm.nih.gov/31188081/

Dietary riboflavin intake in relation to psychological disorders in Iranian adults: an observational study

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10060244/

Dietary niacin intake in relation to depression among adults: a population-based study

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10506255/

A Systematic Review and Meta-Analysis of B Vitamin Supplementation on Depressive Symptoms, Anxiety, and Stress: Effects on Healthy and ‘At-Risk’ Individuals

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6770181/

Biology of Perseverative Negative Thinking: The Role of Timing and Folate Intake

https://pubmed.ncbi.nlm.nih.gov/34959947/

Vitamin B12 Supplementation: Preventing Onset and Improving Prognosis of Depression

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7688056/

The Effects of Magnesium Supplementation on Subjective Anxiety and Stress—A Systematic Review

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452159/

Effect of magnesium and vitamin B6 supplementation on mental health and quality of life in stressed healthy adults: Post‐hoc analysis of a randomised controlled trial

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9292249/

The Role of Vitamins and Minerals in Psychiatry

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3046018/

Additionally...

Factors associated with villus atrophy in symptomatic coeliac disease patients on a gluten-free diet

https://pubmed.ncbi.nlm.nih.gov/28220520/

Influence of Tryptophan and Serotonin on Mood and Cognition with a Possible Role of the Gut-Brain Axis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4728667/

The Effects of Dietary Tryptophan on Affective Disorders

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4393508/

Antidepressant-like Effects of Representative Types of Food and Their Possible Mechanisms

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10574116/

Tryptophan-enriched diet or 5-hydroxytryptophan supplementation given in a randomized controlled trial impacts social cognition on a neural and behavioral level

https://pubmed.ncbi.nlm.nih.gov/34737364/

Effect of Tryptophan, Vitamin B6, and Nicotinamide-Containing Supplement Loading between Meals on Mood and Autonomic Nervous System Activity in Young Adults with Subclinical Depression: A Randomized, Double-Blind, and Placebo-Controlled Study

https://pubmed.ncbi.nlm.nih.gov/31902864/

Nutritional and herbal supplements for anxiety and anxiety-related disorders: systematic review

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2959081/

Nutrition as Metabolic Treatment for Anxiety

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7907178/

Sharing Pathological Mechanisms of Insomnia and Osteoporosis, and a New Perspective on Safe Drug Choice

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6336562/

Passiflora incarnata in Neuropsychiatric Disorders—A Systematic Review

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7766837/

Effects of L-tryptophan on sleepiness and on sleep

https://pubmed.ncbi.nlm.nih.gov/6764927/

The impact of tryptophan supplementation on sleep quality: a systematic review, meta-analysis, and meta-regression

https://pubmed.ncbi.nlm.nih.gov/33942088/

Is tryptophan a natural hypnotic?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC161739/

The Role of Tryptophan Metabolites in Musculoskeletal Stem Cell Aging

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555967/

Nutritional Imbalances in Adult Celiac Patients Following a Gluten-Free Diet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8398893/

Micronutrients Dietary Supplementation Advices for Celiac Patients on Long-Term Gluten-Free Diet with Good Compliance: A Review

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6681258/

Gluten-free diet intervention reduces thiamine intake in two weeks, increases glycaemic response and decreases body weight in four weeks, with no long term nutritional deficiencies

https://pubmed.ncbi.nlm.nih.gov/34583628/

B-vitamins, related vitamers, and metabolites in patients with quiescent inflammatory bowel disease and chronic fatigue treated with high dose oral thiamine

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10601301/

Missing the early signs of thiamine deficiency. A case associated with a liquid-only diet

https://pubmed.ncbi.nlm.nih.gov/30092713/

Randomised clinical trial: high-dose oral thiamine versus placebo for chronic fatigue in patients with quiescent inflammatory bowel disease

https://pubmed.ncbi.nlm.nih.gov/33210299/

Gastrointestinal beriberi: a forme fruste of Wernicke’s encephalopathy?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6040496/

Hiding in Plain Sight: Modern Thiamine Deficiency

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8533683/

Nutritional Aspects of Bone Health and Fracture Healing

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5804294/

And...

There is a significantly inverse relationship between dietary riboflavin intake and prevalence of osteoporosis in women but not in men: Results from the TCLSIH cohort study

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9941537/

And...

Nutrients and Dietary Patterns Related to Osteoporosis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400143/

And...

Vitamin D Deficiency, Osteoporosis and Effect on Autoimmune Diseases and Hematopoiesis: A Review

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8396272/

And...

Riboflavin intake and status and relationship to anemia

https://pubmed.ncbi.nlm.nih.gov/36018769/

And...

Riboflavin Inhibits Histamine-Dependent Itch by Modulating Transient Receptor Potential Vanilloid 1 (TRPV1)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8249943/

Thiamine deficiency made me have a voracious appetite at some times and at other times, I had no appetite at all.  Thiamine affects the satiety center in the brain that tells you to eat more or you've had enough.  

Thiamine deficiency also causes nausea.  I would wake up ravenous, but have nausea so bad I didn't want to eat.  Nausea sometimes occurred after eating.  My food just sat there and didn't seem to move.  Gastroparesis, where your food doesn't get squished through the intestines at a regular pace, can also be attributed to thiamine deficiency.   Later I developed non-stop diarrhea and gastrointestinal pain and cramping (Gastrointestinal Beriberi is caused by Thiamine deficiency).  

Thiamine deficiency causes anxiety.  My doctors threw a variety of antidepressants at me, but they didn't work and made things worse.  Many antidepressants (and other pharmaceuticals like PPIs) can inactivate thiamine so the body can't use it. 

Thiamine deficiency causes fatigue.  The fatigue I felt was awful and unrelenting.  

Thiamine deficiency affected my balance.  I waddled.  My hair started falling out by the handful.  My vision became more blurry.  I had painful migraines.  I began having ophthalmic migraines (thiamine deficiency affects the optic nerves).   I had menstrual problems.  I had cramps in my muscles.  I'd wake at night with Charlie horses.  I felt faint when standing or moving about and sometimes my heart raced too fast or skipped a beat (Postural Orthostatic Tachycardia Syndrome -POTS - another thiamine deficiency disorder).  I started stuttering, and then slurring my words.  My voice became hoarse and at times I could not speak at all.  I forgot things easily.  I got frustrated easily.  I had difficulty concentrating.  I had difficulty with regulating emotions.  I could not read and understand things.  I could not remember verbal instructions.  I could no longer read and knit lace from charted knitting patterns.  I became very despondent.  

But I remembered that half a dozen doctors had asked me if I drank.  I would respond no, alcohol makes me sick. The doctors would scratch their heads, shrug their shoulders, and walk off.  No answers.  But that question rang a bell somewhere amongst the cobwebs.  I had to dig out my notes from university....Thiamine deficiency is most commonly found in (postmortem) alcoholism.  And malabsorption disorders like Celiac Disease!  

I stumbled upon Dr. Derrick Lonsdale who has studied Thiamine Deficiency Disorders outside of alcoholism for years.  Thiamine deficiency presents differently outside of alcoholism.  Eventually, severe thiamine deficiency symptoms outside of alcoholism overlap with alcoholic thiamine deficiency symptoms.  Those doctors saw those same severe symptoms, but they didn't treat it because I didn't drink alcohol.  If it walks like a duck....

So, I started high dose thiamine as Dr. Lonsdale described.  I took over-the-counter Thiamine Hydrochloride and had improvement within an hour.  I added in Allithiamine (TTFD - Tetrahydrofurfuryl Disulfide), a form of Thiamine that can cross the blood brain barrier by itself.  My brain started working again!  

I had other vitamin deficiencies concurrently.  Malabsorption messes with all the nutrients.  Thiamine deficiency symptoms show up first because it runs out fastest.  I had Vitamin D deficiency, Pellagra, Scurvy, and anemia.  

I eat Paleo.  I found that eating healthy fats (Omega Threes) is key.  The satiety center in the brain signals that full feeling after eating sufficient fats.  Olive oil is great.  I ate small meals closer together while I healed.  

A diet that is high in carbohydrates would make me feel awful.  Eating a large amount of carbohydrates at a meal demands an increased amount of Thiamine.  Carbohydrates like white rice and processed foods don't contain sufficient thiamine to digest and convert them into energy.  

I took vitamins and mineral supplements in order to give my body the essential building blocks it needed to repair and recover.  I feel much better now.  I can knit again!

I hope this helps.

References:

Hiding in Plain Sight: Modern Thiamine Deficiency by Dr. Derrick Lonsdale and Dr. Chandler Marrs

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8533683/

And...

Thiamine Deficiency: Appetite and Eating Disorders

http://www.hormonesmatter.com/thiamine-deficiency-causes-problems/

And...

Thiamine deficiency disorders: a clinical perspective

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8451766/

And...

Omega-3 Fatty Acids And Inflammation – You Are What You Eat!

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8846546/

And...

The importance of thiamine (vitamin B1) in humans

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10568373/

B cells defined by immunoglobulin isotypes

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9985177/

And...

Mode of Bioenergetic Metabolism during B Cell Differentiation in the Intestine Determines the Distinct Requirement for Vitamin B1

https://pubmed.ncbi.nlm.nih.gov/26411688/

And...

Metabolism of Dietary and Microbial Vitamin B Family in the Regulation of Host Immunity

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6478888/

And...

TKT maintains intestinal ATP production and inhibits apoptosis-induced colitis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8448773/

Immune cells called B cells need thiamine to become antibody producing cells.  If there's a thiamine deficiency, the B cells cannot become antibody producing cells and there's less of an immune reaction.   Different types of B cells produce different types of antibodies.  

B cells that can produce IgG antibodies are in the bloodstream, so they are the first line of defense.  They can use different methods of making energy, so are not dependent on Thiamine to be able to change into IgG antibody producing cells.  

IgA antibodies are produced mainly in the intestines after B cells which produce IgA antibodies are changed into IgA antibody producing cells.  This change is dependent upon Thiamine.  If there's not sufficient thiamine, fewer B cells can change and fewer IgA antibodies are produced.  

The IgA antibodies stay in the intestines until there's sufficient numbers of them they get into the bloodstream from the intestines.  

Some of us are seronegative.

Clinical and genetic profile of patients with seronegative coeliac disease: the natural history and response to gluten-free diet:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5606118/

Seronegative Celiac Disease - A Challenging Case:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9441776/

Enteropathies with villous atrophy but negative coeliac serology in adults: current issues:
https://pubmed.ncbi.nlm.nih.gov/34764141/

I've experienced the limbs falling asleep.....

Vitamin B12 deficiency neuropathy; a rare diagnosis in young adults: a case report

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5273828/

And...

I've experienced gritty dry eyes and eye pain, light sensitivity....Optic nerve swelling and permanent vision loss occurred in my situation because of delayed diagnosis...

Vitamin B12 deficiency evaluation and treatment in severe dry eye disease with neuropathic ocular pain

https://pubmed.ncbi.nlm.nih.gov/28299439/

And...

Tinnitus and hearing loss...

Therapeutic role of Vitamin B12 in patients of chronic tinnitus: A pilot study

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918681/

And...

Visual loss and optic nerve head swelling in thiamine deficiency without prolonged dietary deficiency

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4039400/

My "friends" used to call me  Helen (as in Keller) because I had such bad problems with my hearing and vision... I was referred to the Helen Keller Institute for the Blind hospital and even those specialists did not diagnose B12, Vitamin A, and Thiamine deficiencies causing my vision problems.  

I have Bell's Palsy, a type of facial numbness and paralysis, which is linked to B12 deficiency.

I have had dark circles around my eyes and puffy eyelids from B12 deficiency.  

B12 deficiency caused urination urgency problems.

I experienced facial rash, nail, and hair changes...

Cutaneous lesions and vitamin B12 deficiency

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2294086/

Niacin B3 caused nail changes, especially toe nail changes that look like fungus but it was the start of Pellagra.  I had Casal's necklace, and the doctors still did not diagnose the Niacin deficiency.

Magnesium deficiency caused night terrors.  Iron deficiency caused black lines in my nails.  Riboflavin deficiency caused a rash around my nose and mouth.  Vitamin C deficiency caused skin problems and hair loss.  Thiamine B1 and Biotin B7 deficiency contributed to hair loss.  Thiamine deficiency caused panic attacks and eventually Wernicke's Encephalopathy. 

Big Thing to note is we can have B12 deficiency symptoms BEFORE blood tests show B12 deficiency.  Same for the other vitamins.  Blood tests don't accurately reflect vitamin deficiencies inside the organs and tissues of the body where the vitamins are actually used.  Blood tests for vitamin deficiencies can reflect how much of that vitamin we've consumed in the previous twenty-four to forty-eight hours.  Supplementing with vitamins prior to blood tests for vitamin deficiencies will reflect the vitamin supplements, not the deficiencies in organs and cells.  

B12 deficiency can be reversed by oral B12 supplementation or B12 shots, but remember, it's unusual to have a single vitamin deficiency in Celiac Disease because the absorption of vitamins and minerals are affected by damage done to the small intestine where most vitamins and minerals are absorbed.  

There are eight essential B vitamins.  Our bodies can not make these or store them for long, so we need to consume them every day.  The eight B vitamins all work together, dependent on each other.  B12 needs folate B9 and pyridoxine B6.  Pyridoxine needs riboflavin B2.  Thiamine B1 and Niacin B3 provide energy and enzymes for the other vitamins to work, along with magnesium and iron and other minerals, and Vitamin C. Also, there are four fat soluble vitamins we need, Vitamins A, D, E, and K 2.

Checking for nutritional deficiencies is part of proper follow up care for newly diagnosed Celiacs.  Blood tests do not accurately measure vitamin status, so talk to your doctor about supplementing with vitamins.  Talk to a nutritionist about including nutrient dense foods in the gluten free diet.

Hope my experiences with vitamin deficiencies can help you and others.

Previously, we examined B cell immunometabolism in the intestine. In the intestine, naïve immunoglobulin (Ig) M+ B cells differentiate into IgA+ B cells in Peyer's patches (PPs) by class switching, and then IgA+ B cells differentiate into IgA-producing plasma cells in the intestinal lamina propria (20). Naïve B cells in PPs preferentially use a vitamin B1-dependent TCA cycle for the generation of ATP. However, once the B cells differentiate into IgA-producing plasma cells, they switch to using glycolysis for the generation of ATP and shift to a catabolic pathway for the production of IgA antibody (Figure 1). Consistent with the importance of vitamin B1 in the maintenance of the TCA cycle, mice fed a vitamin B1-deficient diet show impaired maintenance of naïve B cells in PPs, with little effect on IgA-producing plasma cells. Since PPs are the primary sites of induction of antigen-specific IgA responses, PP regression induced by vitamin B1 deficiency leads to decreased IgA antibody responses to oral vaccines (21).

Wheat products are required by law to be enriched with vitamins and minerals lost in processing.  In other words, wheat products have vitamins added to them. 

Celiac Disease damages the small intestine where the B vitamins are normally absorbed.  We often do not get enough B Complex vitamins while we are healing because of the damage done by Celiac and because the gluten free diet can be deficient in these vitamins.

By supplementing with B Complex vitamins, the body will be ensured of getting all the B vitamins it needs to recover and function properly.

I became very ill with vitamin and mineral deficiencies.  The doctors I saw did not recognise vitamin deficiency symptoms.  I'm a microbiologist, so I had studied this stuff at university.  I knew the pharmaceuticals the doctors threw at me were not helping, the pharmaceuticals only covered up the symptoms, but the real problem remained.  

And I craved gluten, not for the gluten, but because they were a source of the vitamins my body was craving.  

I started supplementing with all eight essential B vitamins.  Our bodies can't make them so they must be consumed every day, hence they are called "essential".

Deficiency in many of the B vitamins will cause altered mentality.

It's rare to have just a single vitamin deficiency.  

I've had Thiamine (Vitamin B1) deficiency that resulted in Wernicke's- Korsakoff syndrome and was written off as crazy by doctors and psychiatric "experts".  High dose (more than 500 mg/day) thiamine therapy was the only thing that corrected that.  Thiamine deficiency is associated with Anorexia, Bulimia, and Binge and Purge disorders, and Obsessive Compulsive Disorder.  

I've had Niacin deficiency that resulted in Pellagra and had mental changes with that.

I've had Cobalamine deficiency (Vitamin B12) and experienced B12 deficiency dementia.  

Vitamin D deficiency caused severe depression.  Magnesium deficiency caused horrible nightmares.  Vitamin C deficiency caused skin problems and delirium.  

If we give our bodies the building blocks of essential nutrients, our bodies can heal themselves.  

I was ill because I was deficient in vitamins and minerals, not because I was deficient in pharmaceuticals.  Doctors don't recognize vitamin deficiency symptoms.  Doctors are trained in medical training institutions funded by big pharmaceutical companies to prescribe pharmaceuticals.  

I've posted previously in this thread studies done on mental health and vitamin deficiencies.  Please read them.  Vitamin and mineral deficiencies will affect your mental health.  Correcting vitamin and mineral deficiencies will help more than putting a bandaid antidepressant on the problems.  

Correcting deficiencies promptly is important. Deficiencies left untreated can cause permanent brain damage which can be seen on MRIs.  

Here's some helpful reading...

Nutritional therapies for mental disorders

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2248201/

And...

Bread and Other Edible Agents of Mental Disease

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809873/#!po=18.0556

And...

The Role of Vitamins and Minerals in Psychiatry

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3046018/#!po=10.0000