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Familial Beriberi: Discovering Lifelong, Genetic, Thiamine Deficiency

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In 2017, at the age of 52, I had an unexpected call from my new doctor informing me “I know what’s wrong with you! Come to my office now!” Lifelong increasing chronic fatigue and untreatable Hashimoto’s thyroiditis were my chief complaints.

Past doctors prescribed high dose thyroid medication, which made me feel worse. An autoimmune diet kept me trim but provided no energy. I read adenosine triphosphate (ATP) is required for thyroid production, though ATP isn’t discussed in treatment. Baggage from Effexor and an adverse childhood were also contributors to my health.

Desperate, every relevant supplement and thyroid medication on the market, I tried. Only two were effective. GABA relaxed me, and d-ribose cured my depression 100%. I became bubbly. My personality changed, but after four weeks they both stopped working. Amour thyroid lifted my brain fog for a week. Then, I had side effects. Eventually, I would learn that I, and many members of my family, across several generations, had beriberi or thiamine deficiency. In my case, I had a defect in a key thiamine transporter that made getting sufficient thiamine from diet all but impossible. Unfortunately, I did not learn this crucial information, until I was in my fifties, after years of illness and suffering.

Women’s Issues and Unrelated Problems Begin

While my problems began decades earlier, they seemed to hit a crescendo as I hit menopause. The HRT patch relieved hot flashes, only to fuel a fruit-sized fibroid that split in half with one part covering my rectum. A GP prescribed colon therapy causing severe leg cramps and constipation. A fibroid ablation enabled normal bowel function. Afterward, ozone baths caused my bowel function to stop and I developed air hunger. An ENT said, “you don’t have sleep apnea, there’s another system in your body that is causing air hunger.” He recommends a university clinic over going to different specialists.  I pursued genetics.

Starting to connect my cognitive decline, prediabetes, and depression in my grandparents to myself, I went to the MTHFR expert that wrote the report.  Her extensive 15-page genetic/supplement report offered no results. After failed treatments from endocrinologists, functional doctors, and big-name clinics like Mercola, I took a chance on Orthomolecular Medicine.

Discovering a Familial History of Beriberi

On the day I was diagnosed with thyroid treatment failure, I found a nutrient interaction article and had a light bulb moment, I’m missing a nutrient for thyroid production. I went to the author, the late Dr. Richard Kunin, San Francisco’s legendary go-to doctor for solving mystery illnesses through nutrients. He was a pioneer in antioxidant therapies, utilizing diet, nutrient and genetic testing since the seventies.  His orthomolecular research was the first to verify the use of a mineral therapy in a drug-induced disease.

When his door flung open, I saw wisdom. A rare commodity. Here was this brilliant doctor and a poster of his early collaborator Linus Pauling, staring down at me. Dr. Pauling coined the term orthomolecular meaning “the right molecule in the right amounts.” A doctor like this comes once in a lifetime and I handed him my three-inch binder.

A true scientist, he was able to assess my biochemical individuality, in two sessions.

In the doctor’s intake, the first clue is asking what my parents ate. They ate both Chinese and Western foods, which seemed like no big deal. After lab results, he searches through 300 genes, to find the biggest picture, the gene. Instead of trying to treat multiple gene defects with a supplement. He addresses the root cause first.

He announces, “You’re deficient in thiamine,” and gives me the SNP, called Transporter 2 (SLC19A3) which provides instructions for making a protein called the thiamine transporter, which moves thiamine into cells. Over time, the transporter dissolves.

I had thiamine and asparagine deficiency and riboflavin and glutathione borderline deficiency. The thiamine or vitamin B1 deficiency caused the other deficiencies, but he stays on point and discusses thiamine and only thiamine. He prefaces the session with a history of beriberi and birds fed white rice.  Looking back, it’s rudimentary B1 history, but as a patient stuck in the Hashimoto’s/Adrenal Fatigue paradigm for so long, my mind went blank. I remained silent, I didn’t know if I could die from it.

To make matters more confusing. I had stopped taking thiamine after an OATS showed B1 adequacy.

When he told me I can’t convert energy from food, I thought how absurd. He reminded me “the bottom line is how well you absorb the thiamine; not how much I tell you to take”. A Meyer’s Cocktail IV is an initial part of treatment. The next step is collecting data to prove the relevance of thiamine as an essential nutrient required to make energy.

When I Added Thiamine, My Body Began To Recharge

For the first time, I saw a difference in labs and body function. At 300 mg of HCL, my increasing A1C levels fell below the prediabetes range. I almost took metformin at one point, recommended by an integrative doctor. I felt the effects of B1 utilizing B6, through a lucid dream. Treating methylation since 2006, he says “B1 is the gateway to methylation.”  With before and after data, he points out B1 upregulating the folate cycling. My energy was increasing. Muscular problems resolved, elevated branched chain aminos were absorbing and TMJ and bruxism disappeared. This was just the beginning. familial beriberi - thiamine deficiency

I found the thiamine experts, Dr. Derrick Lonsdale and Dr. Chandler Marrs during my titration period. Nuances of thiamine used as a drug to make ATP are available with a detailed overview of beriberi, throughout Hormones Matter. Post to post, the doctors’ addressed every missing piece to my complex puzzle and more. They prompted me to take a closer look inside my dad’s past, one he rarely spoke of, and connections were made.

While titrating up, I had a short bout of diarrhea in the middle of the night. When I decreased the dose, I developed POTS for the first time, the room would spin 24/7 whenever I stood up. My GP referred me to the ER. I was unaware that I was having a paradox reaction. I just upped the thiamine, POTS, and diarrhea resolved.

Chronic TD is called beriberi means “I can’t, I can’t” in Singhalese. The problem is Chinese typically under 80, have never heard of beriberi, and in the US, beriberi is known but assigned as a disease that does not exist anymore or a condition only seen in alcoholics and bariatric patients. Genetic beriberi is passed through families, causing the inability to absorb thiamine from foods.

Beriberi In Two Families Going Back Three Generations

My family history revealed apparent genetics expressing as neuropsychiatric disorders and other conditions that appeared unrelated. Thiamine deficiency (TD) is not easily identified, due to its polysymptomatic nature. Besides the brain, the heart, muscle skeletal, digestive system, and autonomic nervous systems (ANS) need thiamine to function.

My maternal side lived in prosperity and ate a traditional Chinese diet and tropical delicacies. There were 7 members, including my grandfather that had Alzheimer’s (AD) and one family member had Parkinson’s. My grandmother had TD from kidney dialysis. There was TD in AIDS. Untreated hyperthyroidism resulted in cardiac failure mortality at 58. An alcoholic uncle had deficits, anxiety, cancer, and AD. An anorexic cousin refuses whole meals, develops a damaged digestive tract, severe IBS-C, chemical sensitivities, and major depressive disorder.

My paternal side lived in poverty. White rice was a diet staple. There was an aunt that died from child mortality in China from starvation.

After migrating to the US, food scarcity persisted. My grandfather had obesity and type 2 diabetes. My grandmother had sadness after her husband sold their daughter’s papers in China, never to see them again. At 61, my 4’10” grandmother fell over and died from beriberi.

Her wake was the first time my dad went to a restaurant at age 16. He often licked food and preserved it for later. Falsely accused of stealing, the detention center fed him regular meals. Five siblings had short stature and high IQs. His Chinese brother pictured right, was saved by the U.S. Army from malnutrition and assigned to be the radar instructor. There was bullying, anger, and irritation in the three boys. One, a bar owner exhibited extreme behavior like bringing a gun over a trivial conflict that would leave in-laws aghast.

Ocular diseases, restless leg syndrome, circadian rhythm disorder, cancer, some OCD and hypermobility, and osteoporosis appear. There was TD from chemotherapy. Two aunts left behind in China lived to be centurions and a daughter has fibromyalgia, depression, and other deficits.

Connect the lineage with a pregnancy gone wrong.

Genetics and a Traumatic Pregnancy Sets the Stage for Life

Pregnancy, a hypermetabolic state, requires sufficient thiamine for the development of a healthy child. My mom, a robust woman, was overmedicated and bedridden for a month post-pregnancy. She recovered but my brother was permanently disabled. My brother was born with uncontrollable hyperactivity and oppositional disorder. Our theory was his oxygen supply was cut off to his brain, but it was thiamine deficiency.

Two years later I was born. As a young child, I was hypoactive and didn’t move much. In grade school hearing loss was detected. Early memories included some clumsiness and not having the strength to swing on monkey bars like other children. My first feelings of frustration were over homework, especially math. My overall health waxed and waned and would not draw attention until high school when tiredness, poor memory and learning disabilities appeared. I was bullied by my older brother.

Nine years later my younger brother was born, bruxism as a baby, was his first sign of thiamine deficiency.

The next generation, symptoms of thiamine deficiency show in a gifted child.

Neurological deficits ranging from severe to minor were a sign of impaired methylation since birth.
My mom’s prenatal diet was traditional and American, and we were bottle-fed. This was in the ’60s when women were weaned off breastfeeding.

Now connect the genetics, the pregnancy and untreated thiamine deficiency in a parent and sibling.

A Genius Mind Uses More Energy and Requires More Thiamine

My dad invented the on-line TV guide in the eighties. In a constant state of fight-or-flight, working through the middle of the night on patents, sugary snacks were comfort foods to compensate for early years of food deprivation. The “night owl” term we used was circadian rhythm dysfunction. Thiamine is an overlooked nutrient required for sleep and the breakdown of cortisol.

When my brother’s hyperactivity was unmanageable, breaking things, beating the ADD out of my brother was habitual. A dysfunctional limbic system causes knee-jerk reactions to uncontrollable rage. I just learned that my seemingly nice uncle, an alcoholic, frequently tried to beat the homosexuality out of his young child.

A psychologist thought violence only happens in alcoholics. I think this limited view needs to be updated to include excess processed food intake. I remember “children should be seen and not heard” commercials as a child when hitting and spanking was more accepted.

In 1983, Dr. Kunin cited Dr. Lonsdale’s research that describes the B vitamin link with violence in Mega Nutrition for Women, “patients whose violent behavior was inexplicable by conventional medical diagnosis were found to be deficient in one or more B vitamins, notably B1, B3, and B6”.

During the Covid-19 shutdown, I thought of TD when incidences of abuse spiked, homelessness and random violence spread, and middle-class families now become dependent on food banks.

Poor Health After Antibiotics

As a young teen, I lost my glow, I looked tired, and my skin had a jaundiced yellow-greenish tint. In high school, after a round of tetracycline for transient acne, I was never the same. My metabolism stopped and I gained 40 lbs. I also have leptin deficiency and so I am always hungry. Napping after school was an everyday event. My limited thyroid test given showed normal thyroid-stimulating hormone (TSH). I was also constipated but didn’t know it until middle-aged after I was diagnosed with Hashimoto’s. In my 20’s I took antibiotics for chronic strep throat. Uninterested in nutrient dense foods, I subscribed to carb loading and high-intensity aerobic activity, the trend of the day.

Changes in My 30’s and the Promise of Modern Medicine

When my dad had side effects from sleep medication, he did his research, bought supplements for every system in the body, and stopped going to doctors. He got the family off of rice and put us on B vitamins. Uneducated in vitamins, I gave up on them too soon. I wasn’t taking enough! My mom’s acupuncturist treated my ADD, but I strayed when a well-meaning friend steered me towards pharmacology, and I took Effexor. The damage showed up over the next decade when increased nervous system and mitochondrial dysfunction begin.

Loud bar music in the back of my unit initiated chronic insomnia in my forties. I had open mouth breathing. Elevated cortisol and night sweats woke me at least 8 times a night. If I was mad, I’d have an instant hot flash and sizzle like a red bull. I lost my sex drive. After quitting Effexor, elevated thyroid TBO antibodies appeared. Later diagnosed with sensorineural hearing loss, the psychiatrist prescribed sound therapy but the condition isn’t curable.

Musculature problems began, I had an unrelenting frozen shoulder from a gym accident, and at one point, I had ataxia and couldn’t walk straight. After a trip, while in Hurricane Ivan, I was unable to walk for a month with ataxia. I once met an advanced multiple sclerosis patient, that experienced the exact same symptom from Ivan. The cause was thiamine deficiency in the cerebellum, the part of the brain that controls movement and walking.

For work, I illustrated 300 skylines from around the world and market them on Etsy. My fine motor skills and artistry remain superior, but my spatial organization was nonexistent. I was very messy. Taking GABA hampered work stress, but I couldn’t cycle it from thiamine deficiency. Managing inventory and college students wore me out. One told me “You can’t retain what I tell you”.  Finding my car in large parking lots was often challenging. The hippocampus circuitry requires thiamine for short-term memory function.

Orthomolecular psychiatry has proven to treat and manage these types of disorders with nutrients and diet, as the first line of defense. There was no need for antidepressants.

After My Diagnosis, I Learned My Parents Were Already Taking Thiamine

When I told my dad about my thiamine deficiency, he pulled out a bottle of thiamine labeled anti-beriberi. He was taking B1 for cardiac support. The heart and brain consume a vast amount of energy and require thiamine to meet the demand. My mom took benfotiamine successfully for shingles, a neuropathic pain.

When I told my original acupuncturist, about my diagnosis he said, “I already know you have beriberi, just take B vitamins and lots of them. You don’t need my herbs.” He had been treating me for dysautonomia, twenty years before I developed POTS. I detested the point because his needling pressure hurt. No questions asked; he needles points by observation and pulse, Western characterization in diseases have no significance.

Part of the treatment for dysautonomia is a needle to the center of the philtrum, this point prevents fainting. Another needle is inserted into the center of the forehead and one on top of the head for balance. Traditional Chinese Medicine (TCM) healers identify liver and lung channels weakness two decades before western medicine.

The New Doctor Damaged My Health In Only Eight Months

Twenty nineteen was a bad year. Dr. Kunin sees Vitamin C deficiency and signs of anemia and then retired. I stopped getting IVs. I would still nap after taking them. My trusted acupuncturist, also a nutritionist moved. I began dry coughing a lot, which later I learned was a sign of TD. Then I met the worst doctor ever.

I showed her, Thiamine Deficiency, Dysautonomia, and High Calorie Malnutrition and she handed it back to me and said “Oh, another patient brought this in the office.” I interviewed another doctor and told him I have TD and he replied with, “what’s your point!” and referred me to a doctor out of state.

I settled on the first doctor, and everything started wrong. She put me on a high-dose thyroid medication without titrating, and Low Dose Naltrexone (LDN), which gave me a stomachache. She wanted me back on LDN after I told her I had side effects. She recommends NAD instead of Meyer’s Cocktails which includes thiamine.

By the time I realized I was in a hyperthyroid state, the damage had begun. A cascade of beriberi symptoms begins. When one symptom would go away, another would begin. The neuropathy was more long-term. I had resting tachycardia, lactic acidosis after five days of yoga stretch that caused feet neuropathy and then trigger finger. All the doctor could say was “I had candida overgrowth”.  The cause of candida was that I had a weakened immune system from TD. I watched videos on lactic acidosis to explain it to her.

When I saw an eleven year old’s homework on glycolysis it made me wonder how much doctors remember from medical school.” I tested the doctor and asked her “What does pyruvate convert to?” She answered incorrectly.

I was developing non-alcoholic Wernicke’s encephalopathy (WE), acute short-term memory loss. I almost walked out of a restaurant thinking I paid the bill. I couldn’t remember putting a credit card back in my wallet and arguing with the clerk after she had handed it back to me. Once I read, “if you think you’re deficient in thiamine, get an IV right away.” After a series of Myers Cocktails with phosphatidylcholine, the progression stopped.

Another doctor got me off the thyroid meds, yet wet and dry beriberi symptoms continued. My left-hand lost circulation and turned hard and purple. The back of my neck hardened and my backside turned into butter. I had unintentional weight loss and my hand reflexes slowed. My minerals were becoming unbalanced. I contacted a refeeding syndrome clinic, for a consult, but was turned away because I wasn’t anorexic. A few months later I traveled to Hawaii and made a mistake.

Orthomolecular Medicine Rescues Me Again

Accidentally packing thiamine HCL instead of TTFD, the HCL initiated my paradox reaction and I had diarrhea several times the first night. Every day I napped from the sun’s UV rays. Excruciating muscle cramps sent me to Dr. Pritam Tapryal, Honolulu’s IV doctor specializing in chronic fatigue syndrome. Thiamine handouts, a stockpile of capsules and vials of B1 were waiting for me.

He calculates that I needed 600 mg of IV thiamine based on the length of time I had been feeling unwell. With an iron load before the second IV, I felt a surge of energy – I got ATP! My vagus nerve stimulated peristalsis and excess fermentation stuck in my body for three months finally released. Elevated liver enzyme activity and low blood pressure normalized.  Afterward, I found a doctor willing to provide high dose thiamine therapy at home.

I went back to the doctor that said “what’s your point” when I told him I had thiamine deficiency and requested 600 mg of parenteral B1 instead of 100 mg. A bit taken back, he shows compassion and custom orders 500 mg of B1 in a Myers Cocktail, after I explained my recent experience. The IV manager thought I was an ICU patient, but I wasn’t. It was the dose I felt best on.

High Dose IV Thiamine Therapy: From  A Patient’s Perspective

A series of high-dose thiamine (HDT) IV treatments, turned into an epigenetic treatment going on two years and two months. I’ve taken 100,000 mg of parental thiamine to this date. Infusions continued to sustain therapeutic effects and increased thyroid production. Unknown cause of malabsorption required ongoing infusions. Resolved through extensive pre-and post-labs.

I self-directed my treatment and gauged myself. I found thiamine articles from all over the world, but high-dose thiamine information was limited to WE treatment only. I received no medical advice on thiamine therapy from allopathic doctors that had clinical nutrition education, or from a young orthomolecular doctor or GP. Familial beriberi - thiamine deficiency

I had two to three IVs per week the first year that included 500 mg of thiamine. The longest time without an IV was three weeks at the beginning of 2020 and eleven days at the end of 2021. Below is a 12-month summary, from a 55-year-old woman with unrecognized lifelong thiamine deficiency from a SLC19A3 gene defect.

Journal From Long Term, IV, High Dose Thiamine Therapy

My high-dose thiamine regimen began 11/21/2019. This is the Meyers Cocktail titration period:

  • 2 infusions of 200 mg of thiamine in 2 weeks in end of Nov. to Dec.
  • 5 infusions 300 mg of thiamine in 2.5 weeks Dec. to Mid Dec
  • 2 infusions 400 mg of thiamine in 2 weeks Mid Dec. to January.
  • 500 mg of thiamine 2 to 3 times a week were taken in the middle of January.

11/2019 Concerned about anaphylaxis. Only a few teeny bumps around lips developed and disappeared after the first day. Visual clarity is the first sign of improvement.

12/2020 – Foot neuropathy and trigger finger for 4 months, resolved with 7 IV’s spread out over 4.5 weeks. The IV thiamine doses were 300 mg or 200 mg. Dexa scan shows osteopenia in lower back and femur and only 3 lbs. of lean muscle mass, muscle wasting, a hallmark symptom of beriberi.

OATS test taken a day after HDT infusion – tested B1 borderline deficient. Borderline and deficient in minerals and vitamins except manganese, doctor thought something was wrong with lab.

1/2020 – Right mucosal lining was demyelinating and slightly bleeding for a month, saw glitter. Zonulin levels over 800, the doctor told me not to be concerned, but I was. Slight rectal bleeding.

An unintentional fast in cold weather caused syncope. Broke out in an intense sweat, became faint and lost appetite. Leaned against buildings every few feet to get home, no thiamine in am. Sitting on bench resolved symptoms. MCV increases to 100, normal range is up to 95.

Tested negative for panel of inborn errors of metabolism. Autoimmune panel negative except – Arthritis – equivocal, Thyroiditis- out of range, Epstein Barr – negative.

2/2020 – New formulation of phosphatidylcholine, with small amount of dextrose without B1 was a mistake.

On three-week break, nighttime driving vision had decreased. Resumed Meyer’s Cocktail after break, fatigued, fell asleep in IV chair after IV. Reduced thyroid medication from I grain a week, increased after break to 3.5 grains a week. A1C 4.8 increased to 5.2 after break.

Right quadrant of my upper teeth dropped down. Oral surgeon said “not pathogenic of disease”.

Last visit with Dr. Kunin. Concerned I looked just as depressed as when we first met. I was happy to see him, unable to express it. Continue a more DIY approach and TCM, “the Chinese have found ways to treat that western medicine has not figured out, and one day technology will be so advanced doctors won’t be necessary”.  He handed me the keys and said, “Figure it out on your own.”

3/2020 – Introduced high fat diet. Lost 3 lbs.in a week. Severe leg cramps from foot to shin. During an IV, felt leg cramping. Normal cholesterol increased from 260 to 400. Stopped diet. No B1 in fat.

4/2020 – Lowered stress from semi-retirement and resting. IBS starts to resolve for the first time at 55. Felt extreme chill one day.  Took injectables at another doctor’s office due to shut down. I took 100 mg B1 in a B complex in intramuscular (IM) with B12 to ease B1 ‘pinch’, plus IM biotin for a month.  Not as effective as HDT infusions.  Combination of B1 with complex and biotin had best results.

5/2020 – Meyer’s Cocktail and 350 mg of NAD back-to-back infusions lifted brain fog profoundly.  Able to do tasks I couldn’t perform prior. I cried with joy, my cells were not permanently damaged from past use of Effexor and antibiotics. Unable to replicate treatment. Oral Inositol reduced elevated triglycerides dramatically, then stopped working. IBS came back off and on.

6/2020 – Tested borderline low on calcium, choline, magnesium, B5, B12, Vit C, K2, zinc on a three month average. GI lab shows mal-digestion, metabolic imbalance, and dysbiosis. Stomach pain from psyllium and flax, phytobezoar build up, rash on neck since 2019 getting worse, insomnia resolved.

7/2020 – Severe anemia showing and severe muscle weakness. I couldn’t lift a 5 lb. weight. Acute memory loss, almost walked out of lab before taking the lab.  Waking up early in am in summer at 8:00.  Hemoglobin normal and then drops frequently, IV doctor sees bleeding. Ophthalmologist finds arcus build up from high cholesterol, strong arteries, and recommends latanoprost for glaucoma after field test.

8/2020 – Decreased parenteral 500 mg B1 to 300 mg to test if high dose thiamine is depleting B12. Began coughing after 7 days. Post NAD IV lab tested  B12 deficiency, causing hemoglobin and T3 deficiency.  Acupuncture treatment creates switch sensations throughout body allowing oxygen flow, heart channel under arm point pulsated – oxygen and lung channels communicate. Leg bruising – Vitamin C deficiency.  Insomnia came back when B1 parental dose decreased, never resolved fully after increasing B1.

9/2020 – ANS dysfunction – uncontrollable body flipping in bed two nights in a row, movements like a fish out of water.  Resumed 500 mg of prenatal B1 after two weeks at 300 mg. Ophthalmologist said “you look more alert”, compared to two months ago. Started IM Mic-B and hydroxocobalamin, 5 days a week. IBS-C decreased with B12 IM. Coughing on Lipothiamine, switched permanently to Allithiamine, cough resolved. Normal zonulin levels return, reduced gut inflammation. GI didn’t order endoscopy after I told him something hit my stomach when walking and had rectal bleeding. He wrote IBS on notes. Stopped EDTA IVs for cadmium after a few treatments, when urine began foaming.

10/2020 – Latent deficiencies appear: B12, CoQ10 malabsorption. B1 not absorbing. Vitamin C deficiency appears, lifelong subclinical scurvy, bleeding gums, gingivitis, pilaris keratosis, bruising, poor iron absorption, rectal bleeding, low tyrosine.  Sick people are low in B vitamins and Vitamin C.  Repeated thiamine depletions cause heavy Vitamin C deficiency in lung, kidney, thymus, and liver.

Tested positive for Intrinsic Factor AB, Pernicious Anemia (PA).  Hematologist defensive when I asked him if TD can cause anemia, cancelled next appt., told me to see a GI. Doctors booked from Covid-19 delays.

Oral surgeon cleared teeth shifting. Orthodontist ordered aligners, short teeth roots in scan.

Trialed compounded thiamine cream from Lee Silsby pharmacy and replaced TTFD.

11/2020 – Stomach pain increasing after meal. Twelve days in, I thought I was going blind. The thiamine cream wasn’t absorbing. Indoor and night vision blurry. Back to TTFD and Myers Cocktail together. My vision came back, but not as clear before getting blurry. Mild paradox reaction, a bowel movement in the middle of the night.

12/2020 – Endoscopy shows chronic gastritis, h. pylori and peptic ulcers. A combination of a lack of nutrients cause ulcers, including B1.  Refused triple therapy (antibiotics and PPI). Treated with cabbage, herbals, mastic gum.  ION Panel indicated GSH and potassium deficiency, lactic acidosis (TD), ketosis, oxidative stress, transmitter deficiencies and metabolic syndrome.

Elliot Overton of EO Nutrition interprets mitochondria in battleship mode, suspects mold toxicity. Unseen mold or water damage. Incontinence and frequent urination. Second ophthalmologist told me don’t take latanoprost. MCV high still high with regular IM B12, since 10/20. With small veins and bursting arteries, it’s difficult to maintain IV’s.

In 2020, my health was like my dad’s. My hearing and vision deteriorated, I was unable to hear people speak with masks on and had difficulties focusing on conversation in noisy rooms. Gingivitis developed into periodontal disease; teeth aligners require lifetime use. My dad is deaf in one ear, and now going blind in the second eye and had the periodontal disease the same year and wears dentures.

Observations at 43,500 mg IV Thiamine After 13 Months

Intravenous therapy can target issues in ways oral thiamine cannot reach.

Improved thyroid production, A1C, insomnia, IBS and CFS, overall energy level partially improved.  Foot neuropathy and trigger finger resolved.  Cocktails with phosphatidylcholine, iron, and NAD, had increased effects, latent deficiencies appear, no nutrient depletions from high-dose thiamine.

Infection, gastritis, ulcers during treatment caused malabsorption. Reducing thiamine caused insomnia to reoccur and acute vision reduction, increased ANS dysfunction caused temporary uncontrollable body movements.  Increased dose of 300 mg to 500 mg of B1 resolved uncontrollable body movements and regained vision.

I saw one patient vomit, and a patient have nausea during 300 mg B1 Meyers Cocktail.

ROS from unknown cause extends treatment into 2021.

High Dose Thiamine IV Therapy, Toxins, Diet, Labs, and Gigong

In 2021, I tapered to two IVs a week and increased the 500 mg to 600 mg mid-year. Hot flashes returned after 5 years of remission causing a three-month setback. Insomnia made me delirious and had to take naps. PEMF bio-mat calms the nervous system to assist in sleep, without it I’ll wake up a few times during the night. For over 10 years, I wake up and urinate once a night. My eyes became blurry and I walked slowly like an old lady for a short period. Daily clear phlegm wants to come out since 2020 when I eat.

In spring my bloodwork showed Stachybotrys and Aspergillus mold. I found growth on papers in a storage box against a wall with the laundry room on another side. Condensation went through the wall.

With my gut healing and IV therapy, my TBO antibodies levels reduced significantly. The increased T3 raised my steroid hormones. Reducing thyroid medication again was a real possibility. IBS-C was resolved by mega-dosing powder magnesium with fiber, B1 and B12. I once had an offer to see the world authority on IBS-C, though all I needed was a good form of high-dose magnesium. I was feeling better until I experienced unexpected setbacks.

Everything Changed With Two Major Endocrine Disruptors

Microscopic brick debris during construction flew under my windows. Debris flew inside over 50 ft. and landed everywhere, never thought my eyes and lungs could clear it. Due to an HLA-DQB1 gene defect, I’m unable to break down mycotoxins (mold).  Mold is an anti-thiamine factor and it oxidizes B1 and B12.

When inflammation started to calm down, my hallway went under remodeling, and material debris and paint fumes went under my door. The chemicals shut down my thyroid. Antibodies rose from 180 to 535. Inflammatory markers that were improving became elevated and deficient. My killer cell function, HNK1 (CD57) level was 50 and now 18.  The doctor thinks I have Lyme. I’m testing for MARCoNS, a staph infection that resides deep in the nasal passage, due to sinus inflammation from the biotoxins.

After trialing Cholestyramine for mold binding, it made me constipated. My acupuncturist gave me a two-hour treatment to undo the damage. To detox, I use an FIR infrared sauna on the mat. I’m getting an ERMI test kit to test other rooms, an air test hardly detected mold.

HDT Isn’t a Standalone Treatment

With the amount of IVs I took, I tested questionable foods. A few small gluten-free snacks put me into a comatose within 20 minutes. Less than two ounces of coffee initiated leg/foot cramping. I never had this problem a few years ago.  Removal of processed carbs is the only way I can maintain my thiamine storage.

Staying in mild ketosis, on a paleo diet is optimal for me. When I tried high-fat and vegan diets, they caused deficiencies. I have a nonfunctional gene cluster FADS1/FADS2, that requires the consumption of EPA and DHA found in seafood. Drinking concoctions of vegetables and minerals activate B vitamins throughout the day.  TD causes nitric oxide deficiency and I replete myself with nitric oxide greens.  My one kryptonite food is liver, it elevates my copper.  Using food as medicine supports my overall immune function as I recover from Chronic Inflammatory Response Syndrome.

My hydrochloric acid is deficient from TD, and I have low gastrin. I’ve taken 13,000 mg of Pepsin Betaine and feel no sensation. Apple cider vinegar doesn’t seem to work. My amino supplements aren’t absorbing.  I also have oxalates, Elliot recommends more B6 and I’ve increased molybdenum to meet my sulfur intake.

I take a blend of B1 that includes: 900 mg Allithiamine, 300 mg benfotiamine and 500 mg thiamine HCL. Over 900 mg Allithiamine and sulfur come up. Before a Meyers Cocktail, I’ll soak in magnesium salts. I’ve increased all the B’s and take them with other essential nutrients throughout the day in moderate to high doses. I require biotin intramuscularly every few weeks, otherwise my nails chip, this started last year. My transporter may be dissolving.

Utilizing Biomarkers and Managing Nutrients

Every six weeks I rotate biochem panels and adjust diet and supplements. My weaknesses this year have been lipids, omegas, aminos, and inflammatory markers. My B12 continues to pool due to suboptimal thiamine levels unable to utilize B12, so I stopped testing. I inject 35 mg of hydroxocobalamin a week, plus sublingual, and hemoglobin is always on the lowest end of normal after I had pernicious anemia. Mold is the suspect cause. I may also have scar tissue from ulcers and scurvy of the colon. The GI doctor recommends an endoscopy once every three years when there’s been a problem.

I’ve found nutrient panels reliable when B1 is extremely deficient. On two occasions my lactate tested normal. Then I had beriberi symptoms after I took the labs on the same day. This was from eating beans and walking in sun, which forced me to sleep. My citric acid markers were normal on an ION panel and I was in ketosis, but the clinician didn’t know I had POTS on the morning of the lab. This was from a three-day fast suggested by a doctor. Thiamine deficiency can worsen on a dime.

Diagnosed with TD on a SpectraCell micronutrient panel, I had long-term B1 deficiency. Normal B1 levels are misleading on my labs once there’s been intake. The Vibrant America panel showed B1 malabsorption at 35,000 mg of parenteral B1.  I’ll continue with this panel and monitor nutrients connected to B1.

My doctor’s friend offered me the two-part transketolase lab for research, but my doctor forgot to arrange the sampling. I was upset at the time, but it doesn’t matter now. I manage myself by how I feel. With Excel journaling, the more elements I add, the more clarity I receive. Observing physical changes are equally valuable to the labs.

A Revisit to Energy Medicine That Compliments Nutritional Balancing

I recently discovered group Primordial Qigong. I haven’t found any other modality that has the same restorative benefits that give energy instead of using energy. Movements connect the body, mind, and soul with the focus on living in the present. Gentle stimulation of systems and body parts creates rejuvenation from within. Who doesn’t want that?

Dysautonomia, the fainting prevention point, is taught in practice. The bank of hands faced together inverted pushed downwards from the forehead over the philtrum encourages balance. Made for masses with no resources, it only requires continuity. This is a welcoming alternative compared to the nutrient-depleting therapies, recommended by for-profit western doctors that made my health worse when they didn’t know what they were dealing with.

At 100,000 mg Of IV Thiamine – It Feels Like I’m on a Train I Can’t Get Off

Overall, the quality of my life has improved. I no longer need to lie down and sleep during the day, even if I feel tired. I’m more active in mind and body. I can sit up and read, wake up earlier, and exercise. My processing speed and speech are faster. The left side of my brain is strengthened. I did audits on my condo association to trace missing dues and one over BlueCross when many claims were unpaid. My brain fog had been too severe to do this previously.

Neuropsychiatric issues appear in less frequency. I still experience forgetfulness and minor learning impairments. Irritation is manageable. I believe some brain function is permanently damaged along with hearing loss. Considering my long-standing history, I’m pleased with the results even though it is only a partial recovery.

Since my body called out for a high dose, there’s a chance I can regress. At 11 days off the IVs, I was deficient in Co2. I don’t know if the thiamine coenzymes can function without high-dose therapy because of my genetic liability. I’m patiently waiting to see how my body changes after the toxins are eliminated and figure out how to taper down from the IVs.

Final Thoughts

Thanks to Dr. Marrs and writers on HM for elucidating thiamine awareness, I learned how to use thiamine as a drug at a time when I needed it most.

Through luck, I found nutritional clinicians that made a significant difference in my health. Educated in Dr. Lonsdale’s thiamine research, they applied his nutrient-based knowledge into their practices. Understanding that beriberi still exists today and is not an ancient scourge from yesterday, is critical.

By assimilating the genetic impact of beriberi and orthomolecular dosing, I’m regaining health in my late fifties. However, no patient should have to spend a lifetime finding a treatment based on luck. There’s no reason to it’s all here: Thiamine Deficiency, Dysautonomia and High Calorie Malnutrition, Derrick Lonsdale and Chandler Marrs; www.orthomolecularmedicine.org

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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This article was published originally on February 14, 2022. 

Beriberi is Alive and Well in America

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Readers of this website must surely be aware that the American medical profession completely resists the possibility of vitamin deficiency as a cause of any disease in America. This is so deeply ingrained that anybody claiming such a diagnosis is considered a fool. This seems to be particularly addressed to the classic vitamin B1 deficiency disease, long known as beriberi. It is unfortunate that we use a Chinese word that, translated to English means: I can’t. I can’t. It is the expression of the profound associated fatigue. There is good reason for denial of its modern existence. It has always been common in countries where rice has been the dietary staple. It existed unrecognized for centuries. In fact, the incredible intricacies of this complex disease took many years to unravel, much of which was performed in China and Japan where there was an obvious interest. It was a series of important historical events that led to its final solution and the history is fascinating. I really think that it is an example of the proverb “those that forget history are condemned to repeat it”. For example, groups of factory workers developed their first symptoms of the disease together after an exposure to sunlight. “Epidemics” of the disease occurred in the summer months. It was only natural that the investigators at that time had concluded that beriberi was an infectious disease. Their search for the responsible micro-organism was a futile endeavor.

The explanation can only be provided from modern knowledge. We now know that ultraviolet light imposes a stress on the human body, requiring mobilization of energy in order to meet it. For example, a car requires more energy to climb a hill. The hill is an analogy for “stress”. The groups of workers described above were in a state of mild deficiency of the vitamin and the stress of the sunlight precipitated full-blown disease, simply because of lack of extra energy required to adapt to the stress. Thus, any form of stress has to be considered in relationship to genetic risk and nutrition if and when the symptoms of beriberi are precipitated.

With this preamble, let me describe some of the clinical experiences that I have been exposed to. First of all, I was lucky enough to be able to think about health and disease in my position in a multi-specialty clinic. I came to the realization that the human body is a wonderful “machine” where the coordination of 70 to 100 trillion live units called cells, depends on chemical energy that has to be transduced to electric energy in order to carry out cellular function. Not only that, I had recognized something that is taken for granted today, that brain cells have an extravagant use of energy. The case that precipitated my lifelong interest in thiamine (vitamin B1) was a six-year-old child who had intermittent brain disease that had confounded all the studies and tests applied in the search for a solution. To put it simply, it was a biochemical approach that showed that he and his brother had a genetically determined condition that, for the most part, allowed them to pursue a relatively normal childhood life. However, each episode of spontaneously resolving brain disease left a little bit more permanent damage. The disease was invariably precipitated by an exposure to a form of stress, represented by a simple viral infection, on one occasion by a mild head injury, and even after an inoculation.

With the help of John Blass M.D. who was working at the National Institutes of Health, we were able to prove that these boys represented the first example of what came to be known as vitamin dependency. In order to prevent brain disease, both of these children required enormous doses of thiamine, but if they were affected by any form of stress such as a viral infection, the daily dose of the vitamin would have to be doubled or tripled in order to prevent a brain disease episode. I came to understand that under these circumstances I was using thiamine as a drug and that it was not a matter of simple vitamin replacement. It was an early example of epigenetics, the relatively new science concerning the way nutrition and lifestyle affect our genes.

You have to understand a very simple idea: thiamine and magnesium are known as “cofactors” to a series of enzymes that represent the machinery of energy production. Both the cofactors are derived from nutrition and have to be bound to their enzymes by a genetically determined mechanism. Not only that: thiamine has to bind to a protein known as a thiamine transporter. The transporter is also genetically determined and conveys thiamine into the cell. All of this takes place in thousands of minute organelles called mitochondria. I refer to these organelles as the “engines” of our cells. That is why glucose can be compared with gasoline in a car engine. Like an excess of gasoline chokes the engine, an excess of glucose chokes mitochondria. Thiamine and magnesium can be compared to a spark plug that ignites the gasoline. Perhaps the reader can begin to understand that this vitamin deficiency disease can literally develop any symptom anywhere in the body according to the distribution of the deficiency and its degree. The brain, heart and nervous system are the most oxygen demanding organs so it is not surprising that they are the first to be involved in thiamine deficiency.

Additional Cases of Thiamine Deficiency

My colleagues knew of my interest and although I was a pediatrician I was asked to comment on the following case. A 67-year-old anesthesiologist at a hospital in Columbus, Ohio came down one day with “a heart attack”. He was subjected to catheterization of the heart that was found to be completely normal. Meanwhile, his son was a medical student and having researched his father’s symptoms, he claimed that the disease was beriberi. The patient was referred to Cleveland Clinic and I was asked to comment on the situation. I found that when he went to his garage to drive to the hospital he would be afflicted by a series of dry heaves. This alone would immediately call to question the possibility of thiamine deficiency. He would give the anesthetic for a series of cases, after which he would go to the pediatric ward and cut himself a large piece of chocolate cake. On returning home, he was too tired to eat dinner and would go to bed, only to repeat the performance the next day. He returned to Columbus with the advice that the patient’s son was correct. I never received a follow-up and don’t know how he was treated but I later heard that he had died. I suspect that he was, in fact, given thiamine in too large a dose that overwhelmed his fragile metabolism.

My next experience was with a brilliant pathologist who was well known in the specialty. She told me that she had extreme fatigue. In fact, a few days previously she had been driving to work but felt so ill that she had turned round and gone home. I discovered that she had a chocolate box in every room in the house. As she went around from room to room she would consume one of the chocolates in each box. I advised her to stop doing this and take a supplement of thiamine, whereupon she rapidly recovered. Note that this was purely a hedonistic urge and had nothing to do with her three meals a day routine.

Ondine’s Curse

A mythological character was a water nymph who supposedly lived in a puddle. She fell in love with a mortal who jilted her and she cursed him with the loss of automatic breathing when he was asleep. There is a disease known as “Ondine’Curse” where this form of breathing ceases, usually at night and the patient dies. So one day I was having lunch with one of the Ear Nose Throat surgeons who knew of my interest. He had seen a woman in the intensive care unit who had stopped breathing and he was called to put in a tracheostomy. He suggested that I should view the case. She was under the care of a rheumatologist and she had had a history of periods of unconsciousness as well as joint pain. In using my knowledge of chemistry, I was able to show that she had thiamine deficiency and began treatment with thiamine.

During her clinical recovery she developed a profound anemia which proved to be due to a deficiency of folate. The importance of this is that her brain was affected by thiamine deficiency but when she was treated with the vitamin, her energy dependent metabolism increased. This exposed a previously adequate sufficiency of folate related to her slow metabolism. The increasingly efficient metabolism stimulated by thiamine required more folate to meet the new demand. She was a chronic smoker that had contributed to the metabolic changes in brain function that precipitated a disease that had gone unrecognized for years. I remember visiting the rheumatologist to ask her whether we could conference the patient to expose this information. She obviously thought that it was an absurd idea and refused to consider a meeting of physicians for further discussion. I learned something else from this patient. She was discharged from the hospital taking supplements of thiamine and folate. When she returned for review, the paralysis in her legs was worse and she had developed a rash on her arms that may occur occasionally in association with deficiency of vitamin B12. It has long been known that B12 and/or folate deficiency could individually be responsible for pernicious anemia (PA). However it had also been known that folate supplementation could not be given on its own for folate deficient PA. It had to be given with vitamin B12 and I had forgotten this. I gave her an injection of vitamin B12 and over the next few days she had some fever and muscle pain but the rash disappeared and she felt better.

The Complexity of Treating Vitamin Deficiencies

I provide these details to show that an understanding of vitamin deficiency disease introduces complexities that require study. When she began receiving thiamine and became clinically worse, it would be easy to blame it as a “side effect” that required administration of the vitamin to be stopped. A physician must first of all have enough knowledge to suspect the possibility and then apply the necessary tests. Obviously, if the collective psychology refuses to accept that possibility, the complaints of the patient, together with the clinical observations of the physician, will be treated symptomatically without a full recognition of the underlying cause. My exposure to a case for which I had no medical responsibility provides an example, for I was merely a visitor. I heard from her that she had been diagnosed with heart disease. She went on to say that her heart rate had dropped to 30 beats a minute, an extraordinarily dangerous situation for which she had received the drug atropine. Atropine blocks the nerve mechanism into the heart, thus controlling the danger symptomatically. She had then been given a diuretic drug and she went through an agonizing 24 hours of almost continual urination. It was clear to me that this was a dramatic exposure of thiamine deficiency heart and nerve disease. She had in fact “wet beriberi”. It has been referred to as “wet” because of the profound collection of fluid in the body and that had been treated symptomatically with the diuretic. The point that I am trying to make is that although the patient had been treated successfully with drugs, the underlying cause had not been recognized. These are uncommon cases, but I am claiming that they are the end-point of years of nutritional and medical neglect and yes, medical ignorance.

Because thiamine deficiency has its major effect in the lower part of the brain, the earliest effects are those of a deregulated autonomic nervous system (ANS). The reader will remember that the ANS conducts the traffic of body organs under the command of the brain. It consists of two basic systems, one of which stimulates action and is called sympathetic. The other one stimulates rest and is known as the parasympathetic. An early symptom of thiamine deficiency is an overdrive in the parasympathetic system, whereas at a later stage of the disease there is usually an overdrive of the sympathetic system. Accepting this factor, it can easily be seen that the patient described above, whose heart rate was drastically slowed, had been endangered because one of the nerves to the heart had carried an overdrive of parasympathetic activity. This, accompanied by a huge collection of fluid in the body, was characteristic enough to look further for the ultimate diagnosis.

Common Presentations of Thiamine Deficiency: The Walking Sick

Looking back at the history of finding the solution to this disease, it is known to have a long morbidity and a low mortality but with a long life of chronic illness gradually leading to some form of mental or physical crippling. In the elderly patient it is often attributed solely to aging. In the 1940s an experiment was carried out in a group of human subjects who were provided with a moderately deficient thiamine diet. Their symptoms were characteristic of those that are presently regarded by most physicians today as psychosomatic. They were irritable, quarrelsome and experienced heart palpitations, headaches, loss of appetite, insomnia, diarrhea or constipation, chronic fatigue and/or intolerance to heat and cold. The vast majority of patients that I treated when I was in practice had a polysymptomatic presentation of this nature, many of whom had been doctor shopping without relief. I was dealing with what I call the “walking sick”, a large group of patients that are haunting the offices of physicians throughout America. Sometimes they had been given a named diagnosis but had not benefited from drug treatment.

The behavioral characteristics of children, particularly those with ADD or ADHD, are dietary in origin, often coupled with some form of genetic risk, not the least of which is superior intelligence. They are being treated symptomatically, but I offer the possibility that failing to recognize these symptoms as nutritional in character may be a failure to recognize them as the forerunner of chronic neurological or heart disease. It is a reflection of high calorie food ingestion overwhelming the action of non-caloric nutrients that enable the necessary synthesis of cellular energy for function, particularly in the brain. In our book “Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition”, we note that our present culture is cursed with a hedonistic ingestion of high calorie malnutrition, responsible for much loss of health. In fact, I have suggested that it is the equivalent of what happened to the ancient Romans whose wine tasted sweet because of lead infiltration from the glaze used in their wine containing jars. They did not know that they were suffering lead poisoning. We don’t seem to grasp the danger of sugar. Each symptom, as it appears, is treated symptomatically with a medication. Rarely is there an interest by the physician concerning diet, particularly the ingestion of empty calories consumed socially. Given the challenge of hedonism, it seems to be part of life joy, particularly in the elderly, to indulge in all the dietary aspects of sweet, sweeter and sweetest. However, it is inappropriate to fail in recognizing the symptoms that might or might not develop as a result. If one or more of the many symptoms is recognized and the patient informed, it is then his/her choice to make the necessary changes.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

Photo: Seated Youth by Wilhelm Lehmbruck 1917. Edited. Wilhelm Lehmbruck, PDM-owner, via Wikimedia Commons.

This article was published originally on April 11, 2019.

Elimination Dieting and Progressive Thiamine Deficiency

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My issues began after the birth of my second child 21 years ago. I would get extreme indigestion for a couple days each month and my skin broke out. This continued for years until I ended up having several rounds of antibiotics. Months later, I developed severe and never ending acid reflux. After struggling for a year, my local health food store owner mentioned the blood type diet and recommended I avoid dairy. The result was magic. Unfortunately, this started a cascade of elimination diets that would set the tone for the next fifteen years.

After eliminating dairy and seeing a resolution of symptoms, at least temporarily, I decided to eliminate gluten too. As with the dairy, the indigestion disappeared temporarily when I eliminated gluten, but other symptoms eventually crept in, including hypothyroidism and bile reflux. I read about a vegetarian diet and decided to give it a try. Again amazing results from removing meat. The bile reflux disappeared.  I thought things were going pretty well, but in these years I started to have other issues: ataxia, fatigue, heat intolerance, numbness and tingling, gait and bladder issues. In addition, I was always starving. I ate a tremendous amount of food each day, but at the same time I was losing weight.

My naturopath had mentioned possible problems with my gallbladder, but I didn’t think too much about it until I had constant pain. It was eventually discovered that I had a non-functioning gallbladder and I reluctantly had it removed, hoping it would solve my problems. I had tried changing my diet to the autoimmune paleo several times, but would always crash after a couple weeks. After surgery, I could eat meat without major issues, but nothing seemed to digest well. I felt like I never really recovered and other issues started to creep in.

My calf muscles would spasm upon standing and I was so weak I was having difficulty walking a block. A year after surgery, I was diagnosed with primary progressive multiple sclerosis, as it matched my symptoms and lesions were seen on my cerebellum and down my spine. The hallmark of PPMS is neurodegeneration without inflammation. The next three and a half years were a quick decline. I quickly became unable to walk unaided, mainly because I was too fatigued and my muscles too weak. PPMS used to be called creeping paralysis and that is exactly what was happening; I was unable to move my arms or legs, my equilibrium was so off that I couldn’t stand without tipping over and I couldn’t look down to even zip up my jacket.

I had really bad edema in my lower legs and feet and they were a nice shade of purple. My brain was easily overwhelmed and not committing things to memory, which left me going in circles. I lost my appetite, but blamed it on my ever changing diet and my fear of eating the wrong food. I would alternate between diets, cutting various food groups with very limited success.

I visited multiple naturopaths, a functional medical doctor, a NUCCA chiropractor and a MS specialist. I have researched endlessly and have a cupboard full of supplements. I had tried B vitamins before but had not noticed a difference. I joined a Facebook group called Understanding Mitochondrial Nutrients and did not think much about the vitamin I needed most, thiamine, until a post by a desperate husband came up in my feed. I began to research thiamine and found I was able to piece together a timeline of my life based on a progressing thiamine deficiency. I am only three weeks into dosing with thiamine (I take 200mg thiamine HCL and 240mg benfotiamine) and a B complex, but it has made such a difference in my balance, fatigue, edema and mental energy. My appetite is back and I can zip up my coat! I am cautiously optimistic, only because I have suffered so much disappointment in the past. I am hopeful that I can make a recovery.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Thiamine Deficiency and Dependency Syndromes: Case Reports

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I have been studying thiamine metabolism since 1969 when I published the first case of thiamine dependency: Intermittent cerebellar ataxia associated with hyperpyruvic acidemia, hyperalaninemia, and hyperalaninuria. The case involved a 6-year old boy experiencing recurrent  episodes of cerebellar ataxia (a brain disease resulting in complete loss of a sense of balance). These episodes, occurring  intermittently, were naturally self-limiting without any treatment and were triggered by inoculation, mild head trauma, or a simple infection such as  a cold. In other words, his episodes of ataxia were repeatedly initiated by an environmental factor. I have called each of these variable factors  a “stressor”. Our studies showed that one of these stressors would unmask the true underlying latent thiamine dependency, falsely giving the impression that the stressor was the primary cause. This may be the principle of post vaccination disease in some cases. It may also be too easy to explain symptoms arising from trauma or infection as primary cause. These recurrent ataxic episodes were prevented from occurring by giving him mega-doses of a thiamine supplement.

Cerebellar Ataxia of Metabolic Origins?

When ataxia, as in this child,  or other symptoms, occur intermittently, as they did in many other patients whom I would treat across my career, it is difficult to identify the true cause. The studies performed by neurologists, neurosurgeons and others inevitably would be  normal, causing diagnostic confusion. In other patients with less serious symptoms, they are considered to be somehow feigned or of psychological origin. Symptoms that appear and disappear in a seemingly random manner and are not supported by conventional laboratory data are often explained this way. Please be aware that ataxia should never be regarded as psychosomatic. The point is that less serious symptoms that cause deviant behavior may not be recognized as biochemical changes in the brain.

With the present medical model, it is difficult to understand and accept that a stress factor can initiate the symptoms of a metabolically caused disease that has been relatively innocuous or silent until the stress is imposed. Let me give you another example.

Loss of Consciousness, Edema, Joint Pain: Rheumatic Disease or Metabolic Disorder

Since I was working at a multi-specialty clinic I was sitting having lunch with an ear, nose, throat (ENT) surgeon who knew of my interest in sudden death in infants (Treatment of threatened SIDS with megadose thiamine hydrochloride). He had been called to put in a tracheostomy to a middle-aged woman who had suddenly stopped breathing. Unlikely as it sounds, he suggested that I should go and look at the situation unofficially.

In the hierarchy of specialization, a pediatrician is not supposed to know anything about adult conditions, so I was not welcome. Because the internists who were taking care of her were rheumatologists, it was considered to be some kind of rheumatic disease, because of aches and pains in joints and limbs. She had had periods of unconsciousness over many years and her body was profoundly swollen, the hallmark of beriberi. Without going into details I was able to prove that this was indeed beriberi.

When I approached the rheumatologist who was her primary physician, I could not convince her of what appeared to her as too bizarre to contemplate. Notwithstanding, I had the cooperation with the nurses who followed my directions.  When the patient was given injections of thiamine, she recovered consciousness and the gross body edema disappeared.

So fixed in the mind of many physicians is the concept that a vitamin related emergency simply does not occur, it was called “spontaneous remission” by my colleagues and “had nothing to do with vitamin therapy”. When I asked the rheumatologist whether we could conference the patient, she ignored the request. Well, this was not the end of the story.

Resolving One Deficiency Often Unmasks Another

After she started the injections of thiamine, with recovery of the nervous system, she began to develop a progressive anemia. It was considered by the internists to be internal bleeding and a thorough search produced only negative results.  So ingrained is the negative attitude to vitamin therapy, I was even in fear that I might be blamed for causing the anemia. In the meantime, I took a specimen of urine and found a substance in the urine that suggested a deficiency of folic acid. Readers will remember that folic acid is a member of the B group of vitamins, as is thiamine. A blood test proved that she was indeed deficient in folic acid. When this vitamin was given to her, the anemia rapidly disappeared. This, believe it or  not, still did not interest my colleagues.

She was discharged from the hospital, receiving supplements of thiamine and folic acid and her nervous system gradually improved. Some months later she developed a rash of a type that had been reported a few months previously as due to vitamin B12 deficiency. She was given an injection of vitamin B12 and over the next few days suffered slight fever and variable joint pains. These were symptoms with which she was familiar and had been responsible for the diagnosis of rheumatic disease.  This sometimes happens temporarily with vitamin therapy, but often enough that I refer to it as “paradox”, meaning that things seem to be worse before they get better. Note that this paradox is not the same as side effects from a drug. The symptoms that cause a patient to see a doctor are temporarily exacerbated. With our present model the patient concludes that this is side effects from the vitamin(s) being used. I had to learn that paradox was the best sign that improvement would follow with persistence. She then continued on the thiamine, folic acid and vitamin B12.

The Role of Lifestyle and Diet Disease Expression – Oft Ignored Stressors

The fact that this woman was a chronic beer drinker and smoker had been ignored.  They were, if you will, the “stressors” that were the dominant cause, perhaps impacting on genetic risk factors. The relationship between alcohol and thiamine deficiency is well known and so she had induced her own disease. Since there was a profound ignorance concerning vitamin deficiency diseases, the beriberi had been referred to by her internists as “rheumatic” in nature. This is because joint and limb pain, usually not recognized for what the pains represent, are often associated with compromised oxidative metabolism, either in the limb itself or in the brain where the pain is interpreted.

Defective oxidative metabolism caused in this patient’s case by thiamine deficiency, causes exaggerated brain perception. The brain induced a pain that gave the false impression that the disease originated in the joints and other parts of the body. Even if the origin of the pain is truly from a joint or muscle, defective oxidative metabolism in the brain will exaggerate the sense of pain perceived by the patient. Although this “phantom” pain is known as “hyperalgesia”, the mechanism is not well known as being due to compromised oxidation in the pain perception brain centers. Thiamine deficiency was responsible for the hyperalgesia experienced by the case of a patient with eosinophilic esophagitis that was posted recently on this website.

Beyond Thiamine: Multi-Nutrient Deficiencies

What interested me in the woman with beriberi was that folic acid deficiency was not revealed until her metabolism had been accelerated by the pharmacological use of thiamine. The folic acid deficiency then became clinically expressed as her metabolism “woke up”. It had been well known for some time that folic acid produced anemia would have to be treated with both folic acid and vitamin B12.

In the case of folic acid deficient Pernicious Anemia, if vitamin B12 was not given at the same time, the patient would develop a disease known as subacute combined degeneration of the spinal cord. Because I had forgotten this fact, I had neglected to give her vitamin B12 until it was finally expressed clinically in the form of a rash. Associating a skin rash with a vitamin deficiency is certainly not commonly accepted as a possible indicator of an underlying cause by physicians.

Vitamin Deficiency Versus Dependency

Returning to the case of the 6-year old boy discussed above, we learned over time that his health was dependent on high doses of thiamine to function. Believe it or not, this child required 600 mg of thiamine a day in order to prevent his episodes of illness. If he began to notice the beginning of an infection he would double the dose. The recommended daily allowance for thiamine is between one and 1.5 mg a day. Here, and in many other cases, huge doses of the vitamin are required in order to accomplish the physiologic effect. This represents what I call vitamin dependency.

Thiamine and magnesium, like many other vitamins, are known as cofactors to enzymes. An enzyme without its cofactor works inefficiently if it works at all. The “magic” of evolution has “invented” this cooperative action which is in itself under genetic control. In technical terms, the vitamin has to “bond” with the enzyme. If this bonding mechanism is genetically compromised, the concentration of the corresponding cofactor has to be increased enormously by supplementation in order to prevent the inevitable symptoms. You can see that this requires a clinical perspective tied to unusual biochemical knowledge. This is in complete contrast to what is usually regarded as vitamin deficiency, arising from insufficient concentrations in the diet.

What is perhaps not known sufficiently is that prolonged vitamin deficiency appears to affect this bonding mechanism. For example, it has long been known that to cure chronic beriberi, megadoses of thiamine are required for months. I have concluded that the megadoses of thiamine given by supplementation to a patient with long term symptoms arising from unrecognized deficiency appears to re-activate the inefficient enzyme. It is as though the enzyme has to be repeatedly exposed to megadoses of its cofactor to stimulate it and restore its lost function.

This may mean that even if the bonding mechanism is normal in chronic deficiency, enzyme function has simply decayed from lack of stimulation. This may explain why genetically determined dependency and long term dietary deficiency will produce the same clinical effect. The dosing of vitamins, if the clinical effects of deficiency are recognized, is not well understood in traditional western medicine. When insufficient doses are given and the symptoms fail to abate, the practitioner views it as evidence that supplements do not work.

Biochemical Diagnoses are Complex

I want the general public to begin to understand the principles that underlie the complexity of biochemical diagnosis. Perhaps a reader might find that a case like this is a reminder of a loved one whose illness was never understood after seeing many different specialists, all of whom were like the blind men and the elephant. Each was confined to his specialist status but none of them could see the overall big picture.

Reading these cases, you might easily come to the conclusion that they represent a rarity. Chronically unrecognized thiamine deficiency is common. Dependency is  not uncommon. It is not as rare as is presently thought. Believe me, cases like these are surprisingly common and are responsible for a great deal of diagnostic confusion.

Vitamins are essential to consumption of oxygen in all life processes. To go against the principles of diet dictated by Mother Nature is a risk to life and limb that is not worth the derived pleasure. When limb pain is experienced without an obvious trauma, it is difficult to accept that it is because of inefficient use of oxidation in the brain, but that is exactly what we found.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Treating Intractable Insomnia and Cerebellar Ataxia With Thiamine

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Twenty years ago, I attempted suicide after years of alcohol and drug abuse. I almost succeeded, but by some miracle I survived. I suffered a cerebellar stroke and as result was left with severe cerebellar damage. The doctors said that I had lost almost 75% of my cerebellum. I couldn’t walk or talk, I could not swallow and was barely functioning, if you could call it that. At some point, I decided I would live and forced myself to improve. I worked the physical therapy and eventually began lifting weights. I wrote about my journey here. Despite my gains in strength and balance though, since the stroke I had suffered from severe and intractable insomnia. Although I was under the care of multiple doctors, none could offer any help beyond increasing this or that medication, none of which worked. Insomnia is common in individuals with cerebellar injury. Then I learned about thiamine.

Persistent Insomnia Treated with Thiamine

Around the time my initial article was published, I began supplementing my diet with thiamine. This vitamin may have been mentioned in passing by some of my physicians, but it was never prescribed or even really emphasized to any great degree. Neither was it ever touted by the medical community during my initial stroke recovery in 2003. I am fairly sure much of the reluctance to use thiamine could be attributed to the pervasive fear of it not benefitting my health.

Being entrenched in the world of mental health and alcoholism for about 25 years (sober 9), I am well aware of Wernicke-Korsakoff’s syndrome. I had heard about massive doses of thiamine being administered to others in medical detoxification facilities. I also have loved ones grappling with Parkinson’s Diseases. I quickly began to see how many of our neurological symptoms were similar, and that thiamine was slyly mentioned to help all of us.

In early 2021, it was strongly suggested that I gradually increase to a large dose of thiamine (not by doctors, mind you, but by others from this website). At the time, I was lucky if I slept 3 hours per night, which of course, exacerbated my ataxia symptoms. I was on so many medications that it raised red flags, but I was never warned about the negative neurological effects. And worse yet, nothing was working.

Once my initial dose of thiamine was entrenched in my system (50 mg of Thiamax), I began sleeping with greater ease. At first, this was approximately an hour, but I discovered that I also slept more soundly and had acquired greater rest during the night. As time progressed, my sleep patterns became increasingly regular.

Better Functioning With Improved Sleep

For several years, I have been making progress in all areas of my life. By August of 2022, thanks to the thiamine, I was off of all prescription medications. I was sleeping through the entire night, soundly. I was also able to complete difficult feats at the gym without falling asleep on a mat in the stretching area (usually resulting in me being taken home, so I didn’t sleep at the gym.) This is one of the reasons that I didn’t train publicly until recently. With my sleep problems, I wasn’t sure if I’d be overcome with an insatiable need to sleep mid-workout.

In addition to the improvements in sleep and the elimination of medication after thiamine came on board, I was able to lift a barbell by myself, while standing. This is no small feat for someone with ataxia. Remember, I was told I would not walk again, or function in any semblance perceived as normal. They said that all my neurological systems had crossed the threshold believed salvageable. In September of 2022, I competed in my first powerlifting meet, where I deadlifted 182 pounds and bench pressed 78 pounds. I am currently deadlifting 225 pounds (January 2023). While I am still ataxic and I still have struggles relative to my injury, I have improved so much since beginning the thiamine.

thiamine for insomnia and cerebellar ataxia
Me lifting 225lbs at the gym.

As I write this, right before the New Year of 2023, I am overcome with the amount of remarkable progress that has been made in my life since August. To deny that would fact would be denial of any amount of truth or reality in existence. I fail to see how anyone can deny the differences in my life since using regular thiamine.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, and like it, please help support it. Contribute now.

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Is Thiamine the Answer?

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Since we have shown that many people with complex disease patterns respond to megadose thiamine and magnesium, irrespective or their symptoms, we have concluded that disease is due to a breakdown of health from energy deficiency. We have proposed that 3 interlocking circles (as in Boolean algebra), labelled Genetics, Stress, and Energy (or Fuel) must be considered singly or collectively as the cause of any disease. Energy is the force that enables any form of mental or physical body function. Its deficiency affects one or more of the three circles.

Genetics is not often a sole cause of disease. It usually requires other factors and genetically determined disease can often be treated by epigenetic energy stimulation. Symptoms of Type 1 diabetes often appear in middle age, often after a mild stress event such as a common cold. Surely it would appear at birth if genetics was the sole cause.

Any form of stress (infection, trauma, prolonged mental stress) demands cellular energy to meet it. The hind brain controls the complex response and is automatic. This part of the brain is highly sensitive to cellular energy deficiency and thus, energy stimulation is the essential factor required to treat any disease.

Beyond Deficiency

It has been shown by Antonio Costantini’s group that mega-dose thiamine treats Parkinson’s disease, presently deemed to be incurable. They have reported similar clinical benefits in Friedreich’s ataxia (another neurodegenerative disease), Multiple Sclerosis and Fibromyalgia, suggesting that each of these diseases, rather than having separate causes, are all energy dependent manifestations of disease. Just last year, a group of researchers linked a damaged thiamine/biotin transporter gene to Huntington’s Disease. Just this month another group has found that thiamine/biotin treatment compensates for the genetic dysregulation, restores function, and rescues neuronal pathology associated with Huntington’s Disease in mice.

A publication decades ago in a prestigious medical journal reported that 252 different diseases had been treated with mega-dose thiamine, with varying degrees of success.

This information, published in peer-reviewed medical literature is startling, because thiamine, in minute doses, is thought to have its sole responsibility as a vitamin. To use it as a completely non-toxic drug offends the present model used to explain disease. Also, it demonstrates that our knowledge of vitamins is incomplete.

Children’s Health and Thiamine

While I was working at Cleveland Clinic in the seventies as a pediatrician, many emotionally disturbed children were referred to me by pediatricians in private practice in the Cleveland area. I found that the diet of these children was full of empty calories due to their indulgence with candy, soft drinks and a variety of substances usually known as “junk foods”. They had been treated with a variety of pharmacological drugs that either had no effect or even made the clinical situation worse. I treated them with large doses of thiamine and their symptoms disappeared. The explanation by my colleagues was the traditional one, “spontaneous remission”, usually used to explain a mystery cure. My explanation was that deficiency of brain energy was responsible for their symptoms. Thiamine was stimulating its cellular synthesis.

The RDA for Thiamine and High Caloric Intake

I looked up the history of the establishment of the Recommended Dietary Allowances (RDA) for these essential substances occurring in natural foods. I found that the original recommendations had been made by a committee of “experts” and there was surprisingly little science involved. There was no attempt to tie the RDA of the vitamin to the calorie concentration.

The dietary supplementation of vitamins to selected foods by the food industry was thought to have completely removed vitamin deficiency disease from America. Consequently, doctors in practice are commonly seeing patients with many symptoms and failing to recognize the ancient disease known for centuries as Beriberi. Because the laboratory tests, used to confirm the nature of the disease, are normal, the many symptoms described by the patient gives rise to a diagnosis of psychosomatic disease by the doctor. Even worse, the patient is told that “it is all in your head” and he or she is advised to “pull him (her)self together”.

Deficiency of thiamine and magnesium, both essential to cellular energy production in the body, need to be in a concentration that is sufficient to oxidize the calorie concentration. That explains why the concentration of blood thiamine is usually normal in this common polysymptomatic disease, because the doctor fails to recognize the overload of “empty calories”. The concentration of thiamine would be normal for a healthy calorie load, as would exist in an organic natural diet.

We have reported high calorie malnutrition as a common cause of this widespread disease. Dysautonomia is responsible for the symptoms because the hind brain, where the control mechanisms of the autonomic nervous system exist, is highly sensitive to cellular energy deficiency. It matters little whether it is called Beriberi or high calorie malnutrition as long as the biochemical cause is understood.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

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Rapidly Deteriorating Health With Thiamine Deficiency

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In May 2020, I experienced my first symptoms with what I now believe to be thiamine deficiency (beriberi). I believe other nutrient deficiencies played a role as well. This was preceded by an especially difficult several months that included a marital separation and possible COVID infection. In addition, I experienced a mild head injury during this time when my son and I accidentally collided while picking up toys together. I have a history of traumatic brain injury, so am susceptible to post-concussive syndrome from mild head trauma.

It was these factors that precipitated the downward health spiral that first began in May 2020 when I was 38 years old. Prior to this time in life, I felt my health to be good. I had gone through some very challenging mental health struggles in the past, a TBI and post-concussive syndrome, as well as a few other issues related to physical health, but for the most part, I would have considered myself to be a fit, healthy, and resilient person. I consumed a paleo diet, which I thought very nutritionally dense, and I exercised regularly. However, looking back on my history suggests risks for thiamine deficiency. Here are some factors that are part of my overall health history:

  • Five pregnancies and nine years of breastfeeding with very little multivitamin supplementation
  • Former short-term fruitarian and vegan diets for purposes of detoxification
  • Former sporadic heavy binge drinking from age 15 to 33
  • Former tobacco smoker from age 15 to 33
  • Consumed extreme amounts of candy as a child
  • Overdosed on pills three times between ages 15 and 17. The third overdose involved Serzone, which has a warning for liver damage
  • Was prescribed antibiotics at least 75 times from age 5 to 33 for chronic UTIs and bronchitis
  • Prior health problems: chronic urinary tract and kidney infections as a child and young adult, chronic bronchitis as a child, candida overgrowth, digestive problems, insomnia, anxiety, depression, PTSD, and depersonalization disorder

In May, the combination of stressors, along with likely longstanding nutrient deficiencies, precipitated a rapid downward spiral leading to multiple hospitalizations, and ultimately, what I believe was severe thiamine deficiency. At its worst, I believe I was headed toward Wernicke’s encephalopathy and heart failure. Since the best physicians could offer was Ativan, antidepressants, and a presumed multiple sclerosis diagnosis (despite a lack of evidence), it was up to me to save myself, particularly because I am a parent to five children. Through extensive internet research, I learned about thiamine deficiency and began to treat myself. This is my story.

Rapidly Disintegrating Nerve Function

The first symptom I remember experiencing was a strange tingling in the center of my chest upon standing. The next symptom was flank pain. I thought perhaps I had a kidney stone and made an appointment with my primary care. During this time, I was also intensely tired in a way I’d never been before, very pale, anxious, uncharacteristically irritable, shaky, short of breath, thirsty, lost weight, and became sweaty at random times.

At the appointment with my primary care, it was decided I would get an ultrasound of my kidneys to check for kidney stones. I didn’t make it to the ultrasound appointment because that same day I stood up after a nap and experienced sudden debilitating chest pain that felt like I was having a heart attack. It started in the area of my heart and moved to my left arm and up to the left side of my neck. I called an ambulance and was taken to the emergency room. They ruled out a heart attack and proceeded with the kidney ultrasound after I shared with them the other strange symptoms I’d been experiencing. Nothing of significance was found on the ultrasound, and I was sent home.

Shortly after that incident, I started experiencing numbness in my legs at random times during the day and night, as if they’d fallen asleep. I went into the ER again after a particularly intense experience of numbness where I felt uneasy about even standing to walk. Again, nothing was found, and I was sent home. My arms began to go numb at night while in bed, in addition to my legs. I’d wake up to this numbness, and shortly thereafter I could feel the numb sensation in my head as well.

I began to experience gastroparesis, and my intestinal motility seemed frozen at times but then would go into overdrive during the night, requiring urgent bowel movements in the middle of the night, which was not normal for me. At the same time, I could feel the sudden rapid digestive motility, I could also feel the blood flow dropping from my brain. As soon as I’d have a bowel movement, the blood flow would return to my brain. These sensations were all so strange and unnerving and unlike anything I’d previously experienced in life.

Loss of Consciousness, Compromised Speech, and Vision Changes

I went to an acupuncture appointment and shared with the practitioner what was happening. She treated me for yin deficiency. That night I woke to use the bathroom, and on the way back to my bedroom, I nearly lost consciousness for the first time. It was a terrifying experience. My ability to speak was compromised, and I tried to communicate to my daughter what was happening, but my voice was in slow motion. My vision was growing tunnel-like and dark. I thought I was having a stroke. My daughter gave me my phone, and I called an ambulance and was able to very slowly articulate what was happening as I lay on the floor, wondering if I was going to die. I was taken on a stretcher to the ER, and the diagnosis from that trip was that I’d had a panic attack. I was given Ativan and sent home. I knew that a panic attack was not the correct explanation, although I was indeed in a state of panic over my current health. I felt very strange, with strange sensations throughout my body and brain, severe anxiety, erratic heartbeats, and tachycardia.

Things grew progressively worse over the next couple days, and my mother drove me to a better hospital four hours away to hopefully get answers. By the time we arrived, I could not walk due to the total body numbness. I was given a neurological exam and had no reflexes in my knees, ankles, and feet. I was then given two bags of IV saline and felt relatively normal a few hours later. Many labs were done, but no nutrient levels were checked. I was kept overnight and examined by a neurologist, but I wasn’t experiencing symptoms during the exam. It was found that my blood sugar was abnormally low during the night (65), and I was told to improve my nutrition and sent home with no real answers.

Was it B12 Deficiency?

I started taking a B complex and multivitamin and tried to eat as healthy as possible, but during the following weeks, I continued to experience near syncope, dizziness, cardiac and GI issues, strange body sensations, and severe anxiety. I’d have pockets of time where I felt relatively normal, but symptoms always returned, and night numbness was a regular occurrence. I often felt ataxic, like I was about to lose my balance or fall. My hearing seemed to change, and my right eyelid began to twitch relentlessly. Nerve pain began in my joint junctions and felt like sparking, electrical, stinging sensations. Over the course of several days, these nerve pains began to affect the base of my spine and slowly moved up my spine to my head. It was a very painful and frightening experience.

When researching symptoms, I came across information about B12 deficiency and wondered if that is what I was dealing with, so I asked my naturopath if he would prescribe methylcobalamin that I could inject at home, and I began daily B12 injections. The nerve pain resolved after a few weeks, which was a tremendous relief. As a result of this resolution, I believed a B12 deficiency to be at the root of my problems. I continued with B12 injections after the nerve pain healed but dropped down to once weekly injections.

Another Hit to My System

Shortly after the nerve pain resolved, I got very sick with a Campylobacter infection. It was strange because no one else in my family got sick, and we’d all been eating the same meals. I went to the ER after several days of relentless diarrhea and high fever. I was given fluids and my stool was tested, which revealed the Campylobacter bacteria, and I was prescribed azithromycin. In hindsight, I wish I’d not taken the antibiotic because I believe it made my condition worse.

After the antibiotic, I felt like I was in a permanent state of semi-consciousness. I felt hypoxic, like I was being asphyxiated. When I’d start to fall asleep, I’d wake up with a jolt because it felt as though I were falling and losing blood flow to my brain. I had constant high-pitched ringing in my ears. Life became a total nightmare. My arms and legs were swirling with strange sensations I’d never felt before – paresthesias and cramping muscles. My heart was in a near constant state of palpitations with alternating bradycardia and tachycardia. When I’d roll from one side to the other in bed or stand up, my heart rate would go from 40s and 50s to 120s and 130s. It felt like my heart was constantly pounding, no matter if the rate was slow or fast. The sound was audible to me day and night, and the pounding seemed to shake my entire body. Sometimes it felt like my heart would stop for an abnormally long amount of time, then sluggishly start thumping again. I would wake up in extreme pain on whichever side I slept on. I recall using my finger oximeter one night and getting a reading of 84% oxygenation.

Maybe Multiple Sclerosis?

During this time, several doctors suggested I might have Multiple Sclerosis (MS). I had an MRI of my brain that showed no lesions, so MS was ruled out. I was eventually diagnosed with POTS by the medical community. I researched POTS and saw that extra salt was often helpful for minimizing dizziness, so I started adding salt and electrolytes to my water. It did seem to help some, so I began drinking about a gallon of water a day with 2-3 extra teaspoons of Celtic or Pink Himalayan salt and added electrolytes.

In late September 2020, my POTS symptoms resolved. My heart had normalized, and I was no longer dizzy or experiencing near syncope, but I was left with “stocking and glove” peripheral neuropathy. I had numbness from my feet up to my calves and numbness in my hands and forearms. I was relieved that the POTS symptoms were gone and felt I could tolerate the numbness and paresthesias. I still felt very weak and struggled with bacterial infections in my ears and sinuses as well as cold intolerance.

Discovering Thiamine Deficiency

Life continued this way until early November, when I decided to try R-Lipoic acid for the peripheral neuropathy and occasional spinal pain and tingling that periodically occurred. This was a devastating mistake. I ingested the first capsule in the morning and second in the evening, and within an hour of the second capsule, nerves all over my body felt like they were on fire. The only thing I’d changed that day was the lipoic acid, so I started researching contraindications to lipoic acid online and found that thiamine deficiency was a contraindication. Lipoic acid and thiamine work in tandem in the Krebs cycle, so by adding one with a deficiency of the other, it creates a draw on an already almost empty tank. In one study, when thiamine deficient rats were administered alpha lipoic acid, it created a toxic reaction. Unknowingly, I’d taken a supplement that made my situation go from difficult to much worse.

I then looked up thiamine deficiency symptoms and recognized my experience immediately in beriberi disease. I found the website, Hormones Matter, run by Dr. Derrick Lonsdale and Dr. Chandler Marrs. I began reading through the information and stories, and my belief that thiamine deficiency was the root of my problems grew stronger. Dr. Lonsdale suggests using a type of thiamine called Allithiamine (thiamine tetrahydrofurfuryl disulfide), as it crosses the blood brain barrier superior to other forms of thiamine. I ordered a bottle and took a large dose of thiamine hydrochloride I had on hand before going to bed.

I didn’t sleep well that night. My nervous system felt like it had been severely damaged. I was shaking, my heart was once again beating erratically with tachycardia upon movement. The nerve pain was intense and spread throughout my entire body. The next day, I went for a short walk and nearly blacked out. The muscles in my legs were painfully cramping. I had no energy. I couldn’t even read. I went to bed that night feeling like I had a head injury.

Each day was progressively worse. I was taking thiamine hydrochloride and benfotiamine every couple of hours, but it didn’t seem to be stopping the downward spiral of symptoms. I felt like I was going to collapse. My brain was not functioning well. I was nauseous and had severe GI distress. All the symptoms I had experienced before, in addition to many new symptoms, manifested again in rapid succession. I went into the ER and attempted to explain that I believed I had a severe thiamine deficiency, hoping I would be given IV thiamine, but I was only handed a thiamine tablet, given some IV fluids and sent home.

Five days went by, and the Allithiamine arrived in the mail. By this point, I was vomiting, could barely walk, and felt like I had a traumatic brain injury. I took one 50 mg capsule and felt relief of the extreme brain injury sensations within half an hour. Encouraged, I continued to take a 50 mg capsule each time I would start to decline. The nerve pain lessened, I stopped vomiting, and my heart rate somewhat normalized, but the most profound effect of the Allithiamine was in reducing the intense brain injury sensation.

I’ve experimented with dosage and arrived at 100 mg every two waking hours being the most effective for keeping most symptoms at bay. In addition to the 100 mg of Allithiamine, I also take 150 mg benfotiamine and 50 mg magnesium glycinate every two hours, a daily high dose B complex, multivitamin, phosphatidylcholine, ubiquinol, digestive enzymes, probiotics, and fish oil. Five weeks out from taking lipoic acid, I still experience constant moderate nerve pains all over my body, problems with bacteria (eye infections, ear pain, sinus infections, sore throat), mild tachycardia upon sudden movement, pounding heart, random sweating, high fasting blood glucose (between 110 and 120), shakiness, dizziness, anxiety, weakness, and exercise and cold intolerance. The Allithiamine and benfotiamine have improved my brain function, nerve pain and paresthesias (from severe to moderate), digestion, and my ability to sleep, and I’m hopeful that with time I’ll see more improvements.

Recovering But Disillusioned With Modern Medicine

I believe the work of Dr. Chandler Marrs and Dr. Derrick Lonsdale and supplementing with Allithiamine saved my life. I believe I was headed toward Wernicke’s encephalopathy or high output heart failure before taking Allithiamine. My quality of life is currently very poor, but I have hope that recovery from beriberi and mitochondrial damage is possible. Some damage may be permanent, but I see small improvement each day, which indicates to me that more improvement is possible.

I wish so much I’d found the Hormones Matter website earlier in the course of my disease, as I’m certain things could have been more easily reversed. I hope that others might benefit from my story and avoid the horrendous decline that I experienced. Just by taking such a simple nutrient as vitamin B1, so many devastating health consequence can be avoided. Why don’t more doctors have awareness of this?

I am disillusioned with the medical community in not identifying my illness despite dozens of trips to the ER with comprehensive symptom lists in hand and visits to internists, cardiologists, and neurologists with detailed descriptions of my ailments. No one ever checked my nutrient status beyond vitamin D, iron, and zinc levels, and B12 and folate at my request. I was treated as though I had an anxiety disorder and offered anxiety medication and antidepressants.

How is it that in 2020, the only thing that comes to mind for the medical community when presented with complex neurological symptoms is MS? Time and time again, I was told I likely had MS, but my MRI clearly showed I did not. Beriberi is a well-documented condition that’s been known for hundreds of years, yet the medical community doesn’t consider it other than Wernicke’s encephalopathy in alcoholics. I hope this can change. Awareness needs to grow. I know there must be many others who have experienced similar symptoms to my own and sought help. We deserve better medical care in what is supposed to be among the most technologically advanced countries in the world. Until and unless things change, websites like Hormones Matter serve as beacons of hope. I am profoundly grateful to the work of Dr. Chandler Marrs and Dr. Derrick Lonsdale.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Thresholds and Tipping Points in Thiamine Deficiency Syndromes

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I recently stumbled upon on a research paper published in 1968. It was not that long ago in the overall course of modern medicine, perhaps even its heyday, when all things were still possible and before the complete fealty to pharmaceuticals arrived. To the youngsters and to those coming of age in the last 20 years, however, anything published pre 1990 is ancient history.  What could such old paper tell me about medicine that is new and useful? It turns out an awful lot.

Back in the day, research was a little simpler and more focused, not on finding out which drug could be fit to which symptoms, but on how things worked. Good experimental design, answered mechanical questions, like if we apply X to Y or if we remove X from Y what happens?

In this paper, Encephalopathy of Thiamine Deficiency: Studies of Intracerebral Mechanisms, the researchers identified a very important component about Vitamin B1/thiamine deficiency – the time course of the disease process. That is, with a diet deficient in thiamine, how long does it take before symptoms emerge, what is the corresponding level of deficiency in the brain, and at what point, after supplementation, does recovery begin; important questions clinically.

Vitamin B1 – Thiamine Deficiency

Remember, vitamin B1 or thiamine deficiency at its worst is linked to severe decrements neurological functioning, like Wernicke’s Encephalopathy that include noticeable ataxic and gait disturbances (loss of voluntary control of muscle movements, balance and walking difficulties), aphasias (language comprehension and/or production difficulties), and if it persists, Korsakoff’s Syndrome (severe memory deficits, confabulations and psychosis). Thiamine deficiency was originally observed in only chronic and severe alcoholics or with severe nutritional deficits as seen in famine. Fortification of food stuffs was thought to relieve much of the nutritional risks for deficit, especially in impoverished regions. More recent research, however, indicates that thiamine deficiency has reared its ugly head once again and this time in modern, non-impoverished, regions where the food supply is ample. How can that be?

Non-Alcoholic Wernicke’s Encephalopathies

Thiamine deficits can be mediated by a number of factors, including by less obvious nutritional deficits where food supply is abundant but nutrition is lacking (a diet of highly processed, carbohydrate and fat laden foods), with thiamine blocking factors found in medications/vaccines, environmental toxicants and some foods, after bariatric surgery and in disease processes like AIDS. Over the course of our research, thiamine deficiency has been observed in previously healthy, young, non-alcoholic patients, post medication or vaccine, along with symptoms of dysautonomia.

What has always struck me about the thiamine deficits we observe is the differential expression and time course of the symptoms. In some people, the reaction leading to thiamine deficit appears linear, progressive and rapid. In others, the symptoms appear to wax and wane and to evolve more slowly. How is that possible? Certainly, individual predispositions come into play. Some individuals may be somewhat thiamine deficient prior to the trigger that initiates the full expression of symptoms, while others have higher baseline stores. Additionally, anti-thiamine environmental exposures and other medical conditions/medications may also come into play.  In the literature, however, the progression of symptoms from bad to worse is almost always direct and rapid, perhaps mistakenly so. Indeed, Wernicke’s Encephalopathy is a medical emergency necessitating immediate IV thiamine.  How is it then, that we see more chronic, remit and relapse patterns of thiamine deficiency, even in some cases where thiamine concentrations are being managed medically?

Cerebral Thiamine Deficiency: Crossing the Black Line

It turns out, there is black line with regard to thiamine deficiency, that when crossed overt symptoms emerge, and a similar black line, that demarks recovery. It is possible then that barring a continuous blockade of thiamine, one can move above and below those lines and the corresponding symptoms may wax and wane. The paper from 1968, cited above, found those black lines, in rodents, but we can extrapolate to humans.

The research. The investigators took three groups of female rodents, a paired group of thiamine deprived and thiamine supplemented, along with a group fed ad lib (as desired) and assessed the time course and concentrations of cerebral thiamine deficiency relative to the initiation and progression of the observable neurological symptoms associated with Wernicke’s encephalopathy in rodents (ataxia, loss of righting, opisthotonos –rigid body arching). The experiment lasted about 6 weeks.

Neither the control group (thiamine supplemented) nor the ad lib group demonstrated neurological deficits at any time during the study. The thiamine deprived group, on the other hand, demonstrated symptoms that began with weight loss, progressive anorexia, hair loss (recall our observations about hair loss) and drowsiness at about 2.5 weeks into the experiment. Interestingly, no neurological signs of thiamine deficiency were seen at that time.

The results. At 4.5 weeks in, the researchers noted a rapid progression of symptoms and decline of health over the course of the next 5 days (the black line). These symptoms included: incoordination with walking, impairment of the righting reflex, reluctance to walk, walking backwards in circles, imbalance, rigid posturing and eventually a total loss of righting activity and severe drowsiness.

One can imagine, if a similar deprivation of thiamine were observed in humans, the corresponding symptoms might also include the initial hair loose and weight loss, perhaps noticeable, perhaps not depending upon the time frame and severity of the thiamine deficiency. It would also include incoordination and difficulty with walking, balance and voluntary movement, perhaps tremors, excessive fatigue or sleepiness and the myriad of neuro-cognitive disturbances noted in Wernicke’s syndrome.

In the cited experiment, one injection of thiamine reversed these symptoms to a nearly normal, or apparently normal neurological state within 24 hours.

Brain Thiamine Thresholds

Animals from each of the groups were sacrificed and examined at each of the stages of the experiment. Brain thiamine and other markers of thiamine metabolism were assayed to determine the cutoff levels of thiamine that demark symptoms and recovery.  This is really interesting and the beauty of this entire study.  Neurological symptoms become apparent when cerebral thiamine concentrations reach 20% of normal.  Recovery begins when those concentrations climb to 26% of normal. At least in rodents, one has to deplete 80% of the brain thiamine stores before overt neurological symptoms become apparent; 80% – that is a huge deficit.  Similarly, it doesn’t appear to take much to right that deficit, only a 6% increase in thiamine concentration set the course for improvement.

If we extrapolate to humans, where life span, genetic and environmental factors likely moderate the degree of thiamine stores and consumption, we still contemplate a rather large thiamine deficit needed before overt symptoms of Wernicke’s emerge. Similarly though, it is also evident that a rather small change in thiamine can have enormous effects on neurological functioning. In the case of the rodents, a mere 6% point change reversed the symptoms. One might suspect equivalent deficit/recovery thiamine parameters in humans.

Waxing and Waning Symptoms:  A Case for Persistent Thiamine Deficiency

If we consider the possible course of non-alcoholic thiamine deficiency, where no extraneous variables like bariatric surgery or thiamine deficient parenteral feeding are present and where dietary thiamine varies daily and is not held constant as it is during experimental conditions or during famine, we can begin to see how thiamine related neurological symptoms may wax and wane. Different exposures and triggers may decrease thiamine periodically, even to the point where overt neurological symptoms present. When those exposures are removed and barring deficiencies in metabolism and diet, symptoms may abate, at least temporarily, and until the next trigger or until the black line is crossed anew and thiamine deficiency becomes the medical emergency observed in overt Wernicke’s.

In contrast, the more persistent or chronic thiamine deficits that do not cross the 80% depletion cutoff (or the human equivalent), may also wax and wane and show all the core neurological symptoms expected in overt Wernicke’s though to a much lesser degree. Additionally, as we have speculated, persistent thiamine deficiency might disable mitochondrial functioning in such a way that the patient presents with a myriad of seemingly unrelated symptoms, that are not typically attributed to thiamine deficiency, such as cardiac dysregulation, gastroparesis, autonomic instability, demyelinating syndromes and hormone irregularities, especially thyroid, but also reproductive hormones. These too may be related to thiamine deficiencies. Although, we cannot and should not rule out other causes as well, sub-optimal thiamine may be involved with a host of complex disease states and medication adverse reactions where neurological symptoms are present. Thiamine deficiency should be tested for and ruled out before more invasive therapeutic options are contemplated.

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