thiamine deficiency Archives - Page 11 of 14

Thiamine Deficiency Amid a Constellation of Mitochondrial and Metabolic Disorders

Published on August 8, 2018

10565 views

This is a bit of a long story because I can’t tell if I have a genetic problem that only shows up under stress or just plain deficits due to extreme stress. I am a 58 year old woman having some pretty severe health problems that I have recently begun to think might be due to thiamine deficiency, malnutrition and/or possibly some sort of genetic problem.

Medical History

I was hospitalized with pneumonia three times before I was 5 years old, once again in isolation ward at age 7. I also had several childhood illnesses including Rubella, chicken pox, and mumps. At age 5, I was diagnosed with exercise induced asthma and prescribed Quibron. Once I hit puberty, my respiratory problems seemed to resolve themselves as long as I avoided aerobic exercise.

At age 9, I was diagnosed with progressive sensorineural hearing loss (an indicator of mitochondrial disease that I only recently learned about). I had a curved loss with 60% gone in the higher frequencies down to about 40% loss in the low ones. My mother was also diagnosed with hearing loss that had gone unrecognized. My daughter also has a mild hearing loss that was diagnosed as an adult.

Major Life Stressors and Emerging Problems with Nutrient Absorption

From 2000 to 2012, had several major life stressors including the death of my second husband to colon cancer, a dog snapped at me and severed my lower lip, my third husband lost his job and attempted suicide, early retirement, bankruptcy, foreclosure on my home and then moving to a new state. I was diagnosed with post-traumatic stress disorder (PTSD) and received weekly trauma therapy for a year.

During the aftermath of the PTSD trigger event, I began having problems with nutrition. I would eat a meal and get no energy from it. After taking an early retirement from my job and losing my house to foreclosure, we packed up and moved out of state.

I never recovered from the exhaustion and stress of the move. We were nearly homeless one night after our car broke down and I had no more money because we had just paid the deposit to rent a house. I managed to leave all our keys in the car at the repair shop. My first husband wired us money for a hotel for the night.

The problems with digestion continued and my health seemed to go downhill. I was tired all the time and my brain was not functioning well. I tried going for walks but would come home exhausted. To make matters worse, we were scraping by on one third of the income I had before I retired and I had no health insurance. I didn’t know how to go about finding help in those conditions. I’ve always been in the system.

Catatonia-like Episodes upon Eating

Starting in 2013, I started having episodes that I call zonking. I would eat something and almost immediately get very sleepy and usually would just fall into a sort of zombie-sleep-like state for 10-30 minutes. Sometimes it seemed sort of catatonic and others is was more like a strong urge to sleep. It wasn’t normal sleep in that there was no dreaming. Sometimes I was in a kind of frozen pose instead of laying my head sideways or getting comfortable. At first it seemed like they were correlated with high-availability carbs, but over time they became an almost daily occurrence with any type of food I ate. These episodes would sometimes disappear for a few weeks and then reoccur. There was no pattern I could discern nor tie to hormonal cycles.

I have been keeping daily logs from 2013-2016. I reported the zonking episodes to my NP and she prescribed Lactulose which just made the diarrhea worse. She ordered an ultrasound on my gallbladder and liver and no major problems were found.

The zonking episodes were really disabling. I would be feeling fine until I ate something and within a 1/2 hour I would zonk out and feel very groggy afterwards. It didn’t feel safe to drive so my husband had to take me shopping or do the shopping himself when I was too tired. I didn’t drive from 2013 to 2016. At times, I didn’t want to eat at all so I could keep myself functional long enough to do something. I found out the limits of fasting pretty quickly.

Left Temple Headaches, Migraines with Visual Aura, and Cognitive Deficits

I also had left temple headaches starting in 2013 and a few migraines also involving left temple pain but mostly just visual aura. I never had migraines previously. After I fell going up the concrete steps to our front door, I became very cautious about moving when I was in one of these states. I noticed that I became very clumsy with tasks that you normally don’t think about like opening a can or a pill bottle.

I also noticed a significant decline in my ability to comprehend speech when I was in one of these states. This was first mentioned in my logs in 2013. I have always had a problem due to my hearing loss but there seemed to be a magic something taking place in my brain that took care of turning sounds into words. Somehow that process was failing when I was in the dizzy and ditzy state.

My condition was deteriorating in 2016 and I was experiencing more severe brain problems that are what I now call dizzy and ditzy. Dizzy and ditzy feels like being very drunk. I was spending more and more time in bed which was making my diabetes worse. When my brain was functional I was researching and trying to figure out what might be causing my condition.

In August 2016, I came across a description of gluten ataxia. The symptoms seemed similar to what I was experiencing so I tried eating a gluten free diet for a few weeks and started feeling better. After two weeks, I decided I was imagining the improvement and tried eating something with gluten in it. After about two hours I began to experience the dizzy state and the left temple headache. From that time I have remained gluten free.

It was my intent to get tested for Celiac at my next appointment, but my husband was hospitalized in October 2016 for sepsis due to undiagnosed type-1 diabetes. This was the worst kind of trauma for me because my second husband died of colon cancer. Knowing that, I applied the techniques I learned during trauma therapy to keep my stress level down. As a result I was able to return to the hospital for his follow-up visits with no increase in blood pressure or other signs of HPA activation. I think it helped me overcome my doctor phobia and I have been increasingly more able to deal with medical situations. My health and energy levels were also improving due to the gluten free diet. I tried various diets and found that I had the best energy levels on a gluten free vegan diet.

Since I did not get in to see my primary until six months had passed gluten free my celiac tests were inconclusive. I found a really good allergist and in January 2017 was diagnosed with 44 food allergies including wheat, barley, oats, eggs, milk, and assorted nuts, fruits, and vegetables and yeast which is everywhere. Six months later, I was diagnosed with multiple environmental allergies. My condition began improving dramatically as I stopped eating the foods that I was allergic to. However I found that I was still unable to eat solid food and get energy from it. Meanwhile my NP added 10 mg glipizide which caused hypoglycemia when I was feeling well and active.

I didn’t experience any more dizzy and ditzy episodes from October 2016 through March 2018.

Diet and Malnutrition

I did have, and still have, episodes where I become very sleepy and nauseous after eating something. This leads to a feeling of being ill and not enough energy for normal activity. My condition improves if I semi-fast for the remainder of the day and then reduce my intake of protein and fat for a few days. As a result, I became more depleted nutritionally as time went by.

I don’t think I’ve managed to convey to anyone just how my diet has shifted from normal and especially what they seem to expect of diabetics. Many days I was unable to even manage 50 mg of protein and if I didn’t eat enough carbohydrates I had difficulty sleeping. I was on homemade liquid meals from 2017-2018 and only recently was able to transition onto whole foods after stopping Metformin.

I still struggle to explain why I suspect nutritional deficits in the face of a body that is down 10lbs but still 220. I think my body compensates by doing things like lowering my body temperature. It was 96-97 on a regular basis over the past 6 years, yet my thyroid panels are normal except for high TSH which may be due to my Biotin supplementation. In May 2018, I had more thyroid testing done.

TSH: 7.5
fT3: 3.1
fT4: 1.34
rT3: 22.2
TPO: 12
Antibody <1.

Sometimes my body heats up immediately after eating. I’ve also had iron deficiency anemia where my hands and feet got painfully cold. Sometimes I get chilled and find my body temperature is 95.8 – even in July.

Other Weird Symptoms

Visual Disturbances

I haven’t been able to match up these phenomenon with technical names so I am just describing them as best I can. There is some overlap as I am not sure what is part of which phenomenon.

Problem: After-images occurring too easily
Duration: 3-4 years
Frequency: Intermittently – seems to be worse when I am having diarrhea episodes
Details: Can’t find exactly what these are called. In normal vision if you stare at something for a long time then look at a blank surface you can see a phantom image of inverted colors. What has been happening intermittently with me is that I will see these images instantly and they take longer to fade than normal. This is especially bad in the mornings. I made up a test for myself to track how bad my vision was on any day by looking at the GOOGLE logo. On bad days it bounces around in afterglow very strongly; other days not at all or not as strong. Sometimes if we are out on a sunny day a glance at a bright reflection off metal will create a strong after image that persist for 20-30 seconds or more. I have to be very careful not to let my eyes linger on anything shiny.

Along with the above problem I also experience a kind of sparkle sometimes where if I look out the window, even on a gray day and then back inside there is a brief field of sparkle in my vision.

Problem: Seeing my pulse in my eyes
Duration: 6 years
Frequency: Not as much these days, but was especially bad when my blood pressure was uncontrolled.
Details: I would see a grayed pattern around the lower outer edge of my vision that would flash in intensity seemingly in conjunction with my heart rate.

Finally, my left eye seems to flutter and roll.

Problem: Left eye flutter and involuntary eye roll and moving illusions in vertical images.
Duration: 9 months in 2015, confirmed by eye doctor.
Frequency: Started very infrequently but has progressed to almost daily.
Details: Irritating flutterly feeling in my left eye. When I looked in the mirror I noticed the left eye was rolling left or attempting to roll left involuntarily. This may be related to another problem I have been having for several years where my vision wobbles. It comes and goes in severity, but if I look at any image that has strong vertical contrast it appears so move. For example a picture of a coliseum or tiger will appear to be moving like the way optical illusions move. The moving illusion also occurs more frequently when I am having bouts of diarrhea.

Migraines With Aura

Problem: Migraines with Aura
Duration: 2 years
Frequency: 3-4 times a year – sometimes in clusters
Details: I get migraines where I see an aura. It starts with a blind spot in the center of my vision, in less severe ones it is more of a sparkle overlay and not as blind. The circle then becomes a semi-circle of the outer edge of each eye that becomes bigger until it moves out of the eye. Then pain comes or not. I can sometimes reduce severity by immediately going into a dark room and lying down. Sometimes I get the headache and sometimes just the visual aura. I mention these here because I have wondered if some of my visual problems are migraine auras that haven’t fully developed.

Allergy Shots and More Symptoms: Ophthalmoplegia, Dizziness, Speech Impairment

In January 2018, I started desensitization shot therapy with my allergist. In February 2018, I had another episode of dizzy and ditzy that was complicated by additional symptoms of hypoglycemia. After consulting with my allergist, he set my shots back a few weeks and set up a standing lab order to see if he could tease out the problem. In March, I had the worst episode of dizzy and ditzy I have experienced to date. It included ophthalmoplegia, dizzy, very sleepy, altered consciousness, and personality changes. I was walking with a sort of limp as if my left leg were injured. I laid down on a bench outside the allergist office until the sleepiness passed. When the people at the allergy clinic got back from lunch they checked my blood pressure which was normal and did a blood draw for labs.

I also had the worst episode of speech impairment ever. I remember thinking it was funny because it sounded like they were speaking so much gobbledy gook. I used mindfulness to notice and try to quantify what it was like. I noticed that my intellect was intact, which distinguishes the condition from brain fog where it’s hard to think at all. But things like trying to speak or find words was hard and I got confused easily. Oddly, I had no problems reading and comprehending research papers and I could write, except I made more typing errors. I had a quarter sized mark on one of my arms from the previous day’s shots, but my allergist did not consider my brain symptoms to be due to the allergies. My movements and general condition was very much like being very, very drunk.

Up until that point I had associated dizzy and ditzy with gluten exposure. Once I was sure there was no gluten in the shots, I was a lot more worried about my condition. I regretted not going to the ER since that might have helped me get a diagnosis. As it was, the allergy doctor only checked my tryptase levels and blood sugar which was 119. That level of blood sugar is hypoglycemia for me. I start getting symptoms under 130. This second episode was much harder to recover from than the first and I had lingering symptoms for months afterwards.

Medication Reactions

The glipizide combined with 1000 mg Metformin ER for the type 2 diabetes was causing me severe problems, even as my energy levels and inflammation was improving. The repeated episodes where I had to lower my protein and fat intake was really difficult with the medications I was on.

One day I had a different sort of drunk feeling with sweating and distorted vision while out shopping. It got better when I ate something. I got home in one piece and spent the entire afternoon eating every hour until things improved. That was the last time I took glipizide. I started looking for a new primary who understood nutrition.

I found a new primary two hours away who seemed like a good fit but this story is already too long to describe what went wrong. Sometimes a bad thing has to happen before good ones. I found myself without a primary and experiencing more dizzy and ditzy symptoms. The problems started at the request of my new primary PA, I changed my metformin dose from 2 500 mg tablets in the evening to 500 mg morning and 500 mg evening. After a few days I woke up with a 206 fasting glucose. So I doubled down and started taking 1000 mg 2 times a day. That made modest improvement of fasting glucose but also caused steatorrhea and diarrhea to return.

Thiamine Pyrophosphate Order Delayed

I began taking 13 mgs of thiamine pyrophostate (TPP) in 2014. Recently, I ran out of the TPP sublingual I normally take due to a shipping delay, so I switched to oral 500 mg Thiamine HCL capsule. Over the next two days, I had cramps in my calves, congestion and coughing after my normal light exercise and a body temp of 95.8 in the evening. Then another episode of dizzy and ditzy with mild ophthalmoplegia and dehydration. I was drinking salt water and still couldn’t retain water. I always drink my water with electrolytes and I went through a whole gallon in a day. My blood glucose was 289 in the evening.

I’ve been having problems with burning feet and neuropathy since March 2018, it comes and goes and makes it hard to get to sleep. I first reported mild symptoms of neuropathy in my logs in 2013. TPP and B2 and sometimes calcium supplements help.

Once TPP arrived I started taking it 3 at a time (3x13mg) as well as extra magnesium glycinate and other B vitamins, but my symptoms weren’t improving as much as I expected so I started looking for other causes.

While researching various genes, I came across a paper on thiamine transporters and metformin. I have at least one mutation in one of those transporters but it doesn’t have any established meaning that I can find. I had not considered thiamine deficiency as a possible cause for dizzy and ditzy even though the symptoms seemed similar because I was taking 13 mg of TPP sublingual daily.

I started easing off metformin and my energy and burning feet symptoms improved. A side effect was the metabolism issues that had kept me on a liquid diet improved and I can eat and metabolize solid food again.

Going off metformin caused a slight rise in my fasting glucose so I had a lab test run myself that shows I still have normal insulin production. My glucose response varies quite a bit but I sometimes get good response when I do daily treadmill with glucose in the 110 range two hours after a meal

One night I had a lot of congestion and couldn’t sleep so I took a dose of 3x TPP and the congestion went away and I was able to sleep. I have had ongoing issues with lung congestion since 2010. I think this may be a return of the lung problems I had as a child. I believe my body compensated with hormones and is now decompensating due to menopause. The fact that the congestion got better after thiamine intake is worrying. But I have a strong placebo response so I have to be careful about creating correlations. The lungs issue has been observed by both my primary and my allergist. I frequently get very thick mucus that may be due to inadequate fat digestion.

Ran out of Thiamine AGAIN!

I had a dizzy and ditzy episode with temple headache 7/11/2018. I went through three bottles of 60 Sublingual TPP in a few weeks and was unable to order more due to factory back order. I researched other versions of thiamine. Benfotiamine was having no effect that I could detect. Sulbutiamine helped with some of the brain problems like short term memory. I had concerns that I wouldn’t be able to absorb some of the other forms due to my fat malabsorption. Fortunately, I came across the blog where Dr. Lonsdale explained what “fat soluble” really means regarding lipothiamine and allithiamine, so I ordered both of those as well as liquid TPP from the UK.

Neither of those had arrived by July 14, when I took my last TPP. I had a return of symptoms over the next few days. I started using a B-complex that had TPP in it, but even with that I had another dizzy and ditzy episode that lasted several days. During that time, I got sleepy every time I ate a meal. My meals are small to start with because of the GERD: one cup lentils with tofu or a tofu taco with avocado. Both of those meals that were normally well tolerated gave me symptoms of sleepiness and fatigue.

I found a comment somewhere about the need for manganese, so I got manganese glycinate supplements and that helped ease the neuropathy until the Lipothiamine and TPP liquid arrived. The first Lipothiamine was like magic, my eyes cleared up in about 15 minutes. They do that sometimes after I eat. The neuropathy symptoms were down by the time I went to bed in the evening. In the morning, my feet were hypersensitive and I had leg cramps due to low magnesium. I still have to take extra magnesium during the day and at night as well as other B-vitamins. I have some mild brain symptoms too but they may be due to the stress of starting with a new primary.

The big difference is in my energy levels, which are sufficient to make it through the day and no burning feet at bedtime. I still have limited ability to metabolize food, I tried to add 1/2 cup brown rice to my daily lunch and it sent me into borderline dizzy and ditzy. A typical day’s intake for me is 1 slice tofu, 1/2 cup lentils, and tofu taco with avocado, some vegetables, and a big leafy green salad with avocado, beans and nuts. Sometimes I can have a snack of fruit but more than that I start having problems. I suspect I have other deficits that may be slowing my recovery. I am waking up at 1 am and having to eat something to get back to sleep.

I had another episode this past week. I was preparing my allergy records for a trip to ER and was very dizzy and clumsy and a band of pressure in my forehead. I had been taking 2 50 mg enteric tablets 3 times a day of Lipothiamine but was experiencing symptoms of illness after eating and tiredness. I was only rescued from ER by modifying Lipothiamine dose so that it would be absorbed in my stomach instead of my intestines. I’ve had symptoms of intestinal malabsorption which haven’t yet been evaluated by a GI. I have checked several nearby GI practices without finding one who takes a self pay patient.

Genetic Testing

Genetic testing has helped me discover other problems I have involving metabolism. I haven’t cataloged all my mutations but I have a diabetes related set of 3 homozygous SNPs called TCF7L2. The way I understand it is that people with this phenotype have increased signaling mechanisms such that when they have excess fat, the pancreas responds by lowering insulin response to food and the liver increases morning glucose. Losing the weight, reduces the expression and returns things to normal. I have other genetic mutations which may be impacting me such as MTHFR(++), MTRR(++), and a rare BCHE mutation that impacts my choline levels. It also makes me vulnerable to pesticide exposure. I have to take Trimethylglycine (TMG) and various B vitamins to keep homocysteine in check. If I don’t take enough TMG and CDP choline, I get depressed.

I am seeing a new primary who is a doctor of Internal medicine. The new doctor’s choices for medications are spot on for my genetic type, they both work on the GLP-1 pathway, but they also increase insulin response. I don’t see how that doesn’t cause hypoglycemia, since I have normal insulin production. I have more research to do before making a decision on new medications.

While I can see that the deficiency symptoms I have been experiencing may be a result of poor diet and digestion, the fact that Thiamine HCL did not work and my condition improved so much after stopping metformin leads me to believe I may have a genetic condition. I really need to find a university that is researching metabolic and genetic conditions so I can get a diagnosis.

Medications and Supplements

Most of these supplements were added in 2017 after I started homemade liquid meals. Prior to this I was taking a sublingual B-complex & Magnesium glycinate.

Current Medications

Singular 10 mg x 1
CoReg 12.5 x 1
Lisinopril 10 mg x 1
Cetirizine HCL 10 mg x 1
Omeprazole DR 40 mg x 1

Most of these were added when I started liquid diet

B-6 Pyridoxal-5-phosphate sublingual 15mg x 1 (more if homocysteine symptoms)
B-1 Thiamine pyrophosphate (TPP) sublingual 13 mg x 1 (the one that is backordered)
*TPP liquid 3 x a day or as needed with malabsorption due to intestinal swelling
*Lipothiamine tetrahydrofuryl disulfate 100 mg 3 times a day with extra Mg.
*Liquid CoQ10 100 mg x 3 times a day
B-2 Flavin mononucleotide sublingual 18 mg x 1
B-3 27 mg as Inositol Hexanicotinate, 25 mg as NAD sublingual 25 mg x 1
Liquid B5 + Carnetine
MethylCobalmin, sublingual 1 mg x 1
MethlyFolate (S6)-5-MethylTetraHydroFolate glucosamine salt sublingual 800 mcg x1
Biotin 5000 mcg sublingual 1 x
Chelated Zinc, zinc glycinate 22 mg x 1
Selenium as L-Selenomethionine, capsule 200 mcg x 1
Kelp 325 mcg Iodine, 325 mcg x 1
TriChromium Chromium Picolinate, Chelavate, & polynicotinate, 500 mcg x 1
Magnesium Glycinate (capsule at home) ~ 800 mg per capsule 50% Mg x 2
Liquid chelated Iron biglycinate 10 mg, Yellow dock 10 mg x 1 (not long term)
D-3 5000 iu with K2 1 sublingual 125 mcg D3+ 90 mcd K2
Ultra K with K2 softgel, K1-1000 mcg + K2 1400 mcg x 1
Algae DHA 200 mg x 1
Phosphatidylcholine softgel 1300 mg x 1
Source Naturals Vitamin A as palmitate 1 x 10,000 iu
Buffered C-1000 complex Calcium Ascorbate 1 g x 2
Southwest Botanicals Mucuna Powder (self capsule) ~ 810 mg x 1
Citicholine (self capsule) ~820 mg, 1-2 as needed
Nootropics Sulbutiamine 200 mg (thiamine derivative) 1 capsule, 200 mg x 4
TrimethylGlycine (Betaine) 1 g x 2 with each meal containing methionine
*Taurine 1000 mg
Liquid Calcium, Magnesium, D3, Phosphorus as needed for sleep

*Recent additions

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.

Share Your Story

If you have a complicated health story to share, send us a note.

NASA/JPL-Caltech/Univ. of Ariz., Public domain, via Wikimedia Commons.

Thiamine Deficiency, Dysautonomia, and High Calorie Malnutrition

by Derrick Lonsdale MD, FACN, CNS

Published on June 14, 2018

11181 views

This book by Lonsdale D, and Marrs C, is available on Amazon books. It is published by Elsevier. Written particularly for physicians who are practicing in the field of Integrative Medicine, it would be of interest to the educated public, particularly those affected by chronic disease.

Beriberi, the classical thiamine deficiency disease, long known to have been caused by consumption of white rice, is thought to have been abolished in developed cultures. It is actually widespread in America due to the colossal ingestion of sugar and is usually diagnosed as psychosomatic disease. Because the standard laboratory studies are negative or nonspecific, it is assumed that no organic disease is responsible.

Beginning with a review of the many symptoms of beriberi, it is described as the “great imitator” of a large number of disease conditions, each of which is thought to have its own etiology. It is relevant in all mitochondrial disease, because thiamine sits astride the vital initiation of energy synthesis. Thiamine deficiency interferes with carbohydrate, fat and protein metabolism, but is particularly important in the etiology of diabetes, types I and II and metabolic syndrome. It also has a place in the etiology of Alzheimer disease and may have an important part to play in cancer.

Evidence is provided to show that the relatively new science of epigenetics is crucial to the understanding of the part played by nutrition and lifestyle in genetic function. If the early symptoms of nutritional deficiency are treated symptomatically and high calorie malnutrition continues, the result is an array of chronic brain diseases. When thiamine deficiency was discovered as the cause of beriberi, the early investigators recognized that therapeutic doses of the vitamin involved the administration of 100-300 mg a day for months. The book reviewed here should be in the library of any Integrative Medicine physician.

Publisher Discount

The publisher is offering a 30% discount off of the list price and free shipping if the book is ordered from their site. Just click the link below enter the promotional code ATR30 at checkout.

Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition

The discount does not apply to Amazon orders.

For a preview of the book, click the preview button under the right side bar image.

Solving the Medically Unsolvable: Gene, Nutrient, and Diet Interactions With Dysautonomia

by Tanya Dawson

Published on May 14, 2018

14174 views

Years of Pain, Fatigue, and Weird Symptoms

I have had chronic fatigue syndrome, excessive Non-REM (NREM) dreaming, mood issues and muscle pain 24/7 for as long as I can remember. I have been to more than 100 health practitioners of various flavors, from the conventional doctors and specialists, to herbalists, energy medicine doctors, hypnotists and acupuncturists as well as taking pretty much every test available. Most tests were frustratingly normal. I had deficiencies in iron and B12 at various times but that came right after being diagnosed with Celiac Disease and starting a strictly gluten free diet.

Still, the fatigue and 24/7 pain persisted, and with the start of menopause, new symptoms emerged. I experienced periods of vertigo, brain fog, unexplained cold sensations in my chest, and after taking bioidentical progesterone for a few days I experienced daily dizziness and eventually got diagnosed with postural hypotension when the cardiologist measured a drop in systolic blood pressure of more than 30 upon standing. This daily dizziness continued for more than three years.

I tried all of the usual dietary interventions as well as the low oxalate diet, the anti-candida diet, the Failsafe diet and other elimination diets. All failed to make a dent in symptoms. The only time I noticed an improvement was when, after several bouts of gastroenteritis, I was forced to subsist on dry gluten free bread, a whey protein based meal substitute drink and skinless chicken. People commented that my skin looked good and I had improved energy, however, over time I returned to my normal diet and the benefits gradually disappeared.

Resolving the Dizziness, Brain Fog, Dysautonomia / POTS with B Vitamins and Diet

For more than three years, I have had daily dizziness pretty much all day as a symptom of dysautonomia/postural hypotension. An OAT test showed low thiamine and I had high hopes that thiamine would be the magic ticket that would get me out of dizzy brain fog hell. Thiamine and a reduced sugar diet did help a lot with energy, mood and general well-being, but unfortunately the reductions in postural hypotension were minor.

I experimented with supplements and lifestyle changes. I increased my meditation time, and did gratitude journaling and worked on taking in the good and rewiring my brain. This helped me better manage the stress of chronic illness and reduced some of my symptoms of depression and agitation.

I also found improvements in taking thiamine and riboflavin (B2) 3-4x a day along with high doses of the other B vitamins once a day. But, again the daily dizziness and brain fog persisted.

My big breakthrough came when I discovered that I had been taking the wrong form of niacin. I had been taking niacin and inositol hexanicotinate for the last three years, but it wasn’t until I returned to taking niacinamide that the symptoms dysautonomia dialed down. I started with a 50mg dose and by the end of the day I noticed that I had been less dizzy. I gradually increased the dose to the full 500mg and the symptoms kept reducing. I also got my brain back! No longer was I feeling constantly brain fogged, sluggish and mentally confused. Now that the niacinamide had my blood circulating properly and fueled my biochemistry things started working. My thyroid numbers had always been on the cusp of hyperthyroidism, yet I had a sluggish metabolism. Within a week, I noticed that with no other dietary changes my post-menopausal muffin top had reduced, my energy increased, and my skin was looking better.

The Missing Pieces: HACL1 and Phytanic Acid

I had high hopes that I would be able to completely eliminate the symptoms of dysautonomia, however, there is still some lingering dizziness. Over the last few weeks, I have been experimenting and have noticed two interesting associations.

The first, is sugar intake. Additional fruit or anything high in sugar increases my symptoms of postural hypotension. This could be linked to thiamine or niacin.

The second, is a reaction to foods high in phytanic acid. I first learned about the HACL1 gene from the Hormones Matter blog and I quickly realized that this made sense of the fact that I reacted to both A1 and A2 cheeses and yogurts as well as butter, but am fine on whey protein. I also react to oily fish and red meats but I am fine with pork and chicken. I live in New Zealand where all of our lamb and beef are grass fed, so all of our dairy products and red meat are higher in phytanic acid than the same products from grain fed animals.

In the past, I had noticed that any of these foods that are high in phytanic acid trigger feelings of rage and anger. There seems to be a threshold, so I can do an elimination diet and reintroduce butter and be fine, but over time, I believe that they phytanic acid accumulates and then the symptoms appear. Once I reach the threshold, I “hulk out” within minutes of eating beef, lamb, fat containing dairy products and oily fish. I have also had similar reactions in the past when I ate sugar or drank alcohol. I had in the past noticed that my dysautonomia was worse with all of these things. It would appear that thiamine is required to process all of these things, either directly in the case of sugar and alcohol or through the HACL1 gene for the other foods. This suggests that my body struggles to maintain thiamine levels and get the thiamine to where it is needed.

HACL1 rs17485390 (C)	TT
HACL1 rs6784844 (T)	CT
HACL1 rs6797119 (T)	CT
HACL1 rs7648958 (A)	AG

Feeling confident after increasing my niacinamide to 1,000mg spaced throughout the day, I reintroduced foods high in phytanic acid and the dizziness increased fairly quickly. I am now sticking to a low phytanic acid with only occasional red meat, fish or butter. (Yogurt and cheese are gone for good and maybe the other foods will need to be completely eliminated too.)

I found an old test that showed that my urinary l-lysine was low. After more research, I discovered that lysine helps maintain tryptophan activity and reduces the draw on niacin in the body. My tryptophan levels were normal on both urinary and blood tests but perhaps a lysine deficiency was indirectly affecting my niacin levels. After an initial dose of lysine I felt almost euphoric. This effect quickly leveled off. I am wondering if, after decades of fatigue, my body likes homeostasis and is counteracting the effects of nutrients that I clearly need. This has happened in the past with medications. After a few doses, they are basically rendered useless. This applies to antihistamines, psychotropics, painkillers, and so on.

Possible Secondary Pellagra

Is it possible that I have secondary pellagra? I initially dismissed the idea of pellagra as the symptoms seemed more severe than mine. My dermatitis was minor compared to the pictures online, I had an explanation for the dizziness (diagnosis of dysautonomia), the diarrhea has been an issue on and off, so it didn’t seem significant, and my mental confusion didn’t seem enough to qualify as dementia and yet I can now see that I did have the 3 Ds of pellagra despite adequate niacin intake. I don’t eat corn and rarely eat grains and have a diet high in niacin but I had many of the symptoms of pellagra including sensitivity to light, dermatitis, diarrhea, dizziness, feeling cold all the time, brain fog and mental confusion, difficulty falling asleep and weakness.

Interestingly, some of these symptoms overlap with thiamine deficiency symptoms and I feel very sure that I have had severe thiamine deficiency because I have also had tingling sensations and muscle pain, as well as a history of high intake of sugar, carbs and alcohol and a very positive response to thiamine and benfotiamine.

Going Forward: More Questions

My plan is to continue with my supplements and a low sugar diet and low phytanic acid foods. I am hopeful that this will completely eliminate the dysautonomia and leave me free to work on my other symptoms. My brain function is good when the dizziness is kept at bay and I feel more optimistic and happy and have a small but noticeable uptick in energy and strength.

Although I have made huge strides in my health, I am left with some lingering questions:

I have been on high doses of many B vitamins for years and yet it seems that my body still craves them. Could years of undiagnosed Celiac Disease have affected the enzymes that take vitamins and converts them to the active form and transports them into organs and tissues? Is it realistic for this to still be happening after eight years of being gluten free?
The literature glosses over the conversion from niacin to niacinamide as something that the body can easily do, however, I have taken high doses of niacin and inositol hexanicotinate without benefit and eat a diet rich in niacin foods without getting the benefits that I got from small doses of niacinamide. Is it possible that some people have challenges converting niacin to niacinamide? I have yet to find any research to support this other than a study suggesting that niacinamide is twice as effective as niacin. However, I was taking triple the dose of niacin with no benefits. I believe that my body is inefficient at converting niacin to niacinamide. If anyone knows of a specific illness that may cause this I would be interested in learning more.
Is my reaction to phytanic acid foods due to a deficiency in thiamine (despite taking very large doses for years) or is there another reason that my body appears not to tolerate phytanic acid foods?
Are there still more vitamin or amino deficiencies that I am yet to discover? In the future I will probably do another OAT or Nutreval to see whether my levels have improved but for now I want to let my body get used to the lower phytanic acid levels and see if things settle.
My body seems to like homeostasis. For the first couple of days that I took niacinamide I noticed that I felt very warm, but I have returned to feeling cold all of the time. The dizziness has improved and it had almost disappeared but then crept back in. Could this be due to more vitamin or amino deficiencies that I am yet to discover, problems with my enzymes or is there some sort of ANS wiring issue that is better addressed by neural retraining?
Sleep is another big issue for me and until I consistently sleep well without excessive NREM dreaming it is possible that these other issues will not fully resolve, but progress is exciting and I am hopeful that the last puzzle pieces will fall into place.

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.

Image by Flickr user Enzo Varialle. CC2.0.

Thiamine, Epigenetics, and the Tale of the Traveling Enzymes

by Chandler Marrs, PhD

Published on April 17, 2018

8021 views

For some time now, we have been covering all the ways in which thiamine deficiency influences disease. The primary mechanisms are through the down regulation of mitochondrial enzymes critical for ATP production. The lack of thiamine impairs mitochondrial functioning significantly leading to complex, debilitating, chronic, and sometimes, deadly illnesses. With mitochondrial energy a requisite for cell functioning and survival it is easy to see how the diminishment of mitochondrial functioning would negatively impact health and how high-energy physiological systems like the nervous and cardiovascular systems might be particularly hard hit. More than just just derailing cell function, as if that wasn’t problematic enough, when mitochondrial energy production slows, the adaptive cascades that ensue include epigenetic modification, not only at the level of mitochondrial DNA (mtDNA), but also, at the level of gene expression from the cell nucleus or nDNA. This is a huge discovery with broad implications about health and disease. It means that all sorts of things considered innocuous, are directly influencing gene activation and deactivation by way of the mitochondria.

Epigenetics: How the Cells Adapt to the Environment

Epigenetic modification refers to the activation or deactivation of chromosomal gene expression absent mutation. These changes can be heritable and often are. Strictly speaking, epigenetics involves changes in methylation, histone modification and/or alterations in non-coding RNA that affect transcription. Epigenetics is the way our genome adapts to environmental circumstances and prepares our offspring to do the same. The majority of epigenetic work focuses on genomic changes. That is, those variables that affect gene expression from the cell nucleus or nDNA. There is a growing body of evidence, however, that mitochondrial DNA (mtDNA) are affected by epigenetic factors in much the same way as nDNA. In fact, given the mitochondria’s role in cell survival, one might suspect that mitochondria are more susceptible to environmental epigenetics, perhaps even the first responders and/or the initiators of chromosomal genetic changes.

Considering that nDNA accounts for over 90% of the proteins involved in mitochondrial functioning, how could damaged mitochondria, even functionally inefficient mitochondria, not affect gene expression in the cell’s nucleus? Though we tend to think of mitochondria as self-contained and discrete entities, black boxes of sorts, where stuff goes in and ATP magically comes out, this is not only not the case, it seems biologically illogical to think that way. So much of mitochondrial functioning is related to its environmental milieu. In fact, increasingly researchers are finding that the mitochondria are the center of the organismal universe, sensing and signaling danger, and effectively, regulating all adaptive responses, including epigenetic modification of the proteins encoded by the cell nucleus.

Beyond the strict definition of epigenetics, it seems to me that any factor that altered mitochondrial function, would eventually alter gene expression by any number of mechanisms, not just the direct ones. That is, because the mitochondria produce the energy required for cell survival, anything that derails their capacity to produce ATP, pharmaceutical and environmental chemicals, for example, should be considered, ipso facto, epigenetic modulators. Energy is a fundamental requirement for life. How could energy depletion not affect gene expression? It does, and now we know how.

Starve the Mitochondria, Alter the Genome

It turns out, when the mitochondria are starving and/or damaged the key enzyme complex that sits atop the entire energy production pathway and is critical for the production of the substrates involved directly (yes, I said directly) with gene expression, migrates from the mitochondria across the cell and into the cell’s nucleus where it then sets up shop and begins its work there. Sit with that for a minute. The entire enzyme complex decides that things are not working where it is, so it hitches a ride with some transporter proteins, several of them along the way, to find a more suitable home. The enzyme complex ‘knows’ that its functions are critical for survival and so it must move or die. What an incredible bit of adaptive capacity. A symbiosis, if you will.

To make matters even more interesting, the traveling enzyme complex just so happens to be the pyruvate dehydrogenase complex (PDC) and you guessed it, the PDC is highly, and I mean highly, thiamine dependent. But wait, there’s more. Several other enzymes involved in mitochondrial bioenergetics are also thiamine dependent. These include: alpha-ketoglutarate dehydrogenase (α- KGDH) in the tricarboxylic acid (TCA) or citric acid cycle, transketolase (TKT) within the pentose phosphate pathway (PPP), the branched chain alpha-keto acid dehydrogenase complex (BCKDC) involved in amino acid catabolism and, more recently, thiamine has be identified as a co-factor in fatty acid metabolism via an enzyme called 2-hydroxyacyl-CoA lyase (HACL1) in the peroxisomes (organelles that break down fatty acids before transporting them to the mitochondria). So thiamine deficiency is problematic. It not only causes dysfunction in the mitochondria, reducing bioenergetic capacity, but if severe enough and/or chronic, it alters the genome. And those changes are likely heritable. That is, your thiamine deficiency likely will affect your children’s ability to process thiamine.

Thiamine Deficiency and Gene Expression

Without sufficient thiamine, the PDC enzyme complex does not function well and because of its geographic position at the entry point into the citric acid cycle, when it is not working at capacity, everything below it eventually grinds to a halt resulting in severe neurological and neuromuscular deficits. Absent congenital PDC disorders, however, when it simply is inefficient or starved for its cofactors, metabolic disorders ensue because we cannot convert carbohydrates into ATP and the sugars that normally would be converted into energy, remain unmetabolized, floating around outside the cells and causing the whole cascade of effects that mark type 2 diabetes. When the PDC is inefficient, ATP levels wane and fatigue ensues. Systems that are highly energy dependent are hit the hardest. Think brain, heart, muscles, GI tract. When mitochondria are inefficient or damaged, reactive oxygen species (ROS) increase. Anti-oxidant capacity decreases and further damage to the PDC ensues. Inflammation increases, immune function decreases. Cell level hypoxia grows. Alternative energy pathways are activated, those that are endemic of cancer. Yes, cancer can be considered a metabolic disorder.

When the PDC is inefficient, mtDNA heteroplasmy, the balance between mutated mtDNA and healthy mtDNA grows with each mitogenic cycle. This, of course, further derails mitochondrial capacity (and increases the need for thiamine). Absent available resources, mitochondrial death cascades are initiated. And now, we know at some point in this disease and death spiral, when ATP diminishes and the litany of adaptive measures fail to maintain sufficient energy availability, the PDC up and leaves its mitochondrion and sets up shop in the cell nucleus, in what is presumably a last ditch effort to save its cell and the organism as a whole. What a remarkable bit of adaptive capacity.

The researchers, who discovered this, ruled out the possibility that the PDC enzyme complex was already in the cell nucleus. It wasn’t. It traveled by way of several transporter proteins. They also found that once in the nucleus, it began producing acetyl-coenzyme A (CoA). Acetyl-CoA is requisite for the acetylation and deacetylation of histones, post translational changes in DNA, but also lysine acetylation, which further affects metabolism – mitochondrial energy homeostasis. With insufficient acetyl-CoA and insufficient acetylation, DNA replication is aberrant. Moreover, without sufficient acetyl-CoA, acetylcholine synthesis, an incredibly important transmitter for nervous system functioning, diminishes.

A Constitutively Active Enzyme: What Could Possibly Go Wrong?

Even more interesting, the PDC in the cell nucleus appears to be constitutively active. Unlike in healthy mitochondria where checks and balances prevail, when the PDC travels to the nucleus it has no feedback control to temper its activity. The enzymes that normally shut down PDC production (pyruvate dehyrodgenase kinase) in the mitochondria, were not present in the cell nucleus, and thus, once the PDC was turned on, it stayed on. That means when the PDC translocates to the cell nucleus it operates independently much like a Warburg effect in cancer metabolism; one that fully supplants healthier metabolic pathways. Can you say tumorogenesis?

This research has enormous implications for everything from cancer to Alzheimer’s disease and everything in between that involves metabolic disturbances like diabetes and heart disease. Metabolism begins and ends with the mitochondria, at the PDC, and the PDC is highly dependent on thiamine. Every pharmaceutical and environmental chemical damages the mitochondria in some manner or another and that damage inevitably reduces ATP capacity. Some chemicals also deplete thiamine directly, thus downregulating the activity of the PDC and the other thiamine dependent enzymes. Even when these chemicals don’t deplete thiamine directly, the western diet is more often than not thiamine deficient, sometimes only marginally, others time quite significantly so with symptoms already expressed, but very rarely recognized. We have known that thiamine was critical for health and survival for some time. Now we have one more reason to tread carefully with lifestyles and exposures that deplete thiamine.

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.

David Goodsell, CC BY 3.0, via Wikimedia Commons

This article was first published on April 25, 2017.

About TTFD: A Thiamine Derivative

by Derrick Lonsdale MD, FACN, CNS

Published on March 21, 2018

77375 views

I recently received notification concerning a “review” posted on HerbCustomer, a commercial website that has been active since February 26, 2010. This so-called “review” was posted on January 16, 2018 by iHerbCustomer entitled “Dangerous allithiamine derivative with no thiamine activity”. The email was posted as well. This person made a potentially libelous statement by referring to me as lying about this thiamine derivative. Its commercial name is Lipothiamine. Its chemical name is thiamine tetrahydrofurfuryl disulfide (TTFD) and this post is to refute the accusations that are made public by this individual.

History of Thiamine Research

Thiamine is the chemical name for vitamin B1 and its deficiency in the diet has long been known as the cause of beriberi. This disease has been known for thousands of years but its underlying cause was only discovered in the closing years of the 19th century. Since beriberi was commonest in the rice consuming cultures, it is not surprising that the major research came from Japan. In the middle of the last century a group of university-based scientists was convened and they wrote a book (Review of the Japanese Literature on Beriberi and Thiamine). This was translated into English, ostensibly because these scientists wished to let people in the West know and understand the pernicious nature of disease resulting from thiamine deficiency. I was fortunate enough to receive a copy of this book from one of the scientists involved. The information in this post is derived from it. Because they were scientists and were well aware of the clinical effects of beriberi, their studies were very extensive. They knew that thiamine existed in garlic and much of their experimentation focused on studies of the garlic bulb. They discovered that there was a natural mechanism in garlic that created a derivative of thiamine and called it allithiamine. Note that this is a naturally occurring substance and the term should be entirely restricted to it.

On a number of occasions I have seen thiamine derivatives being called “The alithiamines” and one commercial product is called Allithiamine with a capital a. The name was given to this naturally occurring product because garlic is a member of the allium species of plants. It can be found in other members of the allium species. Because the Japanese scientists already knew a great deal about the clinical expressions caused by thiamine deficiency, they originally thought that this new derivative might have lost its vitamin dependent activity. They went on to test it in animal studies and found that it had a much greater biologic effect than the original thiamine from which it was derived. They found that it was extremely important that allithiamine was a thiamine disulfide derivative (disulfides are important in human physiology) and they synthesized many different types of thiamine disulfide as well as many non-disulfide derivatives, carefully testing each one for their biologic activity.

What is TTFD?

Without going into the biochemical details, what we now know is that thiamine tetrahydrofurfuryl disulfide (TTFD, Lipothiamine) is, for a number of reasons, the best of the bunch of synthetically produced derivatives and has exciting possibilities in therapy. For example, it has been shown from animal studies that Benfotiamine, a non-disulfide derivative, does not get into the brain whereas TTFD enables absorption of thiamine into the brain where it stimulates energy synthesis. When we take in thiamine, occurring only in our naturally formed food, it is biologically inert. It has to be “activated” within the body that possesses genetically determined mechanisms for its absorption and activation. To cut a technically difficult explanation, let me state that TTFD bypasses this process. It enables thiamine to split away from its disulfide attachment and enter the cells where its activity is required. The concentration achieved in the target cells is much greater than that achieved by the administration of the thiamine from which it was derived.

The Japanese scientists studied the effect of cyanide in mice and found that thiamine propyl disulfide (TPD), a forerunner of TTFD, gave significant protection from the lethal effect of this poison, an incredible discovery that alone should raise eyebrows. They studied this effect and were able to show its mechanism. They also found that it would protect animals from the effect of carbon tetrachloride, a poison that affects the liver. It is using its vitamin actions in a therapeutic manner.

Being myself a consultant pediatrician in a prestigious medical institution, I was able to obtain an independent investigator license (IND) from the Federal Drug Administration, and obtained TTFD from Takeda Chemical Industries in Osaka, Japan, the makers of this product. TTFD is a prescription item in Japan, sold under the commercial name of Alinamin. I have read several publications, showing that it reverses fatigue in both animal and human studies. I was able to study the value of this incredible substance in literally hundreds, if not thousands of patients. Far from being toxic, as this person claims, I never saw a single item that suggested toxicity. Its therapeutic potential is largely untapped in America. This is because the current medical model does not recognize that defective energy metabolism, genetic errors and the nature of stress are the interrelated components whose variable effects in combination are the cause of disease. Do not mistake the use of the word stress, a word that is so commonly used inappropriately. An infection and any form of physical or mental trauma represent a form of stress. It is the ability or the inability to meet the required energy demand to resist that stress that matters in the preservation of health.

Clinical Benefits of TTFD

It is important to understand that the beneficial activity of TTFD is exactly the same as the thiamine from which it is derived. It is the mechanism of its introduction to cells, particularly those in the brain, that enable it to have such an effect on energy metabolism. Because of its strategic position in the cell, thiamine is of vast importance in oxidative metabolism in the complex mechanisms of energy production. There are at least two methods by which thiamine deficiency can be induced. The commonest one is an excess of sugar and fat that overwhelms the capacity of thiamine to conduct the mechanisms involved in energy synthesis. The discovery that thiamine has a part to play in fat metabolism is quite recent. The other one is because of genetic errors involving its biochemical action. However, we now know from a relatively new science called epigenetics that some mistakes in DNA can be overcome by the use of an appropriate nutritional substance like thiamine. The completely non-toxic use of TTFD depends merely on its ability to introduce thiamine into the cells of the body that require its magic. Under these circumstances, the big doses of thiamine are acting like a pharmaceutical by stimulating the missing action. We are not dealing with simple vitamin replacement. This should represent a new era in medicine when nutrient biochemistry takes its place in patient care.

Conclusion

The person that wrote this criticism fails to understand that TTFD and other thiamine derivatives represent a new basic principle of therapy. It recognizes that healing is a function of the body, not the activity of a so-called “healer”. All it requires is the foundation substances needed for repair and sufficient energy to use them. It demands a dramatic change in thinking about health and disease. If you understand the principles involved, it forces the conclusion that the word “cure” is a pipe dream. The only form of pharmaceutical drug that matters is one that safely kills an attacking microbe. Almost all the rest of them merely relieve symptoms and have no effect on the ultimate outcome.

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.

Image by Alexa from Pixabay.

A Scientific Sermon on the Basis of Disease

by Derrick Lonsdale MD, FACN, CNS

Published on March 15, 2018

5852 views

Why a sermon? The title was suggested from a breakfast discussion that I had with a resident in the retirement home in which I live, a retired minister of the United Christian Church. In the nearly 5 years that I have been living here, I have repeatedly sat and listened to my friends talking about their various handicaps and how they are being treated. I was a pediatrician at the Cleveland Clinic for 20 years and left it in 1982 to practice what has become known as “Alternative Complementary Medicine”. Because few people apparently understand the meaning of this, I am trying here to inject a little bit of science to explain it.

From the Unexplainable Comes Insight

In 1982, I began to see adults as well as children. I thought that there might be some interest in why my perspective changed and why I took early retirement from a prestigious orthodox medical institution. As a consultant pediatrician at the Clinic, I was exposed to the referral of children with strange diseases. There is a group of genetically determined rare conditions known as inborn errors of metabolism. The strange thing about them in common is that if they are not recognized at birth, some of these diseases cause the affected child to become mentally retarded. That is why there is a laboratory in each state capital that tests every newborn child for one of these inborn errors. It demands only a finger stick of blood on a strip of filter paper that can be mailed to the laboratory. Perhaps even stranger, many of them can be protected from mental retardation by starting them on a special diet that they have to maintain throughout life. It forced me to understand the necessary biochemistry, the nature of the special diet and why it prevented mental retardation.

One day, because of my studies in biochemistry, I was confronted with a 6-year old child with a weird story. I will refer to him as JV. He had suffered from infancy with intermittent episodes of a condition known as cerebellar ataxia (ataxia is a fancy word used to describe a lack of balance and coordinated movement). The cerebellum is part of the brain that deals with balance amongst many other responsibilities. Each one of these episodes lasted about 10 days, rose to a clinical climax and subsided automatically without treatment, just as though he had been drinking alcohol. Each episode left him a little bit more mentally affected. His clinical presentation was exactly like that of a drunk. He was unable to walk a straight line and his speech remained slurred as long as the attack lasted.

Alcohol has its major effect by inducing vitamin B1 deficiency in the cells that make up the cerebellum. He had been tested with every known method by neurologists and neurosurgeons, all of which produced no information.

To cut a long story short, I had to wait two years before he had one of these episodes when I admitted him to hospital for study. All I did was to collect urine that was subjected to biochemical testing. His urine was collected continuously for 12 hours during the night and separately for 12 hours during the day to see if it reflected differences in night/day metabolic processes. The ataxic episode lasted about 11 days, rose to a symptomatic climax at about the sixth day and gradually subsided without any treatment whatsoever. Of some interest, during the last few days the symptoms would be much less in the morning and gradually worsen as the day advanced. The abnormal chemical changes were reflected in the urine by being alternately high during the day and much lower during the night. Thus, the day/night rhythm of the brain known as circadian (circadian means about 24 hours) was affected. Yes, our brains are constructed to dovetail with the day/night seasonal rhythms of our world.

Without going into complex details I was able to show that he had vitamin B1 dependency. The chemical name for this vitamin is thiamine. Vitamin dependency means that a much greater amount of the vitamin is necessary for its normal action. Vitamins act as what are called cofactors to enzymes. The connection between the vitamin and its respective enzyme is under genetic control and it was this mechanism that was defective.

High Dose Nutrient Therapies to Compensate for Energetic Demands

From this case, I learned that this genetic defect might be overcome by using pharmacological doses of thiamine. It seemed as though the vitamin acted as a drug by stimulating the inefficient enzyme back to a more normal state of function. In a fanciful analogy, some man-made machines require cogwheels that transmit energy from the power source to the action. Enzymes in the body may be roughly compared with cogwheels. They transmit energy derived power to physical and mental action. To continue the analogy, cogwheels require oil and vitamins may be roughly (and I mean roughly) compared to oil given to a cogwheel. They are each essential components that engage with their respective enzymes. Without the appropriate vitamin, the corresponding enzyme gradually becomes dysfunctional.

As I have already noted, the connection between a vitamin and its respective enzyme is controlled by a genetically dependent mechanism. It is the breakdown of this mechanism that introduces dependency. Each of this child’s episodes of ataxia was triggered by a simple infection like a cold, a mild head injury or even an inoculation. I will refer to this as some form of stress. Several reports in the medical literature describe intermittent clinical episodes of their respective disease entity being exacerbated by an otherwise mild infection. This is important because sometimes a mild head injury or an infection is thought to be the cause of the generated symptoms on its own, whereas it may well be triggering the clinical situation in relationship to hitherto marginal energy availability.

The point that I am trying to make is that the injury, and indeed the defense against infection, automatically demands an energy-dependent response. That marginal energy availability may not be enough before the injury to cause symptoms, or perhaps mild symptoms in such an individual might be ascribed to other causes as conceived within our present medical model. For example, a given symptom may be “written off” as an allergy, thus confounding the situation even more. Energy is always required by the brain in order to respond to any form of mental or physical stress. Just as a car consumes more energy when climbing a hill, stress to us is like a hill to be climbed. This action takes place automatically when our capacity to synthesize energy is healthy.

If the increase in energy is not forthcoming, the affected cells do not function properly, giving rise to what we call symptoms. Symptoms are inevitably generated by sensory mechanisms in the brain, another factor which can be very confusing. For example, an injury in an elbow would result in a signal to the brain that generates the sensation called pain. The brain acknowledges the signal by announcing to its owner “I have a pain in my elbow”. The point is this; pain is a brain effect and can explain why there is such a phenomenon as psychological pain.

The Irony of Psychosomatization

I want to impress you however that psychology is always due to electro-chemical brain cell reactions because it has a scientifically plausible explanation. That means that so-called psychosomatic disease is not an invention by the patient. The symptoms are being generated by chemical disturbance in those brain cells and in today’s world, high calorie malnutrition is responsible for polysymptomatic diseases that haunt many physicians’ offices. They are often referred to as “problem patients” and the patient is sometimes told that it is “all in your head”. The irony is that this is the truth. It certainly is in the head but it has a real underlying cause that is being misinterpreted.

I recently read a column in the Wall Street Journal entitled “Is your teen depressed”? With direct quotes from this column “statistics show that teen depression is on the rise. In 2016 around 13% of US teenagers aged 12 to 17 had at least one major depression episode in the past year compared to almost 8% in 2006. The American Academy of pediatrics has recently recommended screening all those youngsters aged 12 and older annually for depression. They define major depressive disorder as having five or more of the following symptoms present for two weeks: depressed mood most of the day, irritability, decreased interest or pleasure in most activities, significant change in weight or appetite, change in sleep, increased educational sluggishness, fatigue or loss of energy, feelings of guilt or worthlessness, changes in concentration and recurrent thoughts of death. They sometimes complain of stomachaches or headaches that don’t have an identifiable cause”. My explanation is the combination of three factors, represented as three interlocking circles of health, genetic risk/stress/nutrition.

Genes, Nutrition, and Energy

Let me explain genetic risk a little. We now know that our genes can be manipulated by nutritional elements and lifestyle. Many genetic diseases do not appear until late in life. If it was only the gene to blame, one would expect it to appear at birth and indeed some do. For example, type I diabetes has genetic determination but the symptoms may not appear until middle age and are often associated with some form of stress such as a cold, a mild injury or even a telegram giving bad news. Some recent research has shown that pharmacologic doses of thiamine might well protect diabetics from their well-known complications.

Thiamine is a vital naturally occurring chemical (the word vitamin was used to express its vital need for life when it was thought to be an amine. When it was synthesized and found not to be an amine the terminal e was dropped) that enables body cells to produce the energy they require for function and we have between 70 and 100 trillion cells that make up the human body, all of which require energy. Vitamins act as what are called cofactors to enzymes. JV actually had intermittent episodes of a classical disease known as beriberi, long known to be caused by deficiency of thiamine. However, because of genetic mechanisms that were at fault, he required huge doses of thiamine in order to prevent his intermittent episodes of beriberi, hence the use of the term dependency.

The RDA (recommended daily allowance) for thiamine is 1 to 2 mg a day and he required 600 mg a day. If he should succumb to a cold, experience a simple injury or some other form of physical stress, he found that he had to double the dose to 1200 mg a day. Contrast this with 1 to 2 mg a day as the RDA indicated for normal healthy people. On one occasion an episode occurred following an inoculation, so I had to assume that the inoculation represented some form of physical stress. Note that the needle stick sends a sensory message to the brain, notifying it of some form of attack. The signal causes the brain to formulate any necessary defensive action. Therefore, if somebody passes out following a needle stick, it is a temporary lack of energy mobilization in the brain.

I must emphasize again: the brain requires energy mobilization to meet any form of stress. Therefore, our energy consumption is in a constant state of flux on a day-to-day basis, much like climbing hills and descending into valleys on a journey For example, when this child was under treatment he was walking in a local park, tripped on a stone and suffered a relatively mild head injury. He became unconscious and was taken to a nearby emergency room. His mother called to notify me of the event. I called the physician in the emergency room and tried to explain to him that this child represented a special case and that he required an injection of thiamine. He thought that I was quite mad: such is the trust that leads to failure of communication between physicians.

Thiamine and Energy

This was such an intriguing experience that I began to perform clinical and library research on vitamins that have continued to the present. Glucose is the “gasoline” that is the major fuel of our cells and thiamine is the equivalent of the “spark plug”. The energy requirement for the brain and heart is enormous because both of them function 24 hours a day throughout life. That is why energy deficiency disease dominates the brain and heart with varying degrees of severity. Because I was a consultant pediatrician, I received referrals from private pediatricians in Ohio and even out-of-state. Some of my common referrals were children with attention deficit, hyperactivity, learning disability and other curious distortions of behavior. Of course I discovered that their diet was atrocious and using pharmacologic doses of thiamine brought them back to normal behavior. Not only that, I found that some of the strange diseases referred to the Clinic also responded to vitamin therapy, so I offer this explanation.

Every cell in the human body is a one-celled organism in its own right. Evolution has endowed each of them with special responsibilities in groups that make up the organs of the body. I think of the body as being somewhat like an orchestra where the groups of specialized cells represent the instrumentalists. The violins, as it were, are separated from the cellos, each representing a bank of instrumentalists. They all know what to do but require a conductor. The conductor in the body is of course that part of the brain that connects with all the organs through the nervous system known as autonomic. We have two types of nervous mechanisms: the voluntary system conveys will, thus allowing conscious control of body movement and thoughts. The autonomic nervous system is purely automatic. Its controls are in the lower part of the brain which is unusually sensitive to deficiency of thiamine. That is why alcohol addiction, heavily related to thiamine metabolism, results in a brain disease known as Wernicke encephalopathy that is well known to be caused by thiamine deficiency.

Signals from the brain to the body organs and from the organs to the brain enable us to adapt to all the vagaries of living in a hostile environment. This signaling system also requires a huge amount of energy and it is not surprising that the brain/body mechanisms deteriorate if there is insufficient energy.

I have come to the conclusion that thiamine is somewhat like the leader in an orchestra. Although the entire vitamin category represents the nutrient necessities of life and each has its own separate responsibility, they all work together. Because of its special place in energy metabolism it stands out with its clinical importance. Because energy metabolism is frequently inferior as the major cause of a disease, the diagnostic category, as we presently represent disease, ceases to matter. A reader might object by referring to genetically determined disease as a leading cause. However, the new science of epigenetics tells us that proper use of nutrients and adjustments of lifestyle can often correct the genetic mistake.

High Calorie Malnutrition: A Disease of Affluence

Now I would like to discuss what I mean by high calorie malnutrition because I believe it is an extraordinarily common cause of disease in our disorganized world. Malnutrition is usually thought of in relationship to starvation. The disease known as beriberi is a classic example of high calorie malnutrition. It was caused for centuries by the consumption of rice. Although the major effect has been in Eastern countries, it has appeared in many different parts of the world including America. The rice grain consists almost exclusively of starch that is broken down to glucose for use as fuel. The vitamins necessary for the metabolism of the glucose are in the cusp around the grain. When you remove the cusp you generate white rice and the Chinese peasants found that white rice looked nicer on the table. Therefore if and when they became more affluent they would take their rice to the rice mill for the removal of the cusps. The use of the rice mill was expensive, hence the association with affluence. They would place the white rice in silver bowls and invite their friends to dinner, not for culinary purposes but to demonstrate their new found affluence. Our constant deviation from the natural rules applied to health costs humanity dear. People with beriberi do not look starved. In fact they may be obese. Because they have bitter complaints and look relatively healthy they are often mistaken for neurotic complainers and treated indifferently. Not only that, if a physician might suspect his patient as having this disease and measure the level of thiamine in the blood he will probably find it to be normal. It is the ratio of calorie concentration to that of thiamine concentration, reminding me of what happens with too much gasoline in the cylinder of a car referred to as a choked engine.

I would like to give you a few examples. When I started my library research on thiamine, I discovered that a medical officer of health in England had been sent out to Hong Kong in the 1940s to investigate a form of sudden death that occurred in breast-fed infants of Chinese mothers. Hong Kong was then a British protectorate. She found that the rice consuming mothers gave their infants thiamine deficient breast milk. Although these infants were often considered to be the healthiest looking members of the family they suddenly died at the age of 3 to 4 months, exactly like sudden infant death syndrome that occurs today. Of historical interest, you may remember that the Japanese invaded Hong Kong and the Chinese people had their rice severely restricted. Although the breast feeding mothers were near to starving, the sudden infant death ceased to occur. When the Japanese were driven from the colony, the mothers had unrestricted rice and the sudden infant death began to reappear. This taught me the danger of empty calories.

At the Clinic, I kept seeing infants that had been classified as “threatened sudden infant death” and would place them on a breathing monitor that indicated when they had an episode of apnea (temporary cessation of automatic breathing) or slowing of the heart. When I gave them thiamine the monitors ceased to fire alarms. By special studies we found that the function of the brain stem in these infants was compromised, clearly indicating an electrochemical underlying mechanism. Although we published our work, it has been ignored. Advancing to my experience with adults after I had resigned from the Clinic a young woman came to see me from out-of-state. She had been diagnosed with a condition known as thrombocytopenic purpura, a disease in which platelets, one of the varieties of cells in the blood that have a function in clotting, were severely deficient. She had been receiving orthodox treatment for 10 years without success. I gave her a series of intravenously administered water soluble vitamins with complete resolution. I can provide lots more examples, but perhaps this has introduced to you the possibility of a different perspective in our constant search for what health really means and how it breaks down into disease. The bottom line, if you will, may come down to simple energy availability. If that is the case, then all disease processes, no matter their origins, would benefit from improving energy capacity.

We Need Your Help

Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism, unbiased by commercial interests, we allow minimal advertising on the site. That means all funding must come from you, our readers. Don’t let Hormones Matter die.

Yes, I’d like to support Hormones Matter.

Image by Jeyaratnam Caniceus from Pixabay.

Two New Cases of Beriberi-like Syndromes: Thiamine Deficiency in Modern Medicine

by Derrick Lonsdale MD, FACN, CNS

Published on January 9, 2018

13509 views

As a result of my participation in Hormones Matter, I receive quite a few emails that record histories of patients who have often languished with inexplicable symptoms, sometimes for years. I am going to record two histories here without identifying any possibility of the involved patients being recognized.

Patient number 1: Cyclic Vomiting, Hyper-salivation, Sensory and Neurological Issues

This is the story of a boy who had what was described as “chronic cyclic vomiting from 11 months until 24 months of age, sometimes 3 to 4 times a day”. Food refusal with chronic vomiting and severe weight loss (failure to gain) was described. His diet was recorded as consisting basically of chicken/beef and vegetables. Frequent use of Paracetamol for ear infections with fever was described. As an infant he experienced hyper-salivation, bad enough for wearing a bib 24/7. Extreme sensory issues were mentioned but were not specified. Dilated pupils from a very young age***, neurological issues with confusion, memory problems, speech difficulty and heart racing/palpitations were mentioned together with eye tracking difficulties. A high concentration of arsenic had been found, presumably in urine, although this was not specified. Candida, a form of yeast, had evidently been a frequent infection. He was reported to have Hashimoto (a thyroid dysfunction) and a high blood glucose ***. He exhibited complete lack of coordination, always “appearing drunk”, talking gibberish and repetitive behavior.

Discussion of Symptoms: Patient 1

Cyclic Vomiting

Sometimes known as winter vomiting, the cause of this relatively common condition is said to be unknown. Recurrent vomiting is one of the symptoms recognized for centuries in the thiamine ( vitamin B1) deficiency disease, beriberi. I had several patients with cyclic vomiting, described in our book (Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition) that responded to thiamine treatment.

Food Refusal

Appetite is governed in the lower brain by several hormones, explaining why a voracious appetite and food refusal could both be a signature of thiamine deficiency, depending on severity and chronicity of the deficiency.

Weight Loss

Severe weight and stature increase (failure to thrive), is a signature finding in familial dysautonomia, a genetically determined disease. Thiamine deficiency also causes dysautonomia. I reported a patient with eosinophilic esophagitis whose dysautonomia resulted in failure to thrive. With thiamine treatment his weight and height increased dramatically (see: Eosinophilic Esophagitis May Be a Sugar Sensitive Disease).

Ear Infections

Extremely common in children, this and jaundice of the newborn are both now known to be the result of inefficient oxygen utilization. Thiamine deficiency is an outstanding cause.

Excessive Salivation

The salivary glands are under the control of the lower brain and this fits with thiamine deficiency.

Extreme Sensory Issues

This is the result of inefficient oxidative metabolism in brain and has been a well known problem in thiamine deficiency beriberi. It is interesting that diabetics are sometimes pulled over and accused of drinking because of erratic driving and subsequent “drunken” behavior. I strongly suspect that this is a thiamine deficiency affect, because thiamine metabolism has recently been found to be closely related to metabolism in diabetes.

Permanently Dilated Pupils ***

This is a cardinal sign of sympathetic nervous system overdrive, fitting in with the diagnosis of dysautonomia.

Neurological Issues: Confusion, Memory, Speech, and Eye Tracking Problems

All of this is the result of inefficient oxidative metabolism in brain.

Tachycardia

This is the term for a fast heart rhythm and is a cardinal sign of dysautonomic sympathetic nervous system overdrive.

Urinary Arsenic

Pressure-treated wood in the United States contains a significant amount of arsenic and is generally touted as being the source for children using playgrounds. This is much more significant than arsenic in drinking water. Arsenic damages oxidative metabolism and could be contributive to the effects of thiamine deficiency.

Candida Infections

Candida is a common form of yeast that infects humans. It dislikes oxygen: consequently this infection is much more likely to occur in people whose oxygen metabolism is inefficient.

High Blood Glucose***

Of course, this means that the patient has some form of diabetes. Both type I and type II diabetes are now known to have thiamine deficiency as part of the syndrome. Alzheimer’s disease may be diabetes type III. Thiamine is absolutely vital in glucose metabolism.

Pattern Suggests Pyruvate Dehydrogenase Complex Disease

Pyruvate dehydrogenase is an enzyme that demands thiamine and magnesium in order to function properly. I would be willing to bet that this boy would be responsive to high doses of Lipothiamine and should be studied in detail by a physician who understands the possibility of inborn errors of metabolism. Note the two starred items above. The observation of permanently dilated pupils indicates excessive activity of the sympathetic branch of the autonomic nervous system. The high blood glucose is a sure indicator that thiamine metabolism is involved, even if there is insulin deficiency.

Patient number 2: ROHHAD

This is a little girl, age not specified. She was described as a patient with ROHHAD. This stands for “rapid onset weight gain, hypothalamic dysfunction and autonomic dysregulation”. The parent described this as “a very rare syndrome and only 150 cases have been recorded worldwide”. Children with this diagnosis are said to have similar symptoms. Most of them have central and obstructive sleep apnea. Many depend on CPAP. This child requires it only during sleeping but many other kids have tracheostomy and all are living on CPAP day and night.

Symptoms of patient 2: Sweaty Palms, Cold Intolerance, Tachycardia and More

At my request, the parent observed that there was no family history of alcoholism or smoking. The mother had been thinking of thiamine deficiency because of the child’s autonomic dysfunction. I have noticed that alcoholism and sugar sensitivity appear to be closely related genetically.

She has palm sweating. Father has blepharospasm (spasm of the eyelids) frequently, lasting for weeks at a time. She also has tachycardia (fast heart rate), excessive vomiting, cold intolerance with persistent cold extremities, peripheral neuropathy, binocular diplopia, double vision, gastrointestinal dysmotility, mood swings, and low pain perception are all symptoms of dysautonomia, the commonest cause being thiamine deficiency. Fortunately the family is working with a physician who had started thiamine treatment for this child. The parent closed with the remarks that “since she started TTFD she is having a fast heart rate at 140 beats a minute and low oxygen saturation with restless sleep. I decreased TTFD from 250 mg to 50 mg but my opinion is that she became more stable with oxygen saturation and pulse rate”.

Discussion of Symptoms: Patient 2

ROHHAD

Rapid weight gain, hypothalamic dysfunction, dysautonomia and sleep apnea are all included in this syndrome. I must point out that the word “syndrome” is always used for a collection of symptoms whose cause is unknown. In fact, all can be caused by thiamine deficiency.

Palm Sweating

Sweating is a result of sympathetic nervous system overdrive. She also has tachycardia, excessive vomiting, cold intolerance, peripheral neuropathy and double vision. Various forms of peripheral neuropathy are cardinal symptom in thiamine deficiency.

Gastrointestinal Dysmotility

The intestine is innervated by the vagus nerve which originates in the brain. This nerve uses a neurotransmitter known as acetylcholine, highly dependent on energy metabolism and therefore also dependent on thiamine. Japanese physicians have used thiamine derivatives for years to treat postoperative intestinal paralysis.

Mood Swings

I learned the hard way about mood swings in children when I found that the dominant cause was poor diet resulting in thiamine deficiency.

Low Pain Perception

Decreases in pain perception are described in familial dysautonomia, a genetically determined condition. Thiamine deficiency results in dysautonomia and may well be responsible for low pain perception.

Points of Consideration: Polysymptomatic Disease and Thiamine Deficiency

Both these children have fallen into diagnostic cracks. It seems only to be the persistence of struggling parents that do their own research and persist in trying to find an adequate explanation that addresses the plight of these children. To me, the problem is obvious. Polysymptomatic disease that affects so many body systems can only be explained by some form of energy deficiency, dependent on oxidative metabolism. Thiamine deficiency, arising from both genetic and nutritional abnormalities is a common cause. It could be a simple thiamine deficiency from diet but this is unlikely in the case of these two children who may have a genetically determined condition that is responsive to megadose thiamine.

We Need Your Help

Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism unbiased by commercial interests we allow minimal advertising on the site. That means all funding must come from you, our readers. Don’t let Hormones Matter die.

Yes, I’d like to support Hormones Matter.

Photo by Hush Naidoo Jade Photography on Unsplash.

A New Model for Medicine

by Derrick Lonsdale MD, FACN, CNS

Published on October 23, 2017

4897 views

What is a Medical Model?

In the Oxford English dictionary the word model is defined as “design to be followed, style of structure”. Then it follows that there must be a model to distinguish health from disease, that differentiates the two states of being. No disease can be treated without knowing exactly what caused it. Let us go back to Hippocrates, 400 BCE, who said “let food be your medicine and your medicine be your food”. What Hippocrates was saying was essentially that nutrition was the core issue in the maintenance of health. At this time and throughout the Middle Ages there was no model for the cause of disease. Consequently, treatment was extremely primitive and almost purely empirical. In the time of ancient Egypt it was believed that mental illness was caused by the presence of evil spirits in a person’s head. They bored holes in the skull to let the evil spirits out. If you think about that, perhaps it relieved the occasional headache because of increased pressure in the skull caused by a brain tumor. Hence, a few successes might have caused it to be retained as beneficial. During the Middle Ages, the only treatment that seems to have been used is bloodletting. It might have been temporarily useful in people with high blood pressure. A few successes yielded the conclusion that it was beneficial for all disease.

The First Controlled Experiment

Semmelweis was a 19 ^th century Hungarian physician. In those days, the incidence of puerperal disease (childbed fever) was absurdly high. Semmelweis made the observation that doctors, delivering their patients, entered the delivery room and went directly to their patients without changing their garments or washing. He came to the simple conclusion that the doctors were bringing something in with their hands that caused the problem. The obstetric ward consisted of a number of beds on each side of the room and Semmelweis directed that doctors delivering their patients on one side should wash their hands in chlorinated lime, while doctors on the other side of the room would continue in the old way. Of course, the incidence of childbed fever was so different that it did not need a statistician to document the difference. Semmelweis’s observations conflicted with the established scientific and medical opinions of the time, particularly as he was unable to explain what was on the hands of the doctors. Some doctors were even offended at the suggestion that they should wash their hands. It is truly an amazing vision of human behavior. Innovation carries with it loss of reputation for the innovator, no matter how successful the innovation. Well, of course everyone today knows that it was microorganisms on the hands of the doctors that caused the disease, but they had not yet been discovered. Poor Semmelweis wound up in a lunatic asylum and died in his 40s after a beating by attendants. Today, he is regarded as the first person to introduce antiseptic medicine.

The First Paradigm in Medicine: Microscopic Organisms

Most people are aware that the invention of the microscope, and the work of historical figures like Louis Pasteur, led to the discovery of organisms, that could only be seen with the microscope, caused what we now call infection. We are all familiar with the fact that a tremendous number of diseases are due to infection by bacteria, viruses or fungi. It was a perfectly logical conclusion that the development of treatment should be aimed at killing these organisms. This was the first paradigm in medicine, meaning that it was accepted by all. A glance at history will tell us that the search for medication that would kill these organisms was hard won. It was difficult to find something that would kill the germs without killing the patient and many patients lost their lives as a result of this search. The discovery of penicillin represented a dramatic change in perspective as it gave birth to the antibiotic age. Millions of lives have been saved. However, we are now entering an era where the development of antibiotic resistance is becoming an increasing problem. More and more potentially damaging antibiotics have been synthesized that present their own problems in therapy.

The Second Paradigm in Medicine: Immunity

It has been said that Louis Pasteur made the statement on his deathbed, “I was wrong: it is the defenses of the body that matter”. I believe that this may well become the second paradigm in medicine. So what are we talking about? Everyone recognizes that we have immunity but the average person has only the vaguest idea of what this really means. In fact, body defenses against infection are exquisitely complex and incredibly efficient when the immune system is healthy. The primary mechanism for health maintenance is exactly what Hippocrates said, not only the quantity but the quality of nutrition. By recognizing this, the concept is offered that preventive medicine, the use of nutrients based on a knowledge of the biochemical machinery that give our cells function, is the second paradigm.

Presently, we stimulate our immunity by the use of vaccines. However, each vaccine gives a protection to a specific microorganism, perhaps the best example being the flu. Most of us are aware that there are many strains of the flu virus and it may not be possible to predict the particular strain responsible for the “next epidemic”. Natural immune defense mechanisms recognize most invaders as “enemies”. Those whose adaptive/immune mechanisms cannot respond will succumb to the infection. Assisting the immunity mechanisms by making energy synthesis as efficient as possible and killing the “enemy” with maximum safety to the patient might just be the way of the future.

How the Body Responds to Environmental Stressors

Each one of us comes with a “blueprint” derived from our parents in the form of genes that carry a code called DNA. This code is unique for each person and provides the structure that makes up a living person. The body is composed of 70 to 100 trillion cells, all of which have to cooperate to produce what we call function. I think of it being like an orchestra where all the organs are made up of cells, each one of which has a specific specialty to provide its contribution. Like instrumentalists in an orchestra, the cells within each body organ have to work together. This requires a conductor, a function that is performed by the subconscious brain. Coordination is administered through an automatic (autonomic) nervous system and a bunch of glands known as the endocrine system that produce messengers called hormones.

Consider what happens when a person is attacked by a pathogenic Streptococcus, for example. The throat becomes sore, the marker of inflammation. Controlled and executed through the brain, it increases local blood supply, bringing white blood cells into the area and is part of a defensive process. Glands in the neck become enlarged and this is also a defensive process, designed to catch and destroy the germs beginning to spread. Body temperature becomes elevated because disease producing bacteria are most virulent at normal body temperature and their efficiency is reduced at a higher body temperature. A standard procedure in medicine for many years has been to reduce the fever and it has always seemed to me to be a disadvantage, based on this explanation. We sweat when the environmental temperature is high and evaporation from the skin results in cooling. When the environmental temperature is low, we shiver and the muscular activity produces heat to maintain body temperature. These are examples of how we are able to adapt to changes in our environment that threaten our well-being. All of this is purely automatic and the only thing to complete the picture is how our food (fuel) is used to create energy. Maximum efficiency of brain metabolism is mandatory. Assist and protect the “conductor”.

How We Create Energy: Enter the Mitochondria

Because any form of burning is the union of oxygen with the fuel, in the body it is termed oxidation. The process is complex and many vitamins and minerals are involved, besides calories. It has long been known that thiamine (vitamin B1) deficiency is the cause of beriberi, the disease that had plagued humanity for thousands of years. Because this deficiency affects every cell in the body, it can degrade the efficiency of virtually any organ. But because different tissues have their own rate of metabolism and the brain and heart are the two tissues that require fast and efficient oxidation, it is the cells in those tissues that are most affected. Therefore, thiamine deficiency has its major effect in the brain and heart, but they are not exclusive.

Glucose is the main fuel, but like any other fuel used to produce energy, it has to be ignited. Thiamine, much like a spark plug in a car, processes this ignition. All simple sugars taken in the diet are broken down to glucose. But before this happens in the body, dietary sugars have two effects. The first is a signal from the tongue to the pleasure zones of the brain. It is this sweet taste that makes sugar addictive. The second is that this excess of sugar overwhelms the capacity of thiamine to oxidize glucose to create energy. A person may have a perfectly normal thiamine level in the blood that is inadequate to meet the demand. It is the ratio of “empty carbohydrate calories” to the concentration of available thiamine that counts. I have called this “high calorie malnutrition” that seems to be an oxymoron since malnutrition is generally considered to be on the way to starvation. The patients with this form of malnutrition may be obese, remain relatively active, do not look ill and multiple symptoms are regarded by their physicians as “psychologic, or psychosomatic”. There appears to be no reason to seek laboratory evidence of malnutrition and the patient is written off as a “problem patient”. It is hardly surprising that the patient leaves the doctor’s office angry and tells friends that “the doctor told me that it was all in my head”.

The irony is that it IS in the patient’s head, but because of electro-chemical changes in brain metabolism. It has always seemed odd to me that physicians often consider that “psychological issues” are somehow “invented” by patients without thinking that every thought, every action, has a mechanism produced in a chemical “machine” called a brain. Distortions are the result of a combination of cellular energy deficiency (malnutrition), coupled with a potential genetic risk and perhaps a stress factor such as an otherwise mild infection/injury, or an inoculation. Any one of the three factors may dominate the clinical presentation, but in most cases the other two are involved.

A New Model: Genetics, Nutrition, and Stress

Throughout life each of us depends on our ability to survive in an essentially hostile environment. The first thing that it depends upon is our genetic inheritance that I have called “the blueprint”. But we also know that the “engines” of our cells, known as mitochondria, have their own genes in which the DNA is more susceptible to damage than our cellular genes. A new model must consider the fact that any stress requires energy in an adaptive response to any form of environmental attack resulting from a mental or physical problem or infection. The only way that we can protect the structural components of our bodies is by the use of the natural ingredients of nutrition, the ancient teaching of Hippocrates. The new science of epigenetics finds evidence that nutrition and lifestyle can make changes to our genes that might be beneficial or not, according to the circumstances. If a person has become sick from an excess of empty calories and refuses to change, the only way to treat that person would be by increasing the concentration of the missing nutritional ingredient in the form of a supplement. It is of paramount interest that in 1962 a paper was written in a prestigious medical journal. The author had found 696 medical journal manuscripts that reported 250 different diseases that had been treated with supplementary thiamine, with varying degrees of success. This suggests the possibility that health is produced by a combination of genetic influence, how we meet the daily impacts of stress and the quality of our nutrition. Disease results from, either genetic failure (cellular or mitochondrial), failure to meet stress because of energy deficiency, malnutrition, or combinations of the three elements.

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 by Sebastian Unrau on Unsplash.

thiamine deficiency - Page 11

Medical History

Major Life Stressors and Emerging Problems with Nutrient Absorption

More Digestive Problems

Catatonia-like Episodes upon Eating

Left Temple Headaches, Migraines with Visual Aura, and Cognitive Deficits

Diet and Malnutrition

Other Weird Symptoms

Visual Disturbances

Migraines With Aura

Allergy Shots and More Symptoms: Ophthalmoplegia, Dizziness, Speech Impairment

Medication Reactions

Thiamine Pyrophosphate Order Delayed

Ran out of Thiamine AGAIN!

Genetic Testing

Medications and Supplements

We Need Your Help

Share Your Story

Related posts:

You might be interested in

Publisher Discount

Related posts:

You might be interested in

Years of Pain, Fatigue, and Weird Symptoms

Resolving the Dizziness, Brain Fog, Dysautonomia / POTS with B Vitamins and Diet

The Missing Pieces: HACL1 and Phytanic Acid

Possible Secondary Pellagra

Going Forward: More Questions

We Need Your Help

Related posts:

You might be interested in

Epigenetics: How the Cells Adapt to the Environment

Starve the Mitochondria, Alter the Genome

Thiamine Deficiency and Gene Expression

A Constitutively Active Enzyme: What Could Possibly Go Wrong?

We Need Your Help

Related posts:

You might be interested in

History of Thiamine Research

What is TTFD?

Clinical Benefits of TTFD

Conclusion

We Need Your Help

Related posts:

You might be interested in

From the Unexplainable Comes Insight

High Dose Nutrient Therapies to Compensate for Energetic Demands

The Irony of Psychosomatization

Genes, Nutrition, and Energy

Thiamine and Energy

High Calorie Malnutrition: A Disease of Affluence

We Need Your Help

Related posts:

You might be interested in

Patient number 1: Cyclic Vomiting, Hyper-salivation, Sensory and Neurological Issues

Discussion of Symptoms: Patient 1

Cyclic Vomiting

Food Refusal

Weight Loss

Ear Infections

Excessive Salivation

Extreme Sensory Issues

Permanently Dilated Pupils ***

Neurological Issues: Confusion, Memory, Speech, and Eye Tracking Problems

Tachycardia

Urinary Arsenic

Candida Infections

High Blood Glucose***

Pattern Suggests Pyruvate Dehydrogenase Complex Disease

Patient number 2: ROHHAD

Symptoms of patient 2: Sweaty Palms, Cold Intolerance, Tachycardia and More

Discussion of Symptoms: Patient 2

ROHHAD

Palm Sweating

Gastrointestinal Dysmotility

Mood Swings

Low Pain Perception

Points of Consideration: Polysymptomatic Disease and Thiamine Deficiency

We Need Your Help

Related posts: