thiamine deficiency - Page 4

Notes On Thiamine Status During Pregnancy

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Thiamine pregnancy

Currently, I am researching thiamine status during pregnancy for a series of articles to be published by the newly formed Thiamine Advocacy Foundation. Over the next few months, I will be publishing snippets of that research, and of course, when the project is finished, I will let everyone know and provide links to the articles. Today, I want to discuss a study published in 1980 about thiamine deficiency in pregnant and non-pregnant women.

For this study, the thiamine status of 60, presumably healthy, pregnant women was assessed across multiple times points (second trimester, third trimester, and in the immediate postpartum. Not all women completed all assessments. Food diaries were collected for three days preceding each test time to identify thiamine intake and a lifestyle survey to assess contraceptive use, smoking and alcohol history was given. Samples and diaries from 20 non-pregnant women were collected as well.

To determine thiamine status the erythrocyte transketolase test with thiamine pyrophosphate activation was used. This is among the reasons I found this study useful. It is only one of only a few studies of this population using the transketolase test. Recall from Dr. Lonsdale’s discussion Understanding the Labs (and here), the transketolase test is arguably a more accurate measure of thiamine status than plasma, serum, and some measures using whole blood.

Using the transketolase test, researchers found that 30% of the non-pregnant women were deficient in thiamine as were 28-39% of the pregnant/postpartum women depending upon the phase of pregnancy. Importantly, not all women were deficient at all test times. This means that the deficiencies likely waxed and waned relative to other variables like intake and stressors. Intake was considered sufficient in all but 10 of the women and for those 10 women it was only minimally below the RDA. Additionally, the researchers reported that previous oral contraceptive use had no apparent effect on thiamine status during pregnancy but that there was a trend for an increased risk of deficiency with previous pregnancies.

While this was a small study, the percentage of women who were deficient in thiamine was striking, especially the non-pregnant controls. If thiamine is deficient before pregnancy, the risk of severe health issues across pregnancy increases. Here though, none of the women who were deficient in thiamine displayed the classical symptoms of thiamine deficiency, although details were lacking. Moreover, all of the women delivered presumably healthy children, or at least healthy weight children, as other parameters were not measured. Again, this finding is important because it suggests that either 1) what we expect to see with deficiency during pregnancy is not completely accurate, 2) that the persistence or chronicity of the deficiency matters, and/or 3) that it is not simply a deficiency in thiamine that causes some of the more severe complications of thiamine deficiency during pregnancy.

I have written previously about the mismatch between classically defined symptoms of thiamine deficiency and what we are more likely to see with modern diets and stressors. I suspect this applies to pregnancy as well. I have also written about how thiamine status is likely to change relative to intake and demand. Rodent studies have shown that the typical neurological symptoms of deficiency do not appear until there is 80% decline of thiamine stores. Since we store a little over two weeks of thiamine, one would have to completely eliminate intake for more than a week before those symptoms might emerge, and even then, it might be a while before they were recognized. This is certainly a factor with hyperemesis gravidarum, the severe vomiting that some women experience during pregnancy but perhaps not in non-HG related pregnancies.

It is important to note, however, HG and thiamine deficiency go hand in hand. Thiamine deficiency, along with other deficiencies, may trigger HG (think gastrointestinal beriberi) in the first place, and once the vomiting begins, will easily deplete thiamine stores. None of the women in the current study developed HG, however, or other complications, so that leads me to believe, that we need additional triggers and we need persistent or chronic thiamine deficiency before noticeable complications arise.

In this study, all we have are indications of deficiency at specific points in time. We have no evidence of how long those deficiencies were present or whether other variables were somehow buffering maternal and fetal health such that the typical complications associated with thiamine deficiency were not observed. Even so, a finding that upwards of 30% of a test population of women, both non-pregnant and pregnant thiamine deficient speaks to how common this deficiency may be and how close to the precipice of more severe health issues a percentage of the population resides. Although observable changes in health were not reported or perhaps even recognized in this report, knowing what we know about thiamine’s role in energy metabolism, it is not unlikely that there were many negative metabolic patterns brewing just below the surface.

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This article was published originally on November 29, 2023.

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Refeeding Syndrome in the Context of Thiamine Deficiency

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Refeeding syndrome in thiamine deficiency

Although this has been mentioned many times in posts and in the comments of readers on this website, there still seems to be a lack of understanding. The commonest complaints have been that “thiamine caused side effects” or “I was allergic to thiamine”, inevitably causing the complainant to discontinue it. I want to emphasize the important meaning of these seemingly adverse effects by illustrating a typical case in my own experience. First of all, please understand that thiamine deficiency has its major effects in the lower part of the brain. It is this part of the brain that controls the automatic (autonomic) nervous system that orchestrates the functions of all the organs in the body. Thiamine deficiency has its dominating effect by damaging this system and the result is known as dysautonomia.

Recognizing Thiamine Deficiency Syndromes

One day I was in conversation with a young woman and was trying to describe the huge number of symptoms that result from dysautonomia. When I finished listing them, I was surprised when she said that I had exactly described the symptoms that she had suffered for years. I had no prior knowledge of this, believing that she was completely healthy. She told me that this polysymptomatic condition had been present for as long as she could remember. Apparently it had never been understood by any physician that she had consulted and she had come to accept that it was “just the way that I am made”. She was in her early thirties and it must have required a lot of courage to do the work for which she was employed. Unrelenting fatigue dominated her life, and this is a major clue to her problem.

Symptom Exacerbation: Refeeding Syndrome

I advised her to start taking thiamine and magnesium supplements, starting with a low dose and advising her that the symptoms would become worse for an unpredictable period of time (refeeding syndrome). Note that this individual was known to be intelligent, was fully employed and that nobody was apparently aware that she had any health problems. Later she told me that after she started the supplements, for a month or more she had suffered an excruciating exaggeration of her many symptoms. Trusting that I knew what I was talking about, she persisted with the supplements. This is of great importance because without this information it might be interpreted as “side effects” and the nutrients withdrawn. It also would probably accompanied by anger and the ultimate symptomatic relief never experienced. Using her own words she then said “after about a month of taking the supplements, all my symptoms disappeared and my energy was better than any that I had experienced in my whole life”.

I will try to interpret what was happening here as an example of refeeding syndrome. It is important to understand that the many symptoms experienced by this woman were due to cellular energy deficiency in the brain. Their variability may have included emotional symptoms such as anxiety, depression, or anger without obvious cause because they would be the result of exaggerations of normal brain activity. The lower part of the brain is highly sensitive to energy deficiency and because it organizes all bodily functions, it can give rise to heart palpitations, chest pain, unusual sweating, pins and needles in the extremities, nausea, abdominal pain, vomiting, insomnia, constipation, diarrhea, or abnormal sense of balance including vertigo. Body pain that has no observable cause (hyperalgesia) or a pain response from a stimulus that does not usually cause pain (allodynia) may occur.

Refeeding Syndrome in Children

A 14-year old boy with sugar induced thiamine deficient eosinophilic esophagitis suffered agonies of hyperalgesia and screamed when I touched his abdomen (allodynia). Postural Orthostatic Tachycardia Syndrome (POTS) is quite a common variant which is particularly frightening to the patient. Let me emphasize once and for all, when symptoms like this go unrecognized, sometimes for years, they become temporarily exaggerated if the necessary nutrients are provided in too high a concentration. Whether this be a single vitamin, a group of vitamins or whole nutrition, this syndrome must be expected. A gradual introduction of the appropriate nutrients is mandatory. Because thiamine is so integral to energy metabolism, I found over the years that it was the most important. Because young children have not been exposed to malnutrition for too long because of their age, refeeding syndrome is seldom if ever encountered. The syndrome is directly related to the time of exposure to malnutrition and its severity. It is therefore an effect in adults and occasionally in adolescents..

Whether intelligence is a genetically determined gift or whether it is acquired during life, the brain consumes a disproportionate degree of energy that can only be met by an appropriate ingestion of food and water. If this is inadequate, symptoms begin to register the inadequacy by producing a sense of fatigue as the dominant one. It is the way that the brain signals its lack of cellular energy. The symptoms are easily removed if the underlying cause is recognized early. Because in many cases they are not recognized and the malnutrition may continue, it is not very surprising that cellular damage would be expected gradually to accrue. Perhaps chronic neurodegenerative disease may follow.

From Catabolic to Anabolic Metabolism

The normal states of damage and repair (anabolic metabolism) would be inadequate and a state of gradual breakdown and inadequate repair would be predicted (catabolic metabolism). Because thiamine deficiency causes the condition known as beriberi, I would like to state once more that the English translation of this Chinese word is “I can’t, I can’t”, severe, intractable fatigue being the dominating effect. Although the refeeding syndrome is poorly understood according to current medical literature it is apparently related to a rapid change from catabolic to anabolic metabolism. The misguided attempts to re-nourish the victims in concentration camps at the end of World War II resulted sometimes in their death. It is at least understood that correcting catabolic to anabolic metabolism, whatever produced the abnormal state, demands low doses of food in starvation and low doses of supplementary vitamins in the long term effects of high calorie malnutrition.

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

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This article was published originally on January 6, 2020. 

Rest in peace Dr. Lonsdale, May 2024. 

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Longstanding Thiamine Deficiency Ignored By Doctors

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Thiamine deficiency isn't all in your head

I would like to begin sharing my story, hoping to help others. My journey is from a nurse’s perspective. I recently learned I am thiamine deficient and likely have been for years. Thiamine deficiency affects the mitochondria, causing a disease process known as beriberi. Beriberi mimics many other illnesses, making it very difficult to diagnose. Let me begin by giving you a background about the woman I was before thiamine deficiency depleted my entire being.

I have always been highly driven. I am perfectionist to a fault. I was an honor student in high school, an active- athlete, a cheerleader for four years. I loved swimming, ice skating, rollerblading, skiing, and all sports. I led many extracurricular activities throughout high school and college. As the oldest of 5 siblings, I was the family leader and caregiver as well. I was always strong mentally and physically. I had survived spinal meningitis at age 5 years, after receiving my last rites while hospitalized in isolation several months. I lost my father shortly thereafter, but I survived.

I was a successful RN for nearly thirty years; a gynecological oncology nurse the first 20 years, and a postpartum nurse caring for mothers and their newborns the last ten years. I was married and had two children and even though I worked full-time, I was an avid volunteer, for activities involving both daughters through their elementary and high school years. I was the first and only woman president of my neighborhood association, organizing many monthly events throughout the year. I cared for my mother through ten years of Alzheimer’s. No family member was hospitalized without me as their private duty nurse advocating. I cared for my father in-law through colon cancer, then moved my mother-in-law in with us for 15 years after he died. I watched over her into her 90’s. Then I suffered loss upon loss: my mother, my father-in-law, several aunts, and two beloved family pets, followed by an awful divorce from my high school sweetheart.

Looking back, I understand why my marriage fell apart, I became a woman I barely recognized. I was in pain all the time. I was tired unable to be the “active fun loving Jane,” I had once been.

In 2006, I developed degenerative disc disease (DDD) in my neck, which ultimately led to a cervical fusion. Nevertheless, I returned to hospital nursing 8 weeks later and worked until I could no longer get through the nonstop days without pain. My nursing manager talked me into management after 28 years as a bedside nurse, which I loved. Then, I suffered a lower back injury that, together with my neck issues, incapacitated me from my nursing career. After losing my career, my marriage, and my home, I moved away from the home town which I loved. Multiple losses, stressors, and what I now believe was thiamine deficiency had me suicidal.

I tell you this, because the thiamine deficiency was insidious. It accrued over time. I was performing and had more energy than most… until one day, I didn’t.

My Silent Demise: Unrecognized Thiamine Deficiency

As I mentioned above, I developed DDD in 2006, and as result, I have suffered for years with intermittent nerve pain and muscle weakness. Over the years, the pain and weakness progressed to the point where by 2019, I could no longer walk or function. I had great fatigue, insomnia, depression, anxiety, and lack of energy. This was in addition to GI distress and signs/symptoms of IBS irritable bowel syndrome. I also had serious bladder issues of great urgency, leaking and even incontinence at times. Over time, I developed significant brain fog and cognitive difficulties. This included a “loss of words,” an inability to read and retain information or eventually, to write; all of which I had always loved doing. I began having memory issues and my nervous system seemed to be shutting down.

Looking back on my history, I had been hospitalized for chest pain 3-4 times ruling out pulmonary embolism or heart attacks. I have had a vitamin D deficiency for over 10 years despite supplementation and good diet and plenty of sunshine. My platelets ran high on and off for years. A hematologist ruled out many disease processes through lots of blood work. He even did a hip bone marrow aspiration and never found answers.

My blood pressure at one point was 200/100. I had tachycardia documented on EKG and on my own nursing checks. Heart palpitations were common. I sought the care of a few cardiologists over the years and had a number of cardiac tests all with no answers. I was frequently dizzy, seeing stars, and nearly passing out on many occasions. Five years ago, I was severely depressed and suicidal. I had lost so much weight, and looked anorexic at 108 pounds. Looking back, I have no idea how or why I had such rapid weight loss. Then the weight issue shifted.

By the end of last year, I had difficulty walking. I gained weight and have now been walking that fine pre-diabetic stage. I seem to be insulin resistant now. Added life stressors, once again caring for my sick and aging 81 year old aunt with multiple medical issues, has led to self-neglect.  I became short of breath on exertion, weak and faint. I began losing my hair. Thankfully, I once had a thick full head and so the hair loss was not immediately noticeable. Even so, I noticed, and I begged my doctor to help me learn why my hair was falling out and thinning so much but my concerns were made light of.

I pleaded with many doctors, asking to learn the cause of my multi-organ system’s failings. I suspected they were medication effect or vitamin deficiency related but several good doctors rolled their eyes when I begged to be tested.

I grew weaker and weaker, sicker and sicker as 2019 came to an end.

The Laundry List of Tests and Doctors Conclude: It’s All in My Head

An MRI in January 2020 showed cervical myelopathy but not significant enough to warrant more surgery (THANK GOD). The orthopedic surgeon and his nurse practitioner, offered Gabapentin (as did 5 other doctors) and physical therapy (PT). I refused the gabapentin because it had made me incoherent in the past. I agreed to try PT but was frustrated, since I had tried physical therapy more times than I can tell over the past ten years. This last time, in February, just the PT evaluation magnified all my symptoms and I barely walked back to my car. Returning to my vehicle, I felt like I was on fire with burning nerve/muscle pain all over.

Again, I adamantly refused meds without learning the cause.

I was sent to have an EMG (nerve-muscle functioning testing). The EMG showed multi-nerve damage, or “multiple peripheral neuropathies.” That was in March of this year. I had been twice before to this same physiatrist having EMG’s years prior due to ongoing “nerve pain.” Like many other doctors, he never suspected thiamine deficiency and implied that it was “all in my head.”

I was sent to another consult, a Brown University rheumatologist, who basically told me the same thing that my pain was “in my head,” as most docs do seeing history of “depression and chronic pain.”  On exam, I actually jumped when he touched my outer thighs and various areas on my body. I was super “nerve sensitive,” which he was attributing to “my mind.” Outer thigh pain/ sensitivity was a symptom of thiamine deficiency I’d later learn. After my RN daughter, acting as my advocate, spoke on my behalf asking for nutritional deficiency testing to rule out causes, he tried ordering labs but had little knowledge of what to order and “could not find the transketolase test or a simple Vitamin B1 test on my screen,” he replied. To appease me, he ordered multiple other labs and sent me on my way with no diagnosis and no return appointment.

For the multitude of GI symptoms, I was sent to a caring gastroenterologist who performed a colonoscopy and endoscopy with insignificant results and biopsies all normal. He too was empathetically puzzled, urging me to request a thoracic MRI due to my history of degenerative disc disease. Upon exam, this doctor was alarmed at my sensitivity at my breastbone area when touched. It was painful and clearly inflamed.

I had all the symptoms of multiple sclerosis (MS) too, so I had a brain MRI with and without contrast that I asked for after researching my symptoms, wanting to rule out MS too. The MRI showed: “a single small focus of flair hyper-intensity within the frontal lobe white matter, nonspecific and could not rule out demyelinating disease or MS…”

They ruled out “pinched nerves” in a thoracic MRI, recommended by the GI doc after not finding answers to my GI symptoms. I had repeated X-rays and a lumbar MRI having a lengthy history of lower back pain too.

The lumbar MRI incidentally found gallstones which sent me to a surgeon who recommended gallbladder removal. In this COVID environment, I have minimized symptoms with better diet and supplements thus far.

Discovering My Thiamine Deficiency: A Bit of Research and a Bit of Serendipity

In February 2020, I had begun reading the book “Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition,” written by Dr.’s Lonsdale and Marrs. From the case studies and the research, I knew that I had thiamine deficiency. The trick now was to get someone to believe me. I brought the book to an upcoming neurologist appointment. Although, with each of the 7 previous consults, blood work was done, it was this last consult, with an astute neurologist, that I found out why. He knew after examining me and listening to me that I was deficient in thiamine. He took the time to research my history and found that I’d been diagnosed as thiamine deficient 5 years ago, but sadly, no one told me. In 2015, lab tests showed that my thiamine was 6 nmo/L , below the lab’s reference range of 8-30 nmol/L. I was still deficient in thiamine in February 2020 with a result of 7 nmol/L. He explained that I “needed to take 100mg thiamine daily, starting immediately and that it would likely take 6-12 months to hopefully reverse symptoms.” He also indicated that I would need supplementation for life now. As I have continued to research and read about thiamine deficiency, I learned that I would likely need much higher doses of thiamine, in the form of something called TTFD. TTFD is a synthetic thiamine that crosses the blood brain barrier getting into the cells better.

A Possible Family History of Latent Thiamine Issues

I continued reading, researching, and learning from case studies and groups. Thiamine deficiency is much more common than thought today. It can be passed on at birth in an unknowing deficient mother. Looking back, I fully believe my mother was deficient given her history of problems in school, high anxiety, and severe depression on and off for years. Her symptoms worsened with divorce when she was still pregnant with her fifth child. Each of her children were born only 12 – 13 months apart! I recall her getting dizzy, feeling faint often. She suffered with leg pain for years.

I am most concerned over the genetic factors influencing me and my family. The first stages of thiamine deficiency see thyroid issues, which my mother, sister, and aunt all had/have. Diabetes runs in my family: my grandmother, aunts, sister, and I’m now at the pre-diabetic stage. Cardiac issues are often seen: my grandmother, mother, aunt, and I have had them. GI issues also are noted in multiple family members. The most worrisome disease is Alzheimer’s disease, which is often seen in late stages of thiamine deficiency according to research. My grandmother, mother, many of her sisters (now deceased) all had Alzheimer’s disease. I am currently seeing early Alzheimer’s and short-term memory loss in my 80 year old aunt and her 75 year old youngest brother.

I have been monitoring my aunt who could not tolerate the Alzheimer’s medications that she was given. I began using thiamine with her in March 2020. We began with a good B-Complex having 100mg thiamine mononitrate and then added 50 mg Allithiamine in mi- July when she got very sick with what I believe was Covid-19. I kept her on this dose through August and then upped it to 100mg in September. I am now seeing improvements. Her energy has improved greatly. Although still forgetful, her memory is improving. She recovered after three weeks with the virus, yet suffered with extreme fatigue many weeks to follow. I will write about her story in a subsequent post.

The Path to Recovery

As a nurse, journaling my symptoms, diet, supplements, and vital signs, etc., I have watched my symptoms, rated on a scale of 1-10 with 10 being worse, go from 7-8s down to 3-4s over the last 6 months, after beginning thiamine replacement. I have been thoughtfully self-experimenting, slowly increasing my TTFD, using the brands called Allithiamine and Thiamax along with magnesium and potassium for proper absorption. Since rebalancing thiamine often brings out other deficiencies, I alternate a good multivitamin/mineral supplement and B-Complex and take probiotics for good gut health and better absorption. Over the last 6 months:

  • My neuropathies, which were tested pre-thiamine in February 2020 and again in June 2020 after a little over 5 months into thiamine treatment, are reversing.
  • I am off all pain meds, antidepressants, and other scripts (weaned under supervision SLOWLY).
  • I am happier, calmer, healthier overall.
  • I am most impressed with my renewed desire and ability to read, write, and research and retain information learned!

I’m now so hopeful for a good recovery by next spring. I understand I will need thiamine supplementation for life now, hopefully in lower doses eventually. Time will tell.

Drugs Don’t Solve Vitamin Deficiencies

With this experience, I have learned that there is no one easy answer for all as far as dosing goes. Replenishing thiamine requires careful rebalancing of other vitamins and minerals, as most people have multiple nutritional deficiencies. Prior to supplementing with TTFD, my labs showed Vitamin D deficiency for over ten years and low thiamine since 2015. If not for the COVID environment, I would have been hospitalized for IV thiamine treatment and looking back now, probably should have been.

I hope my story here can in turn help others find answers which sadly so many Western doctors seem to miss. Nutritional knowledge is barely taught in medical school. I hope that changes, as malnutrition is often the root cause of many diseases. I know all too well how frustrating it can be to go from doctor after good doctor who only know what they are taught: “treat symptoms with drugs.”  Sometimes, it takes one’s own persistence, research, and being proactive to regain wellness. Of course, wellness means cleaning up the diet by avoiding processed foods, carbs, and sugar. Recovery takes eating clean, whole organic foods mainly. It means balancing exercise, sunshine and good mental health. It takes looking at your environmental toxin exposures. It means DE-stressing and cutting back on EMF’s. It takes changing your lifestyle but most importantly, listening to your body and allowing rest and recovery and above all, a well-balanced life.

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 Marija Zaric on Unsplash.

This story was published originally on October 12, 2020.

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Childhood Seizures Precipitated by Thiamine Deficiency

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seizures thiamine deficiency

The seizures started for the first time with a frightened expression in my then 4 year old precious daughter’s eyes, and I thought she had seen a ghost. She held her chest, looked wide eyed, ran over to me and buried her head into my stomach where I felt her heart beating hard and fast. It lasted a few seconds and then I reassured her and on went on. She said it was like strong butterflies in her belly. It also was the morning after her lovely grandparents left after a 3-month visit back to Ireland and we were all very sad.

For approximately one year prior to this, she had been complaining of stomach aches, top and bottom, occasionally under her ribs. She had reduced appetite and a very worrying paleness. She also was very car-sick so we had to prepare for longer journeys. I had been to the ER after Christmas lunch when she had terrible stomach pain. She was checked to be ‘fine’ but I was advised to see a pediatrician to follow up.

Panic Attacks or Seizures?

Basic blood tests confirmed she was in ‘great health’, with the only thing they found in a stool test being h-pylori. So it was their opinion that she wasn’t having seizures but instead must be anxiety/panic attacks as she is a sensitive child. I was always skeptical, but in absence of any other data, we waited a long time for the referred psychologist. After 3 sessions, I realized they had no intel and were chasing the wrong dragon. I kept saying she looked somewhat unwell. The seizures were happening quite infrequently then, perhaps one episode a month, or every 2-3 weeks, but then when she started kindergarten they ramped up a little more frequently. She would stop, look to be catching her breath, hand twisting for a few seconds and then it was over. I thought it was a reaction to the food they fed her there that we didn’t have at home, or a recent childhood vaccination or that she hated being away from me there. I also noticed she reacted with bad behavior and potential episodes after certain foods- e.g. ice cream especially and any food dyes/flavors. So our already healthy diet went up a notch to exclude these. I also did gluten and dairy free on advice from naturopaths. It was strict and sad.

Then these episodes changed to resemble a seizure more directly, not a panic attack. I got rid of the useless pediatrician who was actively gaslighting me to try to minimize the symptoms or their own incompetence and I demanded to see a neurologist. It was again a very long waiting game. When the day came, we were very nervous but were looking forward to some potential answers. He was a neurologist at a prominent Children’s Hospital, so I had high expectations. I still had many questions and areas to workshop but after he ran through my extensive notes and a video I took, he said ”let me stop you, She has epilepsy and ‘NOTHING YOU DO WILL EVER MAKE A DIFFERENCE. She will need medication for life and if that fails an operation”. This was also via video link, as it was during a Covid lockdown. No physical examination and a script sent in the mail. I accepted these, as I know you don’t refuse unless you want trouble, but my intention was to never band-aid or experiment, especially not with a young child and my family’s history of sensitivity to medication. Thank god he lied so blatantly when he said ”there’s no side effects from the anti-seizure meds” to know we weren’t dealing with the truth or someone who could be trusted.

We did another two MRIs, but they were clear. They wanted a third with dye contrast but I refused that and as I learned more about her case, know why I felt so strongly about that.

A Parade of Doctors

We embarked on the alternative/functional medicine pathway, as that is something I am familiar with. I didn’t realize how challenging it was going to be. We went from one to the other. I was constantly seeking experts who possibly knew more than the last. I needed help to decode this horror. I know a healthy child doesn’t get a whisper of issues that then progress to a scream over years for no reason.

With each new practitioner, we did another test. This included blood tests, stool test, hair tests, OAT test, Pyrrole and extensive Genetic testing. She was found to have higher copper ceruloplasmin to be treated simply with zinc, which was always met with a seizure so we stopped that. She had high vitamin D and B12, but another test found that potentially wasn’t a true representation. It can be in the blood reading but not necessarily in her cell. This is where you really throw your hands-up and say what chance do we have if some test results can also be falsely represented!!!!!

The genetic testing provided the best clue that we weren’t dealing with an easy case- she had heterozygous compound MTHFR, and many other compromising genes that are not ideal on many pathways, especially detox. This also got me remembering how I haven’t felt optimal for years. I put it down to extreme stress with my daughter. A huge thing I always wanted to understand was why I was so incredibly sick with Hyperemesis Gravidarum the entire pregnancy with her. I have always believed this had to have impacted her somewhere but could never nail down a connection.

After 5 naturopaths and numerous consults from other medical professionals, listening to one bogus diet restriction after the next, many different versions of expensive supplements that basically all triggered her. Nothing was working. She was having seizures weekly or more particularly is she was sick or overly stressed. The closest theory I could deduce of was a type of MCAS or histamine intolerance and the symptoms were:

  • Crying out prior
  • Frequently occurring in sleep waking her bolt upright
  • Hyperventilation/can’t get air
  • Big scared eyes
  • Drooling, disorientated
  • Body shaking, head was twisting hard to the side like dystonia, arms curled, torso completely contorted.

This would last for about 30 sec-1 min. The horror of witnessing this is imprinted on my soul forever. She began to lose balance so we would have to grab and hold her and I would blow hard in her face to try to get it to finish. It started to become dangerous if we weren’t around to catch her.

I also simultaneously worked back one item at a time to try to fix every variable I could, including environmental. There was a mold spot in our house in the room she slept in the bathroom. It took a long time to get repaired, I pondered about that exposure and if the builder actually fixed the leak properly. Our awful neighbor had smoky barbeques numerous times a week on the fence-line using building offcut wood. The smoke permeated our house. We sold our house to see if that made a difference and moved to the country with my parents’ house in the green clean air.

Thiamine and Riboflavin Deficiencies With Genetic Underpinnings

I finally found a practitioner trained in epigenetics with a naturopath background as I wanted someone like Ben Lynch. His YouTube videos were the only things that made sense to break down a complex health issue. She was a blessing and truly eclipsed the level of detail of knowledge (and empathy) by all others. She looked at the OAT test (shown to 5 people previously) and saw immediately she had very high lactic acid and some other markers indicating thiamine deficiency, critically followed by a riboflavin (B2) deficiency. She advised to not give a B complex and work through one at a time.

When we tried to treat this with thiamine and a B2 capsule. I am sure she had a paradoxical reaction as she had 8 seizures in the night. It was horrifying. I wanted to abort this plan like so many other failed attempts, as I never prolong anything that’s not showing positive traction, but something told me to break it down and do one step at a time. I went back into her genetics myself and looked at the thiamine related genes. She had homozygous defects in a key thiamine transporter (SLC19A2) and an enzyme (thiamine pyrophosphokinase – TPK1) that turns free thiamine into its bioactive form thiamine pyrophosphate. She also had SNPs in several other key thiamine genes, in addition to SNPs in several other mitochondrial genes.

I also came across and watched Elliot Overton’s Thiamine videos on YouTube and how to correctly dose-up. I also read many insightful articles on the Hormones Matter website. I tried again with low dose of b1 (about 5mg), some magnesium and potassium-coconut water. The seizures, in the midst of a horrible flare, stopped immediately and didn’t return for over 2 months. I dosed twice a day and worked up to 50mg of thiamine in total, which is where she is currently. She also got much better color in her face. It truly felt like a miracle!

What Else Are We Missing?

The miracle, however, ended and the seizures have been creeping back in and I’m not sure why. They seem not quite as severe in presentation, however they still occur about once a week to every 2 weeks. I need to understand why and how to help her as my intuition screams at me to find the answer, and quick! She is now 8 years old and I am struggling to comprehend any more of her childhood being stolen.

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

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This article was published originally on September 11, 2023. 

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Thiamine and Heart Function

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Since there are many posts on this website about thiamine, it is entirely possible that some readers will regard it as being an obsession of the author’s. I can well imagine a reader believing that an explanation for so many different conditions is the fruit of such an obsession. I will counter this by stating that a paper in a prestigious medical journal reported 696 separate papers in which over 250 human diseases had been treated with this vitamin as long ago as 1962. I think that the explanation for recognizing the place of thiamine in human metabolism is a professional lifetime of clinical observation, resulting in the conclusion that disease is a representation of cellular energy deficiency. To use a simple analogy, spark plugs used in older cars were necessary to ignite the gasoline. Loss of a single plug made the engine run badly and if they were all affected, the car became completely useless. I have used the analogy frequently: thiamine deficiency is like an inefficient spark plug in the engine of a car.

Heart Disease and Beriberi: Case Stories

Heart disease has been central in beriberi, the classic thiamine deficiency disease, for centuries and the painstaking efforts that uncovered thiamine deficiency as the cause is unfortunately a little-known saga of human effort. Modern physicians have been completely convinced that no vitamin deficiencies exist in America, because of vitamin enrichment by the food industry. So is there any evidence that physicians are beginning to wonder whether thiamine plays a part in modern heart disease? This post is designed to show that there is indeed an awakening that could make a big difference to the role of cardiologists in treating heart disease.

Before I go to some medical literature, I want to describe a personal experience that occurred many years ago because it illustrates the incredible psychological resistance of the medical community to a vitamin deficiency. I was a pediatrician at Cleveland Clinic at the time. In the medical hierarchy, a pediatrician is regarded as being largely ignorant concerning disease in adults. A 67 year old anesthesiologist at a Columbus hospital reported to his colleagues with the symptoms of heart failure. He was subjected to heart catheterization and found to be perfectly normal in that respect.

His son was in medical school and studying his father’s case, he came to the conclusion that he had beriberi. For some reason unknown to me, the patient was referred to cardiologists at the Cleveland Clinic. Because my colleagues knew of my particular interest in thiamine, I was asked to see the patient. The story he gave me made the son’s diagnosis virtually a guarantee. Each day, as he went to get into his car in the morning, he would get the “dry heaves” in the garage. He would drive to the hospital where he gave anesthesia to as many as 10 patients. He would then go to the pediatric ward and cut himself a large piece of chocolate cake. When he got home he was too tired to eat dinner and would go to bed. I gave my reading of the case in the patient’s record and had no further contact. He was returned to the Columbus cardiologists and although I believe that he continued to receive thiamine, he died. I never received any information concerning his further care or whether the cardiologists really believed that this was beriberi. One can only conclude that the state of his heart was precarious and the history of thiamine treatment in beriberi had already showed us that there was a “tipping point” beyond which there was no response to thiamine treatment. Whether the cardiologists were aware of this or not is unknown. It is possible that his failure to respond may well have caused them to reject the diagnosis. What really impressed me was the extraordinary resistance to this diagnosis.

I am reminded of another case in my experience. There was a lady pathologist at Cleveland Clinic who was known to be brilliant. I visited her in the Department of Pathology for a reading on one of my patients. She told me that she was so utterly fatigued that a few days previously she had turned around on her way to work and gone home. I found to my amazement that she had a chocolate box in every room in her house and would take a chocolate at random as she went around her house. Without further advice I simply suggested to her to discontinue that practice and to take a supplement of thiamine, whereupon she recovered quickly. Fatigue is a symptom arising in the brain that notifies its owner of energy deficiency and undue fatigue is a logical result in beriberi.

Recognizing Vitamin Deficiencies in Disease

The problem with thiamine deficiency is that a physician has to change his attitude radically towards the cause of disease. This is because the underlying mechanism is derived from cellular lack of energy. If this is not perceived, a physician can be puzzled by a combination of heart and nervous system disease in a single patient. In the present medical model, he believes that he is confronted with two separate conditions.

Because of this resistance, in 1982 I joined a private practice specializing in nutrient-based medicine and began seeing adults as well as children. I joined a group that came to be known as the American College for Advancement in Medicine (ACAM). This relatively small group of physicians had all come to the same conclusion: nutrient-based therapy is, or should be, the methodology of the future. Many of these physicians were practicing alongside their orthodox colleagues in their local hospitals. One of my

ACAM friends told me the following story. He had a patient in the hospital with a pneumonia caused by antibiotic resistant infection. Together with the antibiotic treatment, he had given the patient intravenous vitamin C and she recovered. A patient in the next bed was under another physician with the same pneumonia and my friend approached him, suggesting that he tried the use of the same treatment. He was told to mind his own business and the patient subsequently died. I know of no better example of resistance and rejection of a principle that has yet to reach full acceptance in American medicine. As long as the psychological resistance to vitamin deficiency remains, it is seldom considered. I am happy to say that this resistance is beginning to break down as we shall see by looking at some of the recent medical literature. Not only that, the therapeutic use of vitamins in pharmacological doses it gradually being recognized for its therapeutic value.

Recent Reports of Thiamine’s Role in Clinical Care

Hear what a physician wrote as recently as 2015. The title of the paper is “Thiamine in Clinical Practice” and the author notes that the active form of the vitamin plays a role in nerve structure and function as well as brain and heart metabolism. Unexplained heart and kidney failure, alcoholism, starvation, vomiting in pregnancy or intestinal surgery “may increase the risk for thiamine deficiency”. Understanding the role of thiamine as a potential therapeutic agent for diabetes, some inborn errors of metabolism and neurodegenerative diseases all warrant further research. Surely, this is an indictment of our present approach by merely trying to control symptoms instead of addressing the primary cause.

A group of Canadian physicians stated that “the management of heart failure represents a significant challenge for both patients as well as the health care system in industrialized countries”. The abstract of their paper notes that thiamine is required in the energy-producing reactions that fuel heart contraction. Previous studies have reported a wide range in the prevalence of thiamine deficiency in patients with heart failure and the impact of its supplementation in patients is inconclusive. Of course, Dr. Marrs and I are appalled because such treatment is not only easy, it is completely non-toxic and therefore safe. If there is clinical evidence, why not use a non-toxic agent? However, the psychological restraints of being accused of being a charlatan are very real and can expose a physician to colleague ridicule.

Another paper reported that a total of 20 articles were reviewed and summarized. Recent evidence has indicated that supplementation with thiamine in heart failure patients has the potential to improve heart contractions. These authors recommend that this simple therapy should be tested in large-scale randomized clinical trials to further determine the effects of thiamine in heart failure patients. Diuretic treatment for heart failure may lead to an increased urinary thiamine excretion and in the long-term thiamine deficiency, further compromising heart function. Nine patients with diuretic treatment for chronic heart failure were studied with thiamine supplementation, producing beneficial effects on cardiac function. The authors state that subclinical thiamine deficiency is probably an underestimated issue in heart failure patients. It has even been shown that thiamine pyrophosphate, the active form of the vitamin, prevents the toxic heart injury caused by the cancer treating agent cisplatin. Dietary thiamine that has not been activated by the body did not prevent this.

It has been known for some time that thiamine in the diet has to be absorbed into the body by means of a protein known as a transporter of which there are quite a few. These transporters are under genetic control and absence of one or more of them will make it difficult for a given person to obtain an adequate amount of thiamine from diet into the part of the body where that thiamine transporter is active. A new thiamine transporter has been discovered whose genetic variants have an effect on blood pressure.

Although this post is about heart disease, I want to end by pointing out that vitamin treatment goes well beyond the consideration of just heart disease. Several years ago I received a letter from an aging physician who had specialized in OB/GYN. This letter was so poignant that I am repeating some of this letter:

I am writing to you, because I have found another mortal being who is particularly interested in the biological activities of thiamine. I had previously thought that I was nearly the lone believer in the benevolent effects of thiamine particularly for the treatment and prophylaxis of the toxemias of pregnancy and its many associated problems. I had even written to the chief of the Cleveland Clinic OB-GYN about the “miracles” I was performing and offered to work with him in further development of the concepts.

It was enclosed in a copy of a book by John B Irwin, M.D., the author of the letter.

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Mural que presenta un corazón en su forma anatómica sobre un fondo de rombos y triángulos blancos, negros y azules, a la altura del número 2 de la calle Alonso Benítez, barrio de Lagunillas, Málaga, España.

This article was published originally on May 30, 2018. 

Rest in peace Dr. Lonsdale. 

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Unraveling Symptoms and Syndromes

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What Is a Syndrome?

A syndrome is the name given to a collection of symptoms and physical signs that have been observed in the past in a single patient or in a group of similar patients. This is often named after the first person to report this set of observations. It is called a syndrome when others have made the same observations, sometimes years later. The terminology is purely descriptive, even though there may be a constellation of abnormal laboratory tests associated with the clinical facts. Unfortunately, the underlying cause is seldom, if ever, known.

Chronic Fatigue Syndrome

Chronic fatigue syndrome (CFS) is also known as myalgic encephalomyelitis (ME). In a review, it is described as a “challenge to physicians”. Its prevalence is reported as approximately 1% in the general German population. The author states that there are no convincing models that might explain the underlying cause as an independent unique disease. A variety of conditions such as chronic infectious disease, multiple sclerosis, endocrine disorders and psychosomatic disease are suggested in a differential diagnosis. There is said to be a significant overlap with major depression.

Another review describes CFS as characterized by debilitating fatigue that is not relieved with rest and is associated with physical symptoms. In order to make the diagnosis, these authors indicate that at least four of the following symptoms are required to make the diagnosis. They include feeling unwell after exertion, unrefreshing sleep, impaired memory or concentration, muscle pain, aching joints, sore throat, or new headaches. They also say that no pharmacologic or alternative medicine therapies have been proven effective.

Fibromyalgia Syndrome

According to the American College of Rheumatology, fibromyalgia syndrome (FMS) is a common health problem characterized by widespread pain and tenderness. Although chronic, there is a tendency for the pain to fluctuate in intensity and location around the body. Deficient understanding of its true cause gives rise to the false concept that it is neurotic. It is associated with chronic fatigue and patients often have sleep disorders. It is estimated that it affects 2 to 4% of the general population and is most common in women. It affects all ages and the causes are said to be unclear. FMS patients may require psychiatric therapy due to accompanying mental problems. Gonzalez and associates concluded that the combination of psychopathological negative emotionality, interpersonal isolation and low hedonic capacity that they found in a group of patients has implications for the daily living and treatment of these patients.

Regional Pain Syndrome

Complex regional pain syndrome (CRPS) is another common and disabling disorder, characterized by defective autonomic nervous system function and inflammatory features. It reportedly occurs acutely in about 7% of patients who have limb fractures, limb surgery, or other injuries, often quite minor. A small subset of patients progress to a chronic form in which autonomic features dominate. Allodynia (pain due to a stimulus that does not usually provoke pain) and hyperalgesia (increased pain from a stimulus that usually provokes pain) are features of CRPS and require a better understanding.

Sleep Apnea Syndrome

Apnea is the term used for a temporary cessation of automatic breathing that usually happens during the night. This syndrome is described as the most common organic disorder of excessive daytime somnolence. Its prevalence is highest among men age 40 to 65 years and may be as high as 8.5% or higher in this population. It is associated with cigarette smoking, use of alcohol and poor physical fitness.

Similar Cause with Different Manifestations

Complex Regional Pain Syndrome is related to microcirculation impairment associated with tissue hypoxia (lack of oxygen) in the affected limb. Without going into the complex details, hypoxia induces a genetic mechanism called hypoxia inducible factor (HIF-1 alpha) that has a causative association with CRPS. It has been found that inhibiting this factor produced an analgesic effect in a mouse model. The interesting thing about this is that thiamine deficiency does exactly the same thing because it induces biochemical effects similar to those produced by hypoxia (pseudo[false]hypoxia). A group of physicians in Italy have shown that high doses of thiamine produced an appreciable improvement in the symptoms of three female patients affected by fibromyalgia and are probably pursuing this research. Dietary interventions have been reported in seven clinical trials in which five reported improvement. There was variable improvement in associated fatigue, sleep quality, depression, anxiety and gastrointestinal symptoms.

Dr. Marrs and I have published a book that emphasizes deficient energy metabolism as a single cause of many, if not all, diseases. The symptomatic overlap in these so-called syndromes is generated by defective function of cellular metabolism in brain. Fatigue is the best symbol of energy deficiency and the English translation of the Chinese word beriberi is “I can’t, I can’t”. Fatigue is a leading symptom in beriberi. When physicians diagnose psychosomatic disease as “it’s all in your head”, they are of course, quite right. However, to imagine or conclude that the variable symptoms that accompany the leading one of fatigue are “imaginary” is practically an accusation of malingering. The brain is trying to tell its owner that it has not got the energy to perform normally and the physician should be able to recognize the problem by understanding the mechanism by which the symptoms are produced. Every thought, every emotion, every physical action, however small, requires the consumption of energy. Obviously we are considering variable degrees of deficiency from slight to moderate. The greater the deficiency the more serious is the manifestation of disease that follows. Death is a manifestation of deficiency that no longer permits life.

Our book is written primarily for physicians, but it is sufficiently lacking in technological language to encourage reading by patients. It emphasizes, by descriptions of case after case, the details of how genetic risk and failed brain energy are together unable to meet and adapt a person’s ability to meet the daily stresses of life. Stress, genetic risk and poor diet all go together. A whole chapter discusses the functions of the autonomic nervous system and how it deviates when the control mechanisms in the lower brain are defective. This system is the nervous channel that enables the brain to communicate the adaptive body actions necessary to meet living in an essentially hostile environment. We show that an excess of sugar and/or alcohol produce deficiency of vitamin B1 and the so-called psychosomatic disease that results is really early beriberi “I can’t, I can’t”. Variability in symptoms caused by this effect is because the cellular energy deficiency distribution varies from person to person and is affected by genetically determined differences.

This is illustrated by the case of a boy with eosinophilic esophagitis whose first eight years of life were marked by repeated diagnoses of psychosomatic disease. At the age of eight, upper endoscopy revealed the pathology in the esophagus. There was a family history of alcoholism and he was severely addicted to sugar. Many of his symptoms cleared with the administration of a thiamine derivative and resulted in a dramatic increase in stature. No pediatrician or other physician whose attendance was sought through those first 8 years evidently had ever questioned diet or the gross ingestion of sweets. They simply treated each condition as a confirmation that they were “psychological”.

It is worth noting that references 1 through 4 refer to both CFS and FMS syndromes being affected by psychological issues. This implies that the patient is “inventing” the poorly understood (and often bizarre) symptoms as a result of neurosis. The unfortunate complainant may easily become classified in the mind of the attendant physician as a “problem patient”. I have become aware that this can rise to such a degree of misunderstanding that the patient is denied access to the physician and even to other physicians in the same clinic. It is indeed about time that an overall revision be made to the absurd concept that the brain can “invent” a sensation that has no importance in solving the electrochemical problem. When we see the statistics of incidence of these common syndromes we have to conclude that there is an underlying cause and effect that pervades the general population. We are very conscious that our cars need the right fuel to work efficiently but rarely take it into consideration that the quality of food is our sole source of energy synthesis.

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

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This article was published originally December 2019. 

Rest in peace Dr. Lonsdale. May 2024.

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Thiamine Insufficiency Relative to Carbohydrate Consumption

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Thiamine (vitamin B1) is an essential micronutrient responsible for key reactions involved in the conversion of the foods we consume into the chemical energy substrate requisite for cellular function, adenosine triphosphate (ATP). Absent sufficient ATP, all sorts of metabolic functions become disordered leading to the disease processes that dominate western medicine. Chronic inflammation, altered immune function, hormone dysregulation, cognitive and mood disorders, and dysautonomias, all can be traced back to insufficient thiamine > inefficient mitochondrial function, reduced ATP, and the compensatory reactions that ensue.

Among the most common but least well-recognized contributors to thiamine deficiency is the regular consumption of a high carbohydrate/highly processed food diet. Although most of these foods are enriched or fortified with thiamine, perhaps staving off more severe deficiencies, the density of sugars overwhelms mitochondrial capacity to process these foods, both the thiamine and any other potential nutrients are excreted, while the carbohydrates themselves are stored as fat for future use. High-calorie malnutrition is a common contributor to thiamine deficiency in obesity but also may develop in presumed healthy athletes whose diets focus heavily on high carbohydrate intake.

Thiamine, along with other B vitamins is often deficient in vegetarian and vegan diets as well. Not only do fruits, vegetables, and carbohydrates contain minimal, if any, thiamine, but some have anti-thiamine factors and are high in what are called oxalates. Anti-thiamine factors found in some fruits and vegetables interfere with the absorption or digestion of thiamine. Oxalates are mineralized crystals of sorts that tend to build up and store in places like the kidneys (kidney stones), but also may store and cause problems anywhere in the body like bones, arteries, eyes, heart, and nerves. Effective oxalate metabolism and clearance requires thiamine. Since vegetarian and vegan diets are also carbohydrate intensive, thiamine deficiency and oxalate issues may be compounded. Thus, a number of common diets not only contain reduced thiamine content but cause an increased need for thiamine by at least three mechanisms; higher carbohydrate consumption overwhelming capacity, which is then magnified by poor carbohydrate and oxalate processing.

Add daily coffee, tea, and/or alcohol consumption to any diet, and whatever thiamine that is consumed is either inactivated by enzymes before being used or is unabsorbable. Add a medication or four and thiamine availability will tank simultaneously with an increased need. Medications both block nutrient uptake and/or increase the need for nutrients by inducing mitochondrial damage. Given that 70% percent of the US population takes at least one medication regularly, while 20% take four or more, it is safe to say, that a good percentage of the population is consuming insufficient thiamine to maintain mitochondrial function and health.

Are We Really Thiamine Deficient?

As an essential nutrient, thiamine must be consumed regularly to maintain sufficient concentrations. The question is how much thiamine is sufficient to maintain health? Current RDA values for daily thiamine intake suggest a little over a milligram per day is adequate for most adults. If this is true, then the minimum value can be attained through just about any diet including those dominant in highly processed, carbohydrate-dense foods, which are commonly either enriched or fortified with thiamine. Everything from bread to cereals and even junk food like Oreos have thiamine. Per the RDA values, none of us ought to be thiamine deficient and none of us ought to require thiamine supplementation, and yet, many of us are and do. Indeed, several studies, across disparate populations show that even by this minimum standard, deficiency is a serious health problem. From our book:

  • 76% of diabetics (type 1 and type 2)
  • 29% of obese patients, 49% of post-bariatric surgery
  • 40% of community-dwelling elderly, 48% of elderly patients in acute care
  • 55% of cancer patients
  • 20% ER patients (random sample, UK)
  • 33% of congestive heart failure patients
  • 38% of pregnant women, more with hyperemesis
  • 30% of psychiatric patients

It takes approximately 18 days to completely abolish endogenous thiamine stores in a diet that is completely devoid of thiamine. Except under total starvation, medical or industrial food production mishaps, and experimentally contrived situations, thiamine consumption is never completely abolished. It waxes and wanes by dietary choices and life stressors. According to rodent studies, it takes a reduction of greater than 80% of thiamine stores before the more severe neurological symptoms are recognizable. In humans, these symptoms include those associated with Wernicke’s encephalopathy, the various forms of beriberi, and dysautonomic function. These include but are not limited to: ataxia, changes in mental status, optic neuritis, ocular nerve abnormalities, diminished visual acuity, high-output cardiac failure with or without edema, high pulse pressure, polyneuropathy (sensorimotor), enteritis, esophagitis, gastroparesis, nausea and vomiting, constipation, hyper- or hypo-stomach acidity, sympathetic/parasympathetic imbalance, postural orthostatic tachycardia syndrome (POTS), cerebral salt wasting syndrome, vasomotor dysfunction, respiratory distress, reduced vital capacity, and/or low arterial O2, high venous O2.

With a less severe thiamine deficiency, symptoms are rarely recognized as such and often attributed to psychological manifestations. A not entirely ethical study done in 1942 involving 11 women on a low thiamine diet over a period of ~3-6.5 months found striking symptoms.

  • During this time all subjects showed definite changes in personality.
  • They became irritable, depressed, quarrelsome, and uncooperative.
  • Two threatened suicide. All became inefficient in their work, forgetful, and lost manual dexterity.
  • Their hands and feet frequently felt numb.
  • Headaches, backaches, sleeplessness, and sensitivity to noises were noted.
  • The subjects fatigued easily and were not able to vigorous exertion.
  • Constipation was the rule, but no impairment, of gastrointestinal motility, could be demonstrated fluoroscopically.
  • Anorexia, nausea, vomiting, and epigastric distress were frequently observed.
  • Low blood pressure and vasomotor instability were present in all patients.
  • At rest, pulse rates were low (55 to 60 per minute) but tachycardia followed moderate exertion. Sinus arrhythmia was marked.
  • Macrocytic, hypochromic anemia of moderate severity (3.0 to 3.5 million red cells) developed in 5 cases.
  • A decrease in serum protein concentration occurred in 8 subjects.
  • Basal metabolic rates were lowered by 10 to 33 points.
  • Fasting blood sugar was often abnormally high.

The study above demonstrated a rapid and dramatic onset of symptoms relative to a diet with limited thiamine. Depending upon caloric intake, the amount of thiamine allowed was approximately 1/3 to 1/5 of the amount recommended by the RDA. Admittedly, the RDA for thiamine is low, to begin with, but even so, this was not a complete absence of thiamine. Since the study took place in the early 1940s, it is difficult to ascertain the specifics of the diet. Nevertheless, it demonstrates a clear association between general health and one’s ability to function, and thiamine insufficiency.

High Carbohydrate Diets Equal Lower Thiamine

More recently, a short and very small study (12 days and 12 participants) of active young men and women (ages 25-30) investigated the relationship between carbohydrate intake and thiamine status. Thiamine was measured in blood, plasma, urine (creatinine), and feces at four time points: at baseline, before the study began, during an adaptation phase where carbohydrate intake represented 55% of the total caloric intake, and during the two subsequent intervention phases, where carbohydrate intake was increased to 65% and 75% of the total caloric intake, respectively. Both caloric and thiamine intake was held constant throughout the study despite the increased intake of carbohydrates. Activity levels were also held constant. Across this short-term study, as carbohydrate intake increased, plasma, and urinary thiamine decreased. Excretion through feces remained unchanged. Transketolase enzyme activity was also measured but remained unchanged. Given the short-term nature of this study, the fact that transketolase remained unchanged is unexpected. In addition to the decreasing thiamine values, there were several changes in lipid profile as well. Despite the short duration of this study, however, the results show a clear relationship between carbohydrate intake and thiamine status; one that would likely be magnified over time and certainly if other life stressors and medical and environmental toxicants were added to the mix.

It is important to note current dietary guidelines suggest carbohydrate consumption should fall between 45-65% of total calories, percentages which, per this study would decrease thiamine availability significantly. From the baseline diet to the 55% adaptation phase, thiamine dropped precipitously, only to drop even further at the 65% phase. A recent study surveying macronutrient consumption showed that average carbohydrate consumption across the US population represented approximately 50% of total caloric intake. Importantly though, the study found that 42% of the carbohydrate consumption came in the form of what researchers termed ‘low-quality carbs’ e.g. sugary processed foods with no nutritional value. Thiamine is only found in pork, beef, wheat germ and whole grains, organ meats, eggs, fish, legumes, and nuts. It is not present in fats/oils, polished rice, or simple sugars, nor are dairy products or many fruits and vegetables a good source. Indeed as mentioned previously, some fruits and vegetables may contain anti-thiamine factors. A diet that is 42% empty calories, that contains limited to no nutritive value, save except what has been added post hoc via enrichment, begs for mitochondrial damage and the illnesses that ensue. And yet, that is precisely the nutritional landscape in which most of us exist.

Admittedly, both studies were very small, but the research connecting thiamine deficiency to ill-health and carbohydrate consumption to thiamine loss is clear. Given the dominance of ultra-processed carbohydrate-dense foods in the modern diet, is likely that high-calorie malnutrition underlies much of the chronic illness that plagues western medicine. To learn more about thiamine deficiency and the havoc it wreaks on health: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition.

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

Yes, I would like to support Hormones Matter.

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Maternal Thiamine Deficiency and Fetal Brain Damage

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Over the last several months, Dr. Lonsdale and I have been working on a book about thiamine deficiency and dysautonomia. Last week I wrote about the presumed connection between the Zika virus and microcephaly where I hinted at a thiamine connection. One might say, that I have thiamine on the brain and that would be a fair assumption. The old adage, ‘if one has a hammer, everything becomes a nail‘, may apply. I may be focusing too much on thiamine and its role on mitochondrial health. Alternatively, it could be that thiamine is just that important. After all, it sits atop at least two of the four energy producing pathways that give us ATP and is deeply embedded within the remainder of the oxidation process. The consequences of impaired oxidative metabolism in the brain are vast and include a range of disease processes like Alzheimer’s disease, amyotrophic lateral sclerosis (Lou Gerhig’s disease), Parkinson’s disease, multiple sclerosis, alcoholic brain disease, and stroke.  Without thiamine, the mitochondrial factories stop producing energy or ATP and without ATP, stuff slows and then dies. So yes, thiamine is critical to health.

It is not difficult to imagine what happens to energy levels when thiamine concentrations diminish even slightly in an adult. An unrelenting fatigue is one of the early symptoms of struggling mitochondria and thiamine deficiency. More fundamentally, however, all the organs tasked with maintaining life, demand energy. When energy stores diminish, those organ systems struggle. The organ systems requiring the most energy, like the brain and the heart, are hit hardest. Maintain a slight deficiency chronically and damage ensues. In Cuba, for example, trade embargo policies resulted widespread thiamine deficiency in the population, which in turn initiated an epidemic of neuropathy – nerve damage. Over 50,000 Cubans were reported to have developed optic neuropathy, deafness, myelopathy, and sensory neuropathy related to embargo imposed dietary changes. In contrast to the more insidious damage initiated by chronically low thiamine concentrations, severe and acute thiamine deficiency is life-threatening, especially in children, but also in pregnant women.

With low maternal thiamine concentrations, the effects on fetal development, especially fetal brain development that requires enormous amounts of energy, are likely to be devastating. And indeed, they are. But we don’t study that very often, even in rats. Do a search on the subject and there is not much research out there. Sure, some researchers have investigated maternal thiamine deficiency in fetal alcohol syndrome (FAS), postulating thiamine might be the mechanism by which FAS develops, but that is about it. Given how critical it is to fetal development, I expected more research.

It is not just alcoholics who are at risk of thiamine deficiency. An increasing percentage of Western populations are likely thiamine deficient. Thiamine depletion occurs with numerous medications and vaccines via multiple mechanisms, many of which are just beginning to be understood. Conventional farming practices use herbicides and pesticides that block vitamin B absorption and so even diets presumed healthy may not be as nutrient dense as in the past. Poor absorption from altered gut microbiomes may be another common mechanism for thiamine deficiency and emerging evidence finds that Type 1 and Type 2 diabetics excrete significantly more thiamine than non diabetics, making them thiamine deficient as well. Not studying this more broadly is leaving millions of folks to suffer with entirely preventable disease processes. During pregnancy, however, this lack of recognition and research is just downright negligent, especially when we consider fetal brain development.

Thiamine During Pregnancy

Thiamine is absolutely critical for both maternal health and fetal development. Women with hyperemesis gravidarum, excessive vomiting during pregnancy, are at a particularly high risk for thiamine deficiency and though there is increasing awareness of maternal Wernicke’s encephalopathy during pregnancy, a condition typically associated with thiamine deficient alcoholics, the full scope of damage associated with maternal thiamine deficiency is insufficiently understood. There is little to no appreciation of the long term effects on maternal health and even less recognition of how the deficiency impacts fetal development in either the short or long term.

Provided mom survives a thiamine deficient pregnancy, what happens to the growing fetus? In 37% of the cases of severe maternal thiamine deficiency, spontaneous fetal loss occurs. If thiamine is critical for mitochondrial energy production, and fetal development requires exorbitant amounts of mitochondrial energy, what happens if one of the key components to that energy production process is lacking? All sorts of things, it turns out, including microcephaly. Beyond a rare congenital defect in thiamine transport believed to affect only consanguineous Amish, there are very few studies that have considered the effects of epigenetic and more functional maternal or fetal thiamine deficits. We know from the Amish cases, that when the fetal thiamine transporters are impaired, microcephaly ensues. Is it so hard to imagine that we might impair those transporters epigenetically or reduce maternal thiamine concentrations functionally by dietary choices, medications or environmental toxicants that leach nutrients and/or by malabsorption?  And yet, as I dig into this, I find only a few studies that have addressed maternal thiamine and fetal brain development. Here they are.

Maternal Thiamine Deficiency and Fetal Brain Damage

A 2005 study from researchers in West Africa showed that the pups from thiamine deficient dams, had significantly smaller brains by weight. Digging deeper, they found far fewer neurons in the hippocampus, the region of the brain responsible for memory consolidation and retrieval, than the pups from thiamine sufficient diets. Brain damage in the offspring could be induced by maternal thiamine deficiency either leading up to, during, or after pregnancy (while lactating) but varied in scope, severity, and pattern. The most significant damage occurred when the dams were deficient during pregnancy.

In the offspring from perinatal thiamine deficiency, hippocampal volume was reduced by almost a third due to neural cell death.  The neurons that survived were smaller than normal and misshapen. The hippocampus is critical to memory. Hippocampal damage in human adults causes all manner of amnesias and aphasias (speaking and language comprehension deficits) and is found in neurodegenerative disorders like Alzheimer’s disease.

The neurons affected most by the thiamine deficiency, the CA1 neurons, are especially susceptible to oxidative damage and insult. Thiamine is integral to brain oxidation and so this makes sense. What we have to remember though, is that in a fully developed human brain, oxidative damage to the CA1 region is associated with hippocampal ischemia, limbic encephalitis, status epilepticus, and transient global amnesia – very serious conditions. To a developing brain, requiring vast amounts of energy to grow, the consequences of hippocampal deficits are largely under-recognized except again in fetal alcohol syndrome.

Another animal study looked at the effects of maternal thiamine deficiency to the cerebellum of the offspring. The cerebellum is the region of the brain responsible for balance and coordinated motor movements. Here again, the damage was severe with a significant reduction of size, loss of neuron viability, and conduction. There have been a smattering of studies across the decades (here, and here, for example) looking at thiamine deficiency and brain damage in non-pregnant rats, but that’s about it.

Not much else is out there.

From these few animal studies, the work on Amish microcephaly and the work connecting neurodegenerative disorders to thiamine deficiency, we can surmise that thiamine is essential to brain development. More specifically, in pregnancies where thiamine concentrations are low, cerebral development of the offspring will be impaired in some pretty significant ways. Namely, the number and size of neurons is reduced, and as a consequent, total brain volume is reduced. If the deficiency is severe enough, microcephaly is possible and has been identified in the two of studies mentioned above. I think this is what is happening in Brazil. That is, a combination of seemingly unrelated factors, coalesce to produce fetal thiamine deficiency which results in microcephaly and other sorts of brain damage. The questions that remain include:

  1. By what mechanisms specifically is thiamine deficiency produced?
  2. What are the risks for maternal thiamine deficiency in other regions?

One of the most direct routes to thiamine deficiency during pregnancy is hyperemesis gravidarum, excessive vomiting. Case studies abound where it is often not recognized until the mother is in critical condition. It is considered a rare complication, but is it? Unless and until those questions are answered more fully and physicians recognize maternal thiamine deficiency as a potential problem, women and children will continue to be at risk for what are entirely preventable complications of pregnancy.

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Image credit: Centers for Disease Control and Prevention, Public domain, via Wikimedia Commons

This article was first published on June 16, 2016. 

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