thiamine Archives - Page 4 of 13

Notes On Thiamine Status During Pregnancy

Published on March 12, 2025

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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.

The Exquisite Simplicity of Health and Illness: Mitochondria and Energy

by Derrick Lonsdale MD, FACN, CNS

Published on March 11, 2025

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For years I have struggled to get people to understand the relative simplicity of what causes us to get sick. Our medical model implies that each disease has a specific cause, and therefore, has a specific treatment. If you look seriously at what makes us tick, there are several obvious factors involved. Yes, we are provided with a “blueprint”, given in code called DNA, by our parents. Since the discovery of DNA, medical research has emphasized almost to exclusion of other factors, that genetics is the primary research area. The most amazing recent finding is that our cellular genes (the blueprint) can be manipulated by our diet and lifestyle.

Diet and Stress

Even though the great Hans Selye studied the effects of physical stress on animals, we have neglected it in relationship to human health. He said that humans were suffering from what he called the diseases of adaptation. What he meant by that was that any form of “stress” has to be met by an adaptation that requires a huge amount of energy. The brain causes the body to go into a defensive mode when we are attacked by a microorganism and it should not be surprising that it requires energy. Sometimes a severe form of stress is associated with fever that should be regarded as an automated defensive action. In fact, I knew of a patient in whom the cause of her persistent fever could not be determined by standard laboratory methods. It was written off as “psychosomatic”, because of personality factors.

The idea, however, seems to me to be a reduction to absurdity based on collective ignorance of the underlying mechanism. The symptoms that we develop are caused by all the actions that make up the defensive mode and we call that the disease. For example, fever is part of the defense because it renders the attacking organism less efficient. Hence, the attacking organism is a “stressor”. Perhaps prolonged mental stress can produce fever in a metabolically abnormal brain because of causative misinterpretation by the brain.

It has long been time-honored that we bring the temperature down artificially as part of the treatment for infection, thus losing an important part of the defense. It wasn’t the flu virus that caused Reye’s syndrome, a disease that caused the death of many children. It was the aspirin given by the mothers to bring their child’s temperature down.

Energy Deficiency and Mitochondria

When you read a telegram giving you bad news, when you ride a bicycle, when you run cross country or shovel snow, we take it for granted that the energy will be forthcoming, that is if we think about it at all. Energy deficiency in the heart muscle could easily explain the “drop-dead” phenomenon occasionally experienced by elderly people in the winter when shoveling snow, usually written off as a heart attack from coronary disease that could easily be part of the event. Could that death have been prevented by analyzing the state of nutrition for that individual?

Another great discovery is that we have a separate set of genes that preside over the functions of our mitochondria. These are the organelles within each of our cells that produce the energy that enables us to function. Sick mitochondria produce sick people, because energy consumed must be met by energy synthesized. We now know that mitochondria have their own genes completely separate from the “blueprint” genes. Mitochondrial genes are passed to the children by the mother. When damaged mitochondrial genes are passed on to children, it becomes a form of maternal inheritance. An obvious question is whether the damage to genes can be caused in adult life from malnutrition or whether the damaged genes passed on to the children are invariably inherited from grandma.

Energy synthesis depends upon an exquisitely complicated set of nutrients that are derived from what we eat, so nutrition becomes the third factor. It is therefore very likely that an element of each of these factors is always involved. Yes, it is true that a genetic mistake may be the primary cause, but a lot of genetic mistakes are really risk factors that begin to produce a given disease in relationship to “stress” and “nutrition”, both of which always play a part.

We now know that the induction of the first symptoms of beriberi, a well-known vitamin deficiency disease that has dogged mankind for centuries, can be fully initiated by sunlight exposure in a person with marginal deficiency. There may be mild symptoms attributed to other “more acceptable” causes or even no symptoms of vitamin deficiency prior to sunlight exposure. In the early investigation of beriberi, the appearance of symptoms in many individuals at the same time misled the investigators who concluded that it was due to a mysterious infection. We now have reason to believe that ultraviolet light imposes a “stress” in an individual whose metabolism is marginal, thus initiating the true underlying cause.

Healing Comes Naturally If We Let It

The human body, as we all recognize, is beautifully designed and healing is a natural phenomenon built into our system. The body knows exactly what to do, but like stress factors, healing requires energy. So, it seems to make absolute sense that we cannot possibly produce healing by the use of compounds that are completely foreign to our cellular system. Shouldn’t we be using methods that assist the healing process by stimulating mitochondria to produce the necessary energy? Surely, the only possible assistance must be through the use of nutrients. At present, we know that there are well over 40 separate non-caloric nutrients that we must get from our food to maintain health and this may not be a full complement.

Feeding the Body Fuel to Heal: Of Vitamins and Minerals

I give this as a forerunner to news that I came across quite recently. I am reasonably sure that it will be known by people who love American sports. Everyone knows the name of Bernie Kosar, the great quarterback of the Cleveland Browns back in the good old days. Bernie understood the highs and lows of football. He had hundreds of concussions, broken bones and torn ligaments over 8 ½ seasons. In retirement he suffered pounding headaches, sleepless nights, anxiety and increased weight. Speech slurring made people think that he was drunk. Amazingly, his family didn’t believe that he had genuine symptoms and thought that he was merely trying to gain attention. The slurred speech was thought to be due to alcohol, the weight gain from overeating. After his retirement, apparently he spent some time in Florida and he learned there of a physician who was using intravenous vitamins to treat the kind of symptoms of which he complained. He tried it and immediately began to feel better. In fact he was so impressed that when he came north to live in Ohio he looked for a physician who could continue this treatment. He was directed to a doctor Pesek, founding holistic physician and CEO of Vital Health in Cleveland, Ohio. Dr.Pesek uses holistic superfoods and megadose vitamins to treat his patients. Kosar gets two or three intravenous infusions of vitamins a month. His headaches have decreased, his sleep is improved and he has lost 60 pounds in weight. This is loss of accumulated water in the tissues, a signature of mitochondrial disease, not loss of fat. In fact he is so impressed that he is going to bring it to the notice of the NFL concussion settlement. He wishes that he had started it earlier. He says that “he knows of guys who are older and some who are younger than me and it goes south quickly”.

Healing the Brain

Because the methodology is “out of the box”, it is likely that a common explanation would be the so-called placebo effect. But that effect has to have a mechanism and perhaps the approach with nutrients actually stimulates this effect. What we know about brain injury is that the damage upsets the normal balance of metabolism. It causes a release of oxygen radicals, a phenomenon that can be likened to the production of sparks in a fire. The damage is cumulative, eventually giving rise to the kind of symptoms experienced by Kosar and also by Mohammed Ali, who went on to suffer from Parkinson’s disease. Neglect the early symptoms, almost always mistaken for psychosomatic disease, and the damage slowly accumulates, eventually becoming irreversible and untreatable. I suggest that this is represented as one of the many neurodegenerative diseases such as Alzheimer’s or Parkinson’s. Under the present medical model, it might easily be assumed that intravenous vitamins are a specific treatment for the effects of concussion and should be reserved for that. The point is that there are many avenues to metabolic imbalance. For example, if type I diabetes was determined by a genetic effect, why do the symptoms not appear for many years? If genes are solely responsible, diabetes should be present at birth. The answer is that other factors come into play including malnutrition and aging. In fact, in the state of genius, it might be that even the best possible diet does not provide sufficient energy, perhaps explaining the long-term illnesses of the historical figures, Mozart and Charles Darwin, both of whom suffered lifelong from symptoms that have often been regarded by historians mostly as psychosomatic.

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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 July 31, 2017.

Rest in peace Derrick Lonsdale, May 2024.

Hormonal Birth Control Plus Poor Diet Is a Recipe for Disaster

by CB

Published on February 17, 2025

5715 views

I am a 29 year old female who began experiencing a decline in my health at 25 years old. This was in 2020. At that point, I had been on hormonal birth control for nearly 10 years. I suspected the birth control was contributing to my ill-health but my doctor disagreed and continued to prescribe different forms to alleviate my symptoms. That did not work and only made things worse. When Depo-Provera was added, I completely crashed and have not recovered, nearly two years later.

When I first began to experience extreme fatigue, abdominal bloating, irritability, restlessness, and massive amounts of hair falling out, I went to my primary care doctor who could find no reason for it on basic bloodwork, except for a low vitamin D level (27mg/mL). They checked CBC, CMP, autoimmune markers, B12, a complete thyroid panel, Lyme titers, mono titers, and iron levels. Since everything was basically normal, my primary care doctor blamed it on my stressful job. At the time, I was working in the emergency room on the night shift. I was not getting the best sleep, and not eating that well either. I was lucky to eat one meal a day and then maybe a snack especially on my busy shifts. On my days off, I was so exhausted that I would eat maybe twice a day. My diet consisted of easy meals like grilled chicken, salads, granola bars, processed cereals, pizza, chicken nuggets, chips, bananas here and there, and overall not a lot of fruits or vegetables.

Enter Depo-Provera

Fast forward to the fall of 2021, after these symptoms persisted, my doctor decided to switch my birth control to the Depo-Provera shot. After taking this shot, havoc was wreaked on my body and brought me down to a level of non-functioning that I never knew existed. Over the next couple months and after taking only one depo shot, I began to experience debilitating symptoms of headaches, fatigue, achy joints/all over body pain that eventually progressed into episodes of heart-racing anytime I would change position. I also experienced shortness of breath, chest pain, difficulty swallowing, a complete loss of appetite, GI issues, brain fog, severely decreased ability to concentrate, severe restless leg syndrome, insomnia, and neurological symptoms so extreme it felt like my brain was “short circuiting” for lack of a better word.

One side of my body would become extremely numb, tingly, and feel weak without any clear deficits. I experienced severe muscle weakness, where it would feel like my body was doing everything it possibly could to keep me upright and breathing. It was so bad, I felt as though I couldn’t even grip my phone and just talking on the phone to family felt like I was dying. I could barely concentrate. I developed severe visual issues, a condition called visual snow syndrome, and still am dealing with it with no improvement. I also developed tinnitus and have a constant high pitched ringing in my ear. I am unable to handle any type of stress, multi-tasking, or any emotional upset without truly feeling like my body is dying from severe neurological symptoms. I became scared to leave the house alone because of these debilitating symptoms. I lost over 30 pounds from feeling so awful and a complete loss of any desire to eat. I would have to force myself to put in fluids or food.

Over the course of many months, I saw multiple neurologists, neuro-ophthalmologist, cardiologist, electrophysiologist, primary care doctor, ENT, TMJ specialist, otologist, binocular vision specialist, rheumatologist, had numerous ER visits, two hospital admissions. I even participated in vestibular/neurological physical therapy over the course of several months. I had multiple head MRIs and CTs of my head and neck, MRIs of my spine, and so much bloodwork looking for autoimmune causes. I had a colonoscopy, a camera down my nose to look at my throat, an audiogram, a sleep study, a tilt table test, an echocardiogram, a stress-echocardiogram, and they even attempted a lumbar puncture on me as well. Conditions such as blood clots, multiple sclerosis, any type of cancer or tumor, etc., were ruled out and the only thing they came up with was a diagnosis of Postural Orthostatic Tachycardia Syndrome (POTS), a suspicion for “some type of migraine variant” and a deficiency in vitamin D and phosphorus on my bloodwork.

Could This Be Thiamine Deficiency?

Fed up and worsening, I paid out of pocket to go to a natural medicine doctor who did heavy metal and mold testing on me along with hormone testing. Nothing really turned up there and so I took it upon myself to order a full vitamin and mineral panel paying over a grand out of pocket. This panel revealed that my serum thiamine was one point away from being flagged as low (8 nmol/L). I then returned to my primary care and two different neurologists to ask if a thiamine deficiency could be the problem or at least part of it, especially after my own research and the known research that birth control depletes many B vitamins. All of the doctors told me that there was no possible way I could have a thiamine deficiency since it is added to so many foods in the United States. They also told me that I could just take a B complex vitamin if I was worried. Even after I told them I was hardly eating because I felt so sick and that when I was eating it was mostly foods like processed toast, frozen chicken nuggets, cans of soup, and other things of that nature, they still dismissed the idea of thiamine deficiency.

May-Thurner Syndrome

On top of all of the debilitating POTS and neurological symptoms, throughout my time on birth control I had complained to my GYN about persistent left sided pelvic pain. It felt like my labia was swollen and at times like something was bulging into my pelvic area. In 2019, I had a CT scan of my abdomen and pelvis done due to some GI symptoms I was having. An incidental finding on it was suspicion for pelvic congestion syndrome (PCS). The report stated that I had very prominent peri-uterine vessels and a dilated left gonadal vein. I took these results to my GYN at the time who clearly stated “PCS is a fake diagnosis and you don’t need to do anything with that.” Since I was young, in my early 20s, I didn’t take it too seriously. Again as time went on, I continued to have the pain and over the years my GYN kept changing my birth control and mentioned endometriosis and small ovarian cysts as possible causes. The birth control would help a little bit for a while but then I would have irregular bleeding and the pain would always come back. It wasn’t until after I took the Depo shot and came off of the hormones that things became worse.

I began to have severe left pelvic pain that persisted for months. I had transvaginal ultrasounds every 6 to 8 weeks to monitor recurring small cysts that they swore were not the cause of my pain. I was tested for PCOS and was negative for that too. It wasn’t until the end of 2022, that I had another transvaginal ultrasound and this one read as having a hydro-salpinx. I had a new GYN at the time who referred me to get an MRI done of my pelvis. This MRI came back as also showing “likely hydro-salpinx” on the left. Since I was having such severe pain, I was referred to a GYN surgeon who said in extremely painful cases it is recommended to take out the tube and it was pretty much nonfunctional when it was as swollen as mine. I elected to proceed with the surgery, as the pain was so extreme. Funny enough, after the surgery when the pathology came back there was no hydro-salpinx and my surgeon said he did not see any endometriosis when he performed the laparoscopy. He said he believed my MRI may have been misread since he did not see any indication of hydro-salpinx during the procedure.

As if that wasn’t enough, after the procedure I had a severe neurological reaction to the scopolamine patch they put on me during the procedure. I had so much testing for this. I was even in the hospital for 5 days with what they thought was “scopolamine patch withdrawal” even though I only had the patch on for 3 days like they told me to wear it.

Fed up and still in pain, I let it go for a few more months thinking it was just “scar tissue” from the surgery or some other easy explanation. It wasn’t until my POTS doctor recommended me to wear an abdominal binder/compression device around my stomach that things worsened so much that I was forced to figure this out. I began having severe left pelvic, hip, and leg pain after wearing this device for only 3 days. I went to the ER because the pain was so bad, but they could only find a small ovarian cyst on my left ovary. They didn’t even consider doing any other work-up. I was then sent to an orthopedic to look at my hip and back to my GYN. Neither could really give an explanation for this pain. Finally enough was enough, I went to a vascular doctor on my own accord to get this PCS, which no one seemed to take seriously, looked at.

At the vascular surgeon’s office, they did a vascular scan of my pelvis and abdomen and were quickly shocked to find that my left iliac vein was almost completely compressed causing my peri-uterine vessels to get almost no blood flow. They diagnosed me with something called May-Thurner Syndrome and said that they usually only see severe cases like mine in women who have had “5 or 6 babies.” I was 28 at the time with one previous ectopic pregnancy many years ago. They quickly scheduled me to get a stent of my left iliac vein placed, as my left leg had begun swelling bigger than my right due to the limited blood flow.

On the day of surgery, my left leg was 2 inches bigger than the right and I was in severe pain. They did a venogram with internal ultrasound and were able to tell me my left iliac vein was 85% compressed. So basically, I was getting no flow through it and hardly any return through that vein up to my heart. They also informed me that the birth control was probably masking the problem but also could have been worsening it when I was on estrogen-containing birth control. They said I was extremely lucky that I did not develop a blood clot, especially when I had taken Beyaz for several years. Now, I am on blood thinners for several months post stent, while waiting to see if this helps with my POTS symptoms at all. So far, I have not seen any improvement except that my leg is no longer swollen.

Still Seeking Answers

I don’t know if thiamine deficiency could be causing my issues, but I have not received any answers other than POTS and my recently discovered May-Thurner Syndrome. I have seen so many doctors and spent so much money with no improvement in my health. This all severely worsened after I took the Depo shot. I have been unable to work for months, was bed bound for a long time, and was completely unable to eat during the worst of my symptoms. Now, I am at least able to move around more than I was and leave the house for doctor appointments, but I am still not working and I am still searching for answers. I would like to feel better and get back to some type of semi-normal life.

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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 August 14, 2023.

Notes on Folate Carriers, Anti-Folate Medications, and Thiamine Deficiency

by Chandler Marrs, PhD

Published on January 22, 2025

5887 views

Folate Carriers, Anti-Folate Medications, and Thiamine Deficiency

A few years back, I wrote a paper about the anti-folate and anti-thiamine properties of a popular antibiotic called Bactrim. It is also sold under the trade names: Septra, Sulfatrim, Septrin, Apo-Sulfatrim, SMZ-TMP and cotrimoxazole. Bactrim is a formulation that combines two drugs, trimethoprim and sulfamethoxazole. Both drugs block folate, albeit via different mechanisms, but trimethoprim blocks thiamine too. The combination has a number of deleterious effects, not the least of which is the possibility for a drug-induced Wernicke’s encephalopathy.

Today, I would like take a closer look at the relationship between thiamine and folate status as it affects transporter activity. It turns out that there is a lot more to the story than simply the drug’s depletion of critical nutrients. There is an interaction at play that determines the potency of these drugs and the severity of the nutrient depletion. That is, the individual’s nutrient status before taking the drug, to a large extent, may determine its effects.

It makes sense, of course, that the individual’s nutrient status would affect drug response. Poor nutrient status in general would exacerbate any illness and increase the risk frank deficiency and drug-induced mitochondrial damage. Beyond these broad strokes, however, there wasn’t a clear mechanism that would account for why some people become so severely debilitated by certain drugs and while others do not.

With regard to anti-folate drugs, a study done over 20 years ago found that nutrient transporter trafficking and directionality may be related to thiamine status. A caveat, this was a cell culture study using murine cell lines, including leukemia cells, and extrapolation to vivo human, non-leukemia cells is necessary. More recent animal research involving the use of methotrexate in liver cancer demonstrates similar effects, although mechanisms are not discussed. High thiamine status reduces methotrexate uptake. Conversely, methotrexate induces thiamine and folate deficiency (here, here).

Returning to the cell study, thiamine concentrations before exposure to anti-folate drugs appears not only to determine how much of drug is taken up by the cell (low thiamine > more drug uptake) but also the degree to which folate and thiamine are depleted. In low thiamine states, the potency anti-folate drug like methotrexate, and I suspect other anti-folate drugs that were not tested, is magnitudes greater than with higher thiamine concentrations. What I found particularly interesting, was that this effect was mediated largely by changes in the folate transporter (RFC1), which controlled not only the influx of folates and anti-folate drugs, but also, the efflux of thiamine pyrophosphate (TPP), the activated form of thiamine. The researchers found that when thiamine was low, more drug was taken up by the cell, while more TPP was spit out of the cell, essentially causing an intracellular deficiency of both folate and thiamine. Of note, a less active form of thiamine, thiamine monophosphate (TMP), appeared to be trafficked into the cell in exchange of the more active TPP.

Since a good portion of the population is likely low in thiamine, this means the potential damage by these drugs is significant and under-recognized. Might some of the adverse effects associated with these medications be related to either folate and/or thiamine deficiency? Possibly, which means supplementation with these nutrients may help.

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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 March 28, 2023.

Childhood Seizures Precipitated by Thiamine Deficiency

by Sonja

Published on January 16, 2025

5541 views

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.

Thiamine and Heart Function

by Derrick Lonsdale MD, FACN, CNS

Published on January 15, 2025

11889 views

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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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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Image credit: Daniel Capilla, CC BY-SA 4.0, via Wikimedia Commons.

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.

Back Pain and B Vitamins: Notes from Personal Experience

by Derrick Lonsdale MD, FACN, CNS

Published on December 18, 2024

16153 views

Throughout the history of medicine, performing research on oneself has been time-honored. Before I describe the experiment on myself, I must digress. As many readers on this website know, I have written a great deal about thiamine and its use in therapy. In particular, I have long been interested in a derivative of this vitamin that is to be found naturally occurring in garlic. It has been synthesized and sold under various trade names. Its chemical name is complex, so I use the initials TTFD. Without going into details, its action is superior to that of the thiamine from which it is derived. I have used TTFD for the treatment of hundreds, if not thousands, of patients. Over the years, I became certain that there was no bad side to its use, whatever the dose. My experiment proved me wrong but in a way that I should have anticipated.

Vitamins Work Together

Vitamins work as a team and thiamine is a member of a group of vitamins known as the B complex that is vital to energy metabolism. We are however beginning to learn that vitamins, either singly or given in a group, can be used as drugs and it requires a great deal of research in order to understand completely these relationships if they are used therapeutically. As I have a particular condition that is precancerous, I have been attempting to find ways and means of preventing the possible onset of cancer by the daily use of a variety of nutrient supplements. We now know that thiamine is implicated in many conditions, including cancer.

For some time I had been taking 100 mg of TTFD a day and one tablet of B complex. I raised the dose of TTFD to 200 mg a day without raising the dose of B complex to see if I could perceive any difference in what I experienced. After about a month with this dose, I was getting into bed one evening and was suddenly afflicted with the worst pain in my left leg that I had ever experienced. It appeared to be muscular pain because any movement would sharply increase the pain and often cause me to cry out involuntarily. Sleep was of course impossible and at about 3 AM, one night last week, I remembered a manuscript that I had come across that purported to relieve pain by an injection of vitamins B1, B6, and B12, administered separately or in combination. I took three tablets of B complex (three times the previous daily dose) and about 15 minutes later I noticed some diminution in the pain. I waited a while before repeating the dose of B complex twice more and within about 45 minutes I was pretty well pain free. It was a shattering experience that demanded some form of explanation, if possible.

The Mechanics and Biochemistry of B Vitamins

My personal explanation is as follows. Each member of the B group of vitamins has a vital part to play in energy metabolism and I had produced an artificial balance between them that severely decreased the efficiency of their combined action. An analogy may help to explain what I am talking about. Imagine a machine that relies on cogwheels, such as a clock. The motor, whether it be clock-work or electric, passes the energy via the cog-wheels to the hands of the clock. The very first cogwheel in the series is the master, because without it nothing happens. The rest of the cogwheels are just as important but only function because of the first one.

The energy that our cells require is passed through a series of enzymes that are the equivalent of the cogwheels. Each enzyme requires one or more cofactors that can be thought of as a special lubricant that differs for each cogwheel. Imagine now that the first cogwheel is an enzyme that requires thiamine and you have added so much lubricant that it causes the meshing with the next cogwheel to slip. The motor keeps running but the transmission breaks down. Like all analogies, this is imperfect. Thiamine is known as the rate limiting factor in the enzyme complex that demands the presence of all the B vitamins. You can think of thiamine as being the dominant member but no less essential than the others.

Vitamins as Drugs

A drug is “a substance that, when ingested, alters physiological actions in the body”. That definition automatically excludes each vitamin and essential mineral, such as magnesium, as a drug under normal healthy circumstances because each is essential to normal human and animal physiology. However, we are completely dependent on appropriate nutrition in order to acquire the vitamins and essential minerals. Because we no longer obey the life rules of Mother Nature, it has become exceedingly easy to develop (non-caloric) nutrient deficiency. It particularly applies to the B complex because of its essential role in liberating energy from glucose. We know from studies of thiamine deficient diets in human subjects that the earliest symptoms are “emotional” in character and may be classified as “psychosomatic”. If the symptoms are not recognized and go on for years, we can assume that the structure of the enzymes deteriorates. If and when clinical and biochemical recognition occurs, it would seem logical to assume that the vitamin cofactor would have to be increased drastically in order to reconstitute the enzyme. The vitamin is therefore used under those circumstances as a drug until reconstitution is complete. When the normal activity of the enzyme is restored, the vitamin returns to its state as a nutrient and its therapeutic dose needs to be reduced.

Prevention Versus Recovery

In my case, the explanation may be different. I was taking a colossal dose of TTFD with insufficient concentrations of the B complex, perhaps causing an imbalance in the selective activities of each. If that is the mechanism, I can only guess that it interfered with oxidative metabolism. Also, I can no longer state that there is no “toxicity” from taking large doses of TTFD. It does seem to imply that the remainder of the B complex should always be used with TTFD. We know that beriberi patients required 100 mg of thiamine three times a day for months. If blood sugar was normal they always responded. If there was hyperglycemia the response was slower. If there was hypoglycemia, some did not respond at all. We can be sure that the thiamine dependent enzymes were sick and that they were being reconstituted by thiamine being used as a drug. Thus, my situation is quite different than treating a thiamine deficient patient. High doses are required only for sick thiamine dependent enzymes that have long been lacking sufficient concentrations of their cofactor(s). Preventive therapy is different than long-term deficiency.

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 julien Tromeur on Unsplash.

This article was published originally on December 21, 2016.

Rest in peace Dr. Lonsdale, May 2024.

The Analgesic Effects of B Vitamins

by Derrick Lonsdale MD, FACN, CNS

Published on December 9, 2024

7613 views

It appears that high doses of vitamins B1, B6 and B12, administered separately or in combination, can alleviate acute pain by potentiating the analgesic effect of non-opioid analgesics such as diclofenac (an NSAID), sold under various trade names. These facts were published in a German paper. In addition, a randomized, double-blind, controlled clinical study was reported in 378 patients with lumbago. The term lumbago is a relatively old one and it is now often referred to as “back strain”.

The patients were divided into two groups, half of them receiving diclofenac together with very large doses of vitamins B1, B6 and B12. The other half received only diclofenac . The investigators concluded that the addition of the B vitamins did indeed enhance the analgesic effect of the drug. The primary mechanism for the anti-inflammatory, anti-pyretic and analgesic action of diclofenac is thought to be by a biochemical mechanism that is well known in the body and described in the paper.

When I read this, I became aware that the mechanism they were describing was the same mechanism that has been described for one of the actions of thiamine tetrahydrofurfuryl disulfide (TTFD, Allithiamine, Lipothiamine) a thiamine derivative that I have mentioned a number of times in posts on this website. When I further researched the mechanisms of action of diclofenac, I read that “diclofenac also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis”. Could it be that the drug has an effect on mitochondrial DNA in people using it to relieve their pain? If so, this would be a serious indictment on its use.

Mitochondrial DNA

We now have reason to believe that our mitochondria (cellular energy producing organelles) have evolved from an original bacterium millions of years ago, and we now know that they have their own genes. These genes, inherited only from the mother, are completely separate from the cellular genes that we inherit from both parents. They are vitally important in the function of mitochondria that are responsible for synthesizing ATP, the energy currency used by the body. The interesting thing is that mitochondrial DNA is like bacterial DNA, has a different conformation from that of cellular DNA, and could be expected to be sensitive to the “DNA related bacteriostatic activity” reported to be one of the effects of diclofenac.

Side Effects of Diclofenac

There are 50 side effects of diclofenac recorded online. It may surprise you to know that 20 of the symptoms reported as side effects are identical to those that are well known in relationship to the thiamine (vitamin B1) deficiency disease, beriberi. Since thiamine is vital to the normal function of mitochondria, perhaps it suggests why three members of the vitamin B complex enhance the analgesic effect of the drug by protecting the patient from harm. This would enable it to be used with reduced dose, thus obviating the possible appearance of side effects.

Side Effects of Pharmaceuticals

It is always wise for a patient who is taking a drug to know what the potential side effects are. With this story of diclofenac, I was reminded of a drug that was produced in the 1930s in order to stimulate weight reduction. The chemical name is dinitrophenol (DNP). The side effects were so severe and occasionally caused sudden death, so it was withdrawn in 1938. Its present use is in experimental research in animals because it inhibits mitochondrial function and enables the researcher to study energy metabolism. Believe it or not, DNP is still available for weight reduction. There is no doubt that it works but it certainly offends the Hippocratic oath accepted by all physicians, “thou shalt do no harm”.

Genetic Susceptibility

We simply do not know the genetically determined susceptibility of an individual in the use of a foreign agent prescribed to relieve a given symptom. The body always recognizes a “foreigner” and sets about breaking it down and getting it out of the body as quickly as possible. If a vitamin is used in a much larger dose than merely replacing it as an essential nutrient, it may be thought of as a drug. This is really a new concept in medicine and has not yet reached the collective psyche of medical practice. Perhaps the body recognizes the huge dose, but uses what it needs and excretes the excess. The trouble with that is that the present concept is that vitamin replacement is thought to be confined to the tiny doses found in natural food that are required by a healthy individual. No thought has been given to the fact that a vitamin may have to be used in order to stimulate and restore the decayed effectiveness of the enzyme to which it must bind. It is as though the roles of the enzyme and the vitamin are reversed. In a sense, the enzyme becomes cofactor to its requisite vitamin rather than the normal enzyme/cofactor relationship.

Energy Metabolism is the Core Issue

What seems to be emerging from all this is that failure of energy metabolism, coupled with genetic risk and the imposition of individual life stresses, provides us with a new medical model for disease. Besides killing the “enemy”, the bacteria, viruses or cancer cells safely, the only real treatment possible is an educated use of nutritional components to coerce damaged cellular systems back into a state of functional efficiency. Healing takes energy and only the body knows how to do that. We should give it every possible assistance. There is much evidence that even cancer cells become maverick because of devious energy metabolism.

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 Inge Poelman on Unsplash.

This article was published originally on July 27, 2016.

Rest in peace Dr. Lonsdale, May 2024.

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