thiamine heart failure

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.


Derrick Lonsdale M.D., is a Fellow of the American College of Nutrition (FACN), Fellow of the American College for Advancement in Medicine (FACAM). Though now retired, Dr. Lonsdale was a practitioner in pediatrics at the Cleveland Clinic for 20 years and was Head of the Section of Biochemical Genetics at the Clinic. In 1982, Lonsdale joined the Preventive Medicine Group to specialize in nutrient-based therapy. Dr. Lonsdale has written over 100 published papers and the conclusions support the idea that healing comes from the body itself rather than from external medical interventions.


  1. My father died of beriberi. I long suspected it but after reading this, I am sure of it. Twenty years before his death he had suffered from Guillain-Barre but had recovered. Now, whether his body demanded more Thiamine because of this history or not, I don’t know; but I do know he ate an exorbitant about of sweets in all forms. For five years before his death, he would dig white, tiny nodules our of his hands with a knife. Mother thought he was crazy but he said they bothered him. His doctors never could find anything wrong with him. His eyes also would sometimes involuntarily cut away when he was looking at you. Like a jerk, and then he could bring them back and focus again. It finally came to the point that he was stricken and couldn’t get up or feel. (He had had increasing neuropathy.) When he was in the hospital, I asked to see his tongue. I expected to see migrating depapillation. Instead I saw a completely smooth and completely red tongue – as if the whole area was wiped clean! I requested he be given Vitamin B1 and it was administered but, alas, it was far too late. He passed away. He refused to eat properly when he was frequently away from home with work and when he was home, he refused to take supplements. Sometimes there’s only so much one can do for others. After he passed away, I found that he had been carrying around nitroglycerine tablets he had been prescribed.

  2. Dr. Lonsdale, I noticed that Patricia’s post from May 30, 2018 mentions several drugs that clearly have a fluorine base. I believe my derranged nervous sytem and connective tissue problems have also been caused by fluorine based drugs initiating profound thiamine deficiency. I was taking amoxicillin and then a fluoroquinolone (Levaquin) and then ecitalopram (Lexapro). Why are fluorine based drugs causing thiamine deficiency? Antibiotics presumably act on our cells as they do on bacterial cells to inhibit them, but is it the fluorine/fluoride that enables this? Perhaps fluorine and fluoride deserve a closer look in relation to mitochondria and thiamine pathways. Our water and food is laced with it in the United States. And if it is fluoride to blame, how do we get it back out of the body? Your thoughts are appreciated.

    • There is some evidence in the medical literature that fluoride has an effect on energy metabolism. The introduction of fluoride in toothpaste has raised some questions concerning dose. It is probably the same old story, moderation in everything. An extremely tiny dose, perhaps that found in natural foods, may be good for developing teeth but it’s addition to toothpaste may exceed the natural requirement and introduce toxicity. The same thing applies to drugs that contain fluoride.

  3. Dr. Lonsdale, if you had a dog or a cat would you personally supplement thiamin to them to supplement their diets that are most likely deficient? I am thinking that this is what I want to do with my fur babies since I have gotten such great results using your recommendations. I was able reach better health after a long bout of chronic illness and finally able to move past the plateau I was unable to move past with the help of Allithiamine. All the pet products I see use the Thiamine monophosphate form would it be better to use Allithiamine and if using Allithiamine is better for pets too how does one figure out dosing for a dog or cat?

  4. Hi Doctor Lonsdale,

    Some of the literature on thiamine deficiency lists “atrophic skin changes” as a possible symptom. I started having a bizarre issue several months ago that has persisted along with several other problems I believe could be caused by thiamine deficiency. My fingertips have become almost continuously wrinkled like when one gets out of a long bath. I seem to have lost collagen or fat in them. I also have developed what resemble bier spots on my palms when they are at my sides. They over vasodilate and become engorged with blood in a mottled patten that does not seem to be classic palmar erythema (liver numbers are good). I should note this has all started after going 100% gluten free. In general my overall health has declined which led me to suspect deficiencies. I just found out my folate level is now below the bottom range. Any insight would be much appreciated. Thank you!

    • Because thiamine deficiency causes energy loss, virtually anything can happen in the body, depending on where deficiency occurs and assuming that the distribution is not uniform. On the other hand, I would suggest that you look at the folate level.

  5. This is an answer to 2 comments by Patricia and 1 comment from Malcolm Maclean.
    Patricia 5/30. 1. There is an interesting relationship between cancer and thiamine that is unfortunately all too frequently overlooked.
    2.In a mouse study, a dose of 2500 times the mouse RDA (for mice) of thiamine stimulated the tumors. A dose of 25,000 times the mouse RDA caused a reduction in the size of the tumor. The mechanism is unknown but needs to be studied.
    3.There are a number of manuscripts concerning the diagnosis of thiamine deficiency as a result of chemotherapy.
    4. I reported thiamine deficiency resulting from parenteral therapy many years ago. The case that I reported was receiving 25 mg a day of thiamine in the fluid. There is a clear-cut ratio between the glucose calories and thiamine adequacy. High dose glucose requires high dose thiamine.
    5. Post I/V thiamine hypoglycemia was an interesting MS.
    Note that most of the MSs concerning these relationships come from mainly Eastern countries, not from America.
    Patricia 5/31. There seems to be some vague association between taurine and thiamine and there is a supplement of magnesium taurate available but the issue is not clear to me.

    Malcolm Maclean. Thiamine, together with magnesium, are both factors to a number of enzymes. If those cofactors are lacking in the diet and the symptoms that develop from it are unrecognized, my experiences is that the enzymes deteriorate in their function and it requires megadoses of the cofactors to restore enzyme function. The history of beriberi tells us this because it took 100 mg of thiamine a day for months to restore a patient’s functions.If there was an associated hyperglycemia, the response was poor. If there was associated hypoglycemia, the patient often did not respond at all. In some cases there is a variable genetic background to the thiamine deficiency and this might require colossal doses. I started a three-month-old baby on 150 mg of thiamine a day and her symptoms rapidly improved. There was a genetic background and as she grew, symptoms would begin to return. The mother, without consulting me, would increase the thiamine hydrochloride herself and the dose eventually reached 7 g.There was no evidence of toxicity but she did die of toxic shock syndrome from an infection at the age of 27 years. I have never seen any information advocating 6-8 g and certainly this would be absurd in the vast majority of cases. Please understand that we are talking about phenomena that should have detailed research to make them commonplace. Using thiamine as a drug is brand new.The phenomenon of the initial symptoms becoming worse before getting better (paradox) requires study.

  6. Hello Dr Lonsdale, I have very much enjoyed reading your texts devoted to Thiamine deficiency. I had independently come to the conclusion that Thiamine deficiency is widespread and largely unrecognised, before fortunately chancing upon your excellent web pages.
    I have a question:
    You have enormous experience in the use of Thiamine as a supplement.
    Somewhere I read that long-term Thiamine deficiency can cause the Thiamine dependent enzymes to “go to sleep”. Further, it was proposed that in order to overcome the loss of function of these enzymes, it was necessary to “mega-dose” these enzymes with Thiamine in order to “wake them up”. I believe Thiamine 6-8 grams daily was advised for initial dosing.
    I can’t find the web page where I read this.
    Is this your experience?
    If so, what has been your typical advice on Thiamine dosing in chronic Thiamine deficiency?
    Thank you for giving this your attention. I would really appreciate if you would find the time to copy your reply to my email address. The reason being that I may not be able locate your web page reply.
    Malcolm Maclean

  7. Dr. Lonsdale, apparently not only cisplatin causes deficiency of B1. I have read about cases of cancer treating agents like doxifluridine, ifosfamide, and 5-fluorouracil causing problems as well. I even noticed that in the Mayoclinic website, when you look into the Capecitabine page, it says that Thiamine may be a good addition to the treatment. But interesting that it doesn’t say anything about Thiamine in the 5-FU page and 5-FU agent is very close related to the Capecitabine agent.

    Severe Encephalopathy, Lactic Acidosis, Vegetative Instability and Neuropathy with 5-Fluorouracil Treatment – Pyrimidine Degradation Defect or Beriberi?

    Wernicke’s Encephalopathy in an Acute Myeloid Leukemia Patient: A Case Study

    A Case of Wernicke’s Encephalopathy Following Fluorouracil-based Chemotherapy

    • My doctor treats cancer, and he says cisplatin causes secondary cancer over time. He custom doses B vitamins to treat specific cancers. Perhaps it’s the B1 deficiency that precipitates secondary cancer. My brother went through a few rounds of cisplatin and his white blood cell count is low, which can be caused by nutrient deficiencies.

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