Beriberi, the Great Imitator

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beriberi great imitator
Because of some unusual clinical experiences as a pediatrician, I have published a number of articles in the medical press on thiamine, also known as vitamin B1. Deficiency of this vitamin is the primary cause of the disease called beriberi. It took many years before the simple explanation for this incredibly complex disease became known. A group of scientists from Japan called the “Vitamin B research committee of Japan” wrote and published the Review of Japanese Literature on Beriberi and Thiamine, in 1965. It was translated into English subsequently to pass the information about beriberi to people in the West who were considered to be ignorant of this disease. A book published in 1965 on a medical subject that few recall may be regarded in the modern world as being out of date and of historical interest only, however, it has been said that “Those who do not learn history are doomed to repeat it”. And repeat it, we are.

Beriberi is one of the nutritional diseases that is regarded as being conquered. It is rarely considered as a cause of disease in any well-developed country, including America. In what follows, are extractions from this book that are pertinent to many of today’s chronic health issues. It appears that thiamine deficiency is making a comeback but it is rarely considered as a possibility.

The History of Beriberi and Thiamine Deficiency

Beriberi has existed in Japan from antiquity and records can be found in documents as early as 808. Between 1603 and 1867, city inhabitants began to eat white rice (polished by a mill). The act of taking the rice to a mill reflected an improved affluence since white rice looked better on the table and people were demonstrating that they could afford the mill. Now we know that thiamine and the other B vitamins are found in the cusp around the rice grain. The grain consists of starch that is metabolized as glucose and the vitamins essential to the process are in the cusp. The number of cases of beriberi in Japan reached its peak in the 1920s, after which the declining incidence was remarkable. This is when the true cause of the disease was found. Epidemics of the disease broke out in the summer months, an important point to be noted later in this article.

Early Thiamine Research

Before I go on, I want to mention an extremely important experiment that was carried out in 1936. Sir Rudolf Peters showed that there was no difference in the metabolic responses of thiamine deficient pigeon brain cells, compared with cells that were thiamine sufficient, until glucose (sugar) was added. Peters called the failure of the thiamine deficient cells to respond to the input of glucose the catatorulin effect. The reason I mention this historical experiment is because we now know that the clinical effects of thiamine deficiency can be precipitated by ingesting sugar, although these effects are insidious, usually relatively minor in character and can remain on and off for months. The symptoms, as recorded in experimental thiamine deficiency in human subjects, are often diagnosed as psychosomatic. Treated purely symptomatically and the underlying dietary cause neglected, the clinical course gives rise to much more serious symptoms that are then diagnosed as various types of chronic brain disease.

  • Thiamine Deficiency Related Mortality. The mortality in beriberi is extremely low. In Japan the total number of deaths decreased from 26,797 in 1923 to only 447 in 1959 after the discovery of its true cause.
  • Thiamine Deficiency Related Morbidity. This is another story. It describes the number of people living and suffering with the disease. In spite of the newly acquired knowledge concerning its cause, during August and September 1951, of 375 patients attending a clinic in Tokyo, 29% had at least two of the major beriberi signs. The importance of the summer months will be mentioned later.

Are the Clinical Effects Relevant Today?

The book records a thiamine deficiency experiment in four healthy male adults. Note that this was an experiment, not a natural occurrence of beriberi. The two are different in detail. Deficiency of the other B vitamins is involved in beriberi but thiamine deficiency dominates the picture. In the second week of the experiment, the subjects described general malaise, and a “heavy feeling” in the legs. In the third week of the experiment they complained of palpitations of the heart. Examination revealed either a slow or fast heart rate, a high systolic and low diastolic blood pressure, and an increase in some of the white blood cells. In the fourth week there was a decrease in appetite, nausea, vomiting and weight loss. Symptoms were rapidly abolished with restoration of thiamine. These are common symptoms that confront the modern physician. It is most probable that they would be diagnosed as a simple infection such as a virus and of course, they could be.

Subjective Symptoms of Naturally Occurring Beriberi

The early symptoms include general malaise, loss of strength in knee joints, “pins and needles” in arms and legs, palpitation of the heart, a sense of tightness in the chest and a “full” feeling in the upper abdomen. These are complaints heard by doctors today and are often referred to as psychosomatic, particularly when the laboratory tests are normal. Nausea and vomiting are invariably ascribed to other causes.

General Objective Symptoms of Beriberi

The mental state is not affected in the early stages of beriberi. The patient may look relatively well. The disease in Japan was more likely in a robust manual laborer. Some edema or swelling of the tissues is present also in the early stages but may be only slight and found only on the shin. Tenderness in the calf muscles may be elicited by gripping the calf muscle, but such a test is probably unlikely in a modern clinic.

In later stages, fluid is found in the pleural cavity, surrounding the heart in the pericardium and in the abdomen. Fluid in body cavities is usually ascribed to other “more modern” causes and beriberi is not likely to be considered. There may be low grade fever, usually giving rise to a search for an infection. We are all aware that such symptoms come from other causes, but a diet history might suggest that beriberi is a possibility in the differential diagnosis.

Beriberi and the Cardiovascular System

In the early stages of beriberi the patient will have palpitations of the heart on physical or mental exertion. In later stages, palpitations and breathlessness will occur even at rest. X-ray examination shows the heart to be enlarged and changes in the electrocardiogram are those seen with other heart diseases. Findings like this in the modern world would almost certainly be diagnosed as “viral myocardiopathy”.

Beriberi and the Nervous System

Polyneuritis and paralysis of nerves to the arms and legs occur in the early stages of beriberi and there are major changes in sensation including touch, pain and temperature perception. Loss of sensation in the index finger and thumb dominates the sensory loss and may easily be mistaken for carpal tunnel syndrome. “Pins and needles”, numbness or a burning sensation in the legs and toes may be experienced.

In the modern world, this would be studied by a test known as electromyography and probably attributed to other causes. A 39 year old woman is described in the book. She had lassitude (severe fatigue) and had difficulty in walking because of dizziness and shaking, common symptoms seen today by neurologists.

Beriberi and the Autonomic Nervous System

We have two nervous systems. One is called voluntary and is directed by the thinking brain that enables willpower. The autonomic system is controlled by the non-thinking lower part of the brain and is automatic. This part of the brain is peculiarly sensitive to thiamine deficiency, so dysautonomia (dys meaning abnormal and autonomia referring to the autonomic system) is the major presentation of beriberi in its early stages, interfering with our ability for continuous adaptation to the environment. Since it is automatic, body functions are normally carried out without our having to think about them.

There are two branches to the system: one is called sympathetic and the other one is called parasympathetic. The sympathetic branch is triggered by any form of physical or mental stress and prepares us for action to manage response to the stress. Sensing danger, this system activates the fight-or-flight reflex. The parasympathetic branch organizes the functions of the body at rest. As one branch is activated, the other is withdrawn, representing the Yin and Yang (extreme opposites) of adaptation.

Beriberi is characterized in its early stages by dysautonomia, appearing as postural orthostatic tachycardia syndrome (POTS). This well documented modern disease cannot be distinguished from beriberi except by appropriate laboratory testing for thiamine deficiency. Blood thiamine levels are usually normal in the mild to moderate deficiency state.

Examples of Dysfunction in Beriberi

The calf muscle often cramps with physical exercise. There is loss of the deep tendon reflexes in the legs. There is diminished visual acuity. Part of the eye is known as the papilla and pallor occurs in its lateral half. If this is detected by an eye doctor and the patient has neurological symptoms, a diagnosis of multiple sclerosis would certainly be entertained.

Optic neuritis is common in beriberi. Loss of sensation is greater on the front of the body, follows no specific nerve distribution and is indistinct, suggestive of “neurosis” in the modern world.

Foot and wrist drop, loss of sensation to vibration (commonly tested with a tuning fork) and stumbling on walking are all examples of symptoms that would be most likely ascribed to other causes.

Breathlessness with or without exertion would probably be ascribed to congestive heart failure of unknown cause or perhaps associated with high blood pressure, even though they might have a common cause that goes unrecognized.

The symptoms of this disease can be precipitated for the first time when some form of stress is applied to the body. This can be a simple infection such as a cold, a mild head injury, exposure to sunlight or even an inoculation, important points to consider when unexpected complications arise after a mild incident of this nature. Note the reference to sunlight and the outbreaks of beriberi in the summer months. We now know that ultraviolet light is stressful to the human body. Exposure to sunlight, even though it provides us with vitamin D as part of its beneficence, is for the fit individual. Tanning of the skin is a natural defense mechanism that exhibits the state of health.

Is Thiamine Deficiency Common in America?

My direct answer to this question is that it is indeed extremely common. There is good reason for it because sugar ingestion is so extreme and ubiquitous within the population as a whole. It is the reason that I mentioned the experiment of Rudolph Peters. Ingestion of sugar is causing widespread beriberi, masking as psychosomatic disease and dysautonomia. The symptoms and physical findings vary according to the stage of the disease. For example, a low or a high acid in the stomach can occur at different times as the effects of the disease advance. Both are associated with gastroesophageal reflux and heartburn, suggesting that the acid content is only part of the picture.
A low blood sugar can cause the symptoms of hypoglycemia, a relatively common condition. A high blood sugar can be mistaken for diabetes, both seen in varying stages of the disease.

It is extremely easy to detect thiamine deficiency by doing a test on red blood cells. Unfortunately this test is either incomplete or not performed at all by any laboratory known to me.

The lower part of the human brain that controls the autonomic nervous system is exquisitely sensitive to thiamine deficiency. It produces the same effect as a mild deprivation of oxygen. Because this is dangerous and life-threatening, the control mechanisms become much more reactive, often firing the fight-or-flight reflex that in the modern world is diagnosed as panic attacks. Oxidative stress (a deficiency or an excess of oxygen affecting cells, particularly those of the lower brain) is occurring in children and adults. It is responsible for many common conditions, including jaundice in the newborn, sudden infancy death, recurrent ear infections, tonsillitis, sinusitis, asthma, attention deficit disorder (ADD), hyperactivity, and even autism. Each of these conditions has been reported in the medical literature as related to oxidative stress. So many different diseases occurring from the same common cause is offensive to the present medical model. This model regards each of these phenomena as a separate disease entity with a specific cause for each.

Without the correct balance of glucose, oxygen and thiamine, the mitochondria (the engines of the cell) that are responsible for producing the energy of cellular function, cannot realize their potential. Because the lower brain computes our adaptation, it can be said that people with this kind of dysautonomia are maladapted to the environment. For example they cannot adjust to outside temperature, shivering and going blue when it is hot and sweating when it is cold.

So, yes, beriberi and thiamine deficiency have re-emerged. And yes, we have forgotten history and appear doomed to repeat it. When supplemental thiamine and magnesium can be so therapeutic, it is high time that the situation should be addressed more clearly by the medical profession.

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  1. Hi Dr. Lonsdale,

    I was wondering if you have a post or could possible write one specifically on how thiamine deficiency affects digestion?

    I have been referring so many people to your research and articles to help with things such as Chronic fatigue syndrome, diabetes, thyroid disorders, reflux, and especially bad digestion. I have tried so many different supplements over the years to help with my chronic indigestion problems, but nothing has ever helped quite so much as taking large doses of thiamine HCL. If you could write a post about how thiamine deficiency regulates the digestion system specifically, it would be a big help to me and so many others. Thank you for your time and God bless .

    1. Thiamin deficiency beriberi produced many symptoms including what might be loosely called “indigestion”. In one stage of the disease, there could be a low acid content in the stomach. If thiamin was given to the patient the acid content of the stomach became excessive before it became a normal concentration. In another stage of the disease the stomach could have an excess of acid. If thiamin was given to the patient, the acid content would become low before it became normal. In other words hypoacidity (too little) or hyperacidity (too much) could be seen in a given patient according to the stage of the disease. I would assume that when you took thiamin, you may have gone through this process.

  2. I’m a 44 year old woman in the US. I have been battling a b-vitamin deficiency (self-diagnosed) off and on for the past nine months. The deficiency occurred because of a thyroid issue. But looking back, I think it was also the other way around as well. My thyroid issue occurred because of micronutrient deficiency.

    It’s such a breath of fresh air to read your articles. It’s been a real struggle dealing with the medical community. I’ve had a few doctors roll their eyes at me or worse, just stare blankly at me, when I ask about how vitamin and mineral deficiencies might be playing a role in my recovery. The more I learn, the more sad and frustrated I feel that none of the doctor’s I’ve seen know about this stuff.

    My thyroid started acting badly a year ago. I was diagnosed with hypothyroidism after I’d already started to feel better from certain foods, and supplementing with vitamins, so I decided not to take medication. I didn’t really know what I was doing when I started back then, and some of the things I tried made me go into hyperthyroid a little bit. I believe the hyper-metabolic state used up my stores of b-vitamins, maybe zinc and some other things. This was made very obvious last New Years Eve, after three cocktails led to me waking up the next day with more than just the usual hangover symptoms. Especially strange were my ruby red lips, and a rash on my hands and wrists. A week or so later, I developed a sore tongue and mouth.

    I slowly recovered from the New Years Even thing, but it took two months for my tongue to feel normal. But then new symptoms started, like zapping pain in my toes and fingers. At some point I read that B6 toxicity can cause nerve damage which feels like zapping in the toes and fingers. I was worried that was happening to me, so I tried taking a lot of all the b-vitamins and just a little of B6, and seemed to do well. But after three months of large doses of b-vitamins and just 4mg of B6, my tongue got sore again, and I got a headache that wouldn’t leave. I also felt very emotional and sad, and my period came and stayed, for several weeks. I decided I should try B6 again since it was the only vitamin I wasn’t taking much of.

    I started with 25mg of B6, and immediately felt happier, my period stopped, and I thought everything would be great from there. Well, it’s been very up and down. I think that I got so low in B6 that even just 25mg of B6 seems to make me hyperthyroid. I read that B6 brings iodine into the thyroid. And then when I get hyperthyroid, I get symptoms of thiamine deficiency again. Symptoms of both the wet and dry beri beri.

    Because I was worried about taking B6, I also added Alpha Lipoid Acid along with the B6, but it made me even more low on thiamine, which I later read can happen to people who are already low in thiamine. I had heart palpitations, and chest pain, edema, joint pain, and a feeling like it was hard to breath. It took me two weeks to make the connection to the ALA. I stopped the ALA, and increased my thiamine dose to 500mg twice a day, and I’m doing much better.

    I’ve continued with the B6, and now I’m up to 100mg in a B-100 complex extended release tablet, which i take twice a day. I had been taking iodine for the past year, but it seems it’s not compatible with taking the B6, so I stopped. Amazingly, one month after starting a lot of B6, the three breast lumps that I had for the past four years have gone away. So that is kind of a miracle to me. My periods are more normal, and I just feel so much happier. But I still have this sore tongue every day. It comes and goes. I can’t figure out what is causing it. Thiamine? Maybe I’m not absorbing thiamine well, even at 500mg twice a day. I also still have a little bit of zapping in my toes, although that is much better than before.

    I just convinced my doctor to order a bunch of blood work and asked them to check my b-vitamins along with zinc and copper, iron and vitamin A and D. But I’m not sure how reliable some of those checks are.

    Do you have any experience with someone like me? Any recommendations for how to progress? I’ve been taking a 500mg thiamine supplement plus a co-enzymated carboxylase version. I also have taken benfothiamine, with no much noticeable change. But I saw you recommended lipothiamine for someone and I’m going to order that and see how I feel on it.

    After more than a year doing my own self-guided recovery, it would be awesome to hear from an expert on the subject.

  3. This is a very interesting comment. There are several questions and I will take them one by one
    1. It is true that dietary thiamine has a limited absorption. This is because of the transporters that are required. It is also true that there are a number of synthetic thiamine derivatives. The best one, in my view, is thiamine tetrahydrofurfuryl disulfide (TTFD). Without going into the technical issues, this derivative does not require the transporters and it can be used as a “drug” to stimulate enzyme activity that is dependent on thiamine. The trade name for this is Lipothiamine and it comes in a dose of 50 mg. The usual dose is one or two tablets a day but it has no toxicity and much bigger doses can be used if necessary.
    2. You are quite right about autistic children. The real name of the game is unquestionably in the consumption of junk food, particularly sugar. Although it is now well known that sugar is toxic the exact cause of the toxicity is unknown. My answer is that thiamine is an absolutely essential for its metabolism and the lower part of the brain is highly dependent on thiamine. This part of the brain organizes all our adaptive mechanisms, both mental and physical so it is hardly surprising that individuals affected by this are maladapted to the environment. But thiamine does not work on its own. It is a member of a massive team of nutrients although it might well be the most essential.3.Post sugar seizures—-NO SUGAR + thiamine/magnesium supplement.

    1. I am a 76 year old male with many of the symptoms that you describe including neuropathy. You mention much bigger doses being used. How does one do this and what dose would be most advantageous? Should the dose be divided for the day? I have also heard of benfotiamine. Can both of these thiamines be taken together? I’m not familiar with supplements and I consider myself very lucky that I came upon your research. You really seem to be the only expert in this field as I found many references and all authored by you. Thank you.

  4. Hello Dr Lonsdale, I am a great admirer of your work and also believe that ‘simple’ nutritional support is the key to correcting metabolic imbalance that leads to disease. I had a couple of questions, if I may? There are a number of forms of B1 available, and the difficulty is in figuring out dosages. For most forms I have heard only about 5 mg can be transported out of the gut at one time. Is this also true of alliathiamine? It comes in only one dose, 50 mg. How much of that is actually crossing into the blood (assuming no transporter issues)? What is your take on the co-enzyme forms of B1, or ‘active’ B1?

    I am interested in how thiamine deficiency affects the autistic population, not just at the time of their initial regression into autism, but at other times of metabolic crisis. Often these kids experience immune system vulnerability and even those under the care of biomedical doctors who are supplementing, their poor gut health causes chronic malnourishment. I have observed that many will have sudden onset of issues post illness, which look similar to what is called PANDAS, or an auto-immune issue induced by strep, but it is NOT strep induced. What is your experience with thiamine and metabolic crashes resulting in tics and OCD type behavior?

    Finally, have you ever associated absence seizures with thiamine deficiency? For example, I know a child who experiences absence seizures shortly after eating sugary foods. He blanks out and stares into space. Could this be related to thiamine? No other known seizure issues other than the staring after or even while eating high carb/sugar foods.

    Again, thank you for your continued involvement in the health community! I have only recently come to connect some dots via copper dysregulation and its association with Wilson’s Disease and thiamine. Many ASD children have profound copper dysregulation that has not yet been found to have a genetic component. Your research is filling in the bigger picture for me and other parents seeking to help their children.


    1. I did not see this comment at the time. There will be a new post published here that is relevant to this question.

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