stumbling while walking

Beriberi: The Great Imitator

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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 A book published in 1965 on a medical subject that few recall may be regarded in the modern world as being out of date and of historical interest only, however, it has been said that “Those who do not learn history are doomed to repeat it”.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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This article was published originally on November 4, 2015. 

Neuropathy and Multiple Sclerosis Treated with Biotin, Thiamine, and Magnesium

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Neuropathy From Unknown Causes

I was diagnosed with “Neuropathy from unknown causes” back in 2005. It started in my feet (coldness, loss of feeling, cramps, stiffness). Then, over the years the numbness worked its way up to my calves, with severe cramps, then thighs and even my biceps got involved (squeeze the bicep, get a cramp). Sometimes I would have numbness in the hands and face. I started having a gait issue occasionally with a foot drop. Overall my legs got extremely stiff. Muscles felt like piano wires and no amount of stretching helped. I also had acid reflux issues on and off and a pain in the low left abdomen which often expressed out the back at the lower left hip. I used to love lifting weights but stopped as instead of soreness then recovery with more strength, lifting seemed to cause soreness that just increased no matter how long I spaced recovery between sessions. Doctors said they eliminated serious possibilities and whatever it was wouldn’t kill me. They noticed some brain lesions, but joked – well who doesn’t have those :-). Still around 14 years later so they were right.

Over the last couple of years, I started to have frequent stumbles which progressed to several serious falls last year. Luckily, I avoided serious injury. My diagnosis hasn’t been changed nor looked at since 2005, but to be fair, when rushing through the last appointment with my doctor I forget to mention the stumbling and falling as a new symptom. There seems to be a genetic factor at play as my father suffered from stiff legs and a walking issue and neuropathy. Both brothers are having similar issues and an Aunt had Parkinson’s Disease.

Enter Thiamine

I ran across your work with thiamine and have started high dose of the TTFD form of thiamine (allithiamine and lipothiamine) about 100 mg 3x a day. I saw a quick resolution of the stumbling and falling issue, my balance has been fantastic, a reduction in muscle pain throughout my body, acid reflux vanished, and a big improvement in cramping in thighs and calves. I also have tinnitus and haven’t seen much change there, it comes and goes.

My brother has also started. He had water on the heart after having chemotherapy, low energy, constant diarrhea, bloating, weight gain, and the neuropathy in the legs. He is doing very well with only 50 mg a day.

We both noticed after 3-4 days, a relaxation of chronic muscle spasms and increased flexibility, especially in the shoulders. My brother says he could raise either arm and touch the middle of his back for the first time in over 40 years. My brother is also losing body fat around the belly quickly, he is overweight, while my weight has been steady instead of the usual battle to stop gaining weight. I also feel far stronger.

Recently, I got busy and missed some doses and the muscle cramping returned quickly and getting back to 100 mg 3X a day (along with a B-complex) cleared things up quickly. I felt things were still very good but not quite as effective, so I recently up’ed to 100 mg, 100 mg, 150 mg, 150 mg, for a total of 500 mg as I also wanted to see if I could tackle the tinnitus. In the mornings, I was waking up with my feet feeling a bit tight and after taking my morning dose I could quickly feel the feet unwinding. I noticed that the higher dose just before bedtime seemed more effective, and waking without the tight feeling in the feet.

As for questions – I am 6’4″, 240 lbs, and 64 years old. My dosage is 2.8 mg/kg. My remaining issues are tinnitus and some eye issues (vitreous detachment, lots of floaters and flashes in both eyes).  The only things I might attribute as side effects – I get hungry after my morning dose – as if I’m experiencing low blood sugar but not the other doses. I’m sometimes twitchy in the mornings (maybe a case for that higher dose before bedtime). I sometimes feel a bit spacey/hard to focus shortly after a dose which passes, and these occasional stabbing/shooting pains sometimes in nerves that haven’t bothered me before – I think this more to do with the relaxing muscles and nerves getting pinched due to my new freedom of movement and adjusting to that. That seems to only happen from sitting around and hold a posture too long then moving not when I am working on projects.

The Road to Recovery: Thiamine, Biotin, and Magnesium

The above was taken from a comment I made on the post “Beriberi is alive and well in America” in April. I had been led to the post doing searches on beriberi as I was struck how similar my symptoms were to the disease. Dr Lonsdale proposed thiamine+biotin+magnesium. I tried the thiamine first in the different forms and the lipothiamine worked by far the best. It mostly reduced the electric shocks in the feet/legs. I accidentally took 50 mg biotin thinking I was taking 5 mg and it had a near immediate and profound effect throughout my body erasing my stiffness/numbness/tingling and giving me great relief in my tightly cramped feet. It also brought back normal sensation. One effect was a powerful feeling of pulsation (blood flow) at the base of the skull after taking the biotin. I had been experiencing a lot of falls and stumbling as well and that completely stopped once I started the biotin.

During my experimentation phase, I was looking at the doses given for Biotin Dependent Basal Ganglia Disease and decided to try about 800 mg of biotin. I quickly got a severe nausea and started throwing up copious amounts of green bile, picture “The Exorcist”. In hindsight I wonder if that was a paradox reaction. So I dialed that back to about 10 mg biotin + 50 mg thiamine + occasional magnesium and was doing quite well. Not all my symptoms were gone but all in all manageable. I was also a bit bad on self – care as I would go keto/low carb, no alcohol for winter/spring and drop 30 lbs but back to an anything goes with high carbs, occasional alcohol for summer and fall with a worsening of symptoms but tolerable along with rapid weight gain.

A Switch to Conventional Medicine: Prednisone

This fall I decided that once and for all I was going to get a good health checkup and also a mainstream diagnosis and as part of that dropped the thiamine/biotin so to not affect some scheduled routine blood tests. I immediately had a big flareup in pain and stiffness which got me first sent to Rheumatology where they said they didn’t understand why I was there, then to a physiatrist who found some spinal stenosis and prescribed a course of prednisone. The prednisone worked like magic. All my symptoms vanished except for my calves and feet where the pain and tightness was gone but the spasms and electric feelings were very high. I had the opposite of expected side effects on the prednisone. I didn’t feel hunger, drank a lot of water and lost weight, no bloating, minor increase in BP. I had also been experiencing on/off chills with a low body temperature to the point I would wear a winter coat indoors at times. The prednisone vanished this, lighting up an internal furnace of heat and energy. I felt great, my motivation increased, and I got a lot of projects done, whereas before I was dragging. Even my tinnitus was greatly reduced and even vanished at times. My heart rate which was around 60 popped up to 75. Unfortunately, I broke my sleep tracker which pre-prednisone told me I was dropping into low 50’s and even high 40’s heart-rate while sleeping. The stomach pain, head pain, stiffness, numbness all gone!

Then came the taper. I started to feel the cold again as I tapered off and on and the tinnitus came roaring back. I started to feel like I had a pain sensitivity dial. My pain was extreme in the mornings and evenings, reduced during the day. My average body temp dropped from 98.4 to 96.8. Now the numbness and tingling wasn’t just in the legs, hands and feet but everywhere. Spasms everywhere. I felt I was in a real crisis. My primary referred me to an endocrinologist but it was a 2.5 month wait.

Possible Multiple Sclerosis

With the prednisone taper and return of my symptoms, I convinced my doctor to give me another MRI of the head, as the last one was 2005. That found 10 lesions that had progressed slightly but he didn’t feel that accounted for my symptoms. I now have a neurologist scheduled in a month after communicating my list of symptoms after the prednisone taper.

2005 MRI

HISTORY: Loss of feeling in feet and pain and numbness in hands, face, and feet. Occasional tremors. Polyneuropathy on EMG.

FINDINGS: There are a few small scattered foci of prolonged T2 relaxation in the central and subcortical white matter of the frontal lobes. A few similar lesions are seen in the temporal lobes. These are nonspecific as to etiology given their distribution and appearance. None of them shows abnormal Gadolinium enhancement. The rest of the brain appears normal. The arteries at the base of the brain and the dural venous sinuses are patent and the facial structures appear normal.

CONCLUSION: Nonspecific scattered white matter lesions in the frontal and temporal lobes. The differential diagnosis includes demyelination from multiple sclerosis, sequelae of vascular headaches, early small vessel ischemic disease, and vasculitis.

My latest findings showed some progress of the lesions and they went from a few in two regions (6-7 I assume) to 10.

2019 MRI

HISTORY: Neuro deficit(s), subacute. Paresthesia.

FINDINGS: Diffusion-weighted images are normal. There is no evidence for intracranial hemorrhage or acute infarct. There are some scattered signal hyperintensities in the supratentorial white matter. These number approximately 10 and are not associated with any mass effect or enhancement. These have slightly progressed since the prior exam. Brain parenchyma is otherwise normal. Ventricles and  subarachnoid spaces are within normal limits. Vascular structures are patent at the skull base. Postcontrast images do not show any abnormal areas of enhancement or any focal mass lesions.

IMPRESSION

  1. Several small scattered white matter lesions without enhancement or mass effect. These have slightly progressed since 2005. They are nonspecific and could be due to gliosis, chronic demyelination, or chronic ischemic change. They can occasionally also be seen in patients with headaches.
  2. No evidence for intracranial hemorrhage, acute infarct, or any focal mass lesions.

My doctor still didn’t think the lesions accounted for all my symptoms and recommended waiting for the endocrinology. Both the 2005 and 2019 reports list multiple sclerosis as a possible differential diagnosis along with a couple of other things but nothing further was done. In 2005, the diagnosis was neuropathy of unknown causes.

Back to Biotin, Thiamine, and Magnesium

The brain lesions triggered some research and I discovered that high doses of biotin are being studied and in France prescribed for MS. This was enough to sink in. Being in extreme pain and figuring it is some time before any new testing, I went back to the thiamine+biotin+magnesium combination.

The results were dramatic. I immediately felt my pain sensitivity reduce to normal, so a bit of back pain was a twinge, not like something stabbing into my soul and the size of a beach ball. Stiffness, numbness, and tingling vanished in most of my body with just a bit of numbness in mouth, lips, and tongue. I could now pronounce some words again that I couldn’t just days before. I still felt the cold, especially in my feet but this is lessening every day and my average body temp is now 98.2. My heart rate is down again, but mostly low 60’s. I still cannot stand on one leg with my eyes closed but can manage with two and not sway much or start to keel over.

This time I decided that given MS patients were benefiting and tolerating 300 mg of biotin to give it a try. I increased from 50 mg to 300 over a few days. I had a touch of nausea, very minor, and no throwing up this time. Every day my symptoms are getting better. The higher dose of biotin has been more effective on the tinnitus and it sometimes is nearly gone. Currently, I am using 300 mg biotin, 250mg lipothiamine, and 350 mg magnesium and now feel back to my “normal”.  My toes still curl and jump a bit, my feet get tight ranging from 25% normal to 85% normal. If I touch my thigh my toes curl. My mouth, lips, tongue are a bit numb. Prior though, I was also having pain in the left side of my head, in the jaw, “TMJ pain”, as well as pain Northeast of top of the ear, behind and below the ear going down the neck, and my left eye hurt a lot whenever I moved it. That is all gone now with the thiamine, biotin and magnesium combo, just as it was with the prednisone.

I suspect that the prednisone was shutting down all the inflammation, and allowing me to feel great and energetic but without the biotin and thiamine and not eating much I was burning the candle at both ends and paid a terrible price once I tapered.

I have done some genetic research but it all dead ended. Any research related to thiamine deficiency disorder or biotin thiamine responsive basal ganglia disease doesn’t list any of my SNP’s except for a couple that have been studied and listed in clinvar database as benign and 23andme dna data does not have many of the SNP’s for BTBGD. If I want to pursue that route I’ll have pay for special testing.

My Promethease report (which is free now everyone!) does list 29 mutations that increase multiple sclerosis risk but I suspect that is a general container for a lot of subtypes of neurological disorder. It is possible I do have MS and it is overtaxing my ability to absorb and deliver thiamine to the brain. I have a couple of homozygous mutations on SLC19a3 (Thiamine transporter gene) but there is no data on them or any of my heterozygous mutations on SLC19a2 or SLC19a3.

At this point I’m doing well and plan on continuing with the thiamine+biotin+magnesium at the current level and I am debating if it is worth pushing on with the specialists. I also plan on going on the keto/low carb/no alcohol diet permanently. I’ve learned my lesson.

I want to thank again Dr. Lonsdale, Dr. Marrs, and this site for the information they provide. I cannot imagine where I’d be at this point without the knowledge I’ve gained here.

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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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