neuropathy

Progesterone for Peripheral Neuropathy

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Some 20 years ago, during my very first neuro class taught by an accomplished neurologist from a prominent research university, I had a conversation about hormones and the brain. It was a brief conversation during which he admitted not only knowing nothing about how hormones affected the brain or nervous system functioning, but also, how he and others had no interest in considering the question. He believed hormones were too complicated to consider relevant. One didn’t ‘mess with hormones’ as he put it.

Lucky for us, some intrepid neurologists have moved the science of neuroendocrinology past the foibles of ‘don’t mess with hormones’ to hormones might be important therapeutic options. Nowhere is this more evident than in the areas of traumatic brain injury and diseases of demyelination. Here we see advances in hormones used as viable and important treatments where once there were none. Although the research is yet in its infancy and suffers from the typical one-size-fits-all approach, it marks a huge step forward in clinical neuroendocrinology.

What is Neuropathic Pain?

Neuropathic pain, the often chronic and difficult to treat pain that comes from nerve injury and demyelination affects approximately 3% of the population. The number of individuals suffering from neuropathy is likely much higher when one considers diseases such as endometriosis and the ill-understood, under-recognized neuropathy emerging post medication or vaccine adverse reactions. The experience of neuropathic pain in hands, feet, arms and legs is described as burning, freezing, electrical, tingling, prickling and more often than not, severe and unrelenting. As the nerve injury progresses and the pain continues, the rawness and intensity of the pain becomes indescribable to someone who has not experienced nerve pain firsthand.

Hormones and the Nervous System

Since the late eighties, researchers have known that steroid hormones, such as progesterone were not limited to reproductive functions and that many steroids were active in the nervous system. Not only were those steroids synthesized peripherally in ovaries, adrenals or adipose tissue able to cross the blood brain barrier, but all the core substrates for steroid synthesis were available in the brain too, meaning the brain could make its own steroids, de novo, from scratch. Researchers initially deemed steroids made or active in the brain as neurosteroids. Eventually, that nomenclature fell by the wayside as researchers realized there was tremendous crosstalk between peripheral and central hormones, no matter where the hormones were synthesized.

It should be noted, that hormones exert influence all over the body and brain via receptor binding. (A discussion on hormones and receptors can be found here: Promiscuous Hormones and Other Fun Facts.) In addition to steroid hormone receptors on (cell membrane) and in (nuclear) hormone-specific cells, like those in ovary, testes, adrenals, uterus, endometrium, hormone receptors are co-located on neurons, glial cells, oligodendrocytes and Schwann cells (myelin producing cells), immune cells, cardiomyocytes (heart), hepatocytes (liver), adipocytes – essentially every cell, organ or tissue in our body is modulated in some way by a hormone. Hormone influence is particularly important in the in the nervous system, where everything from neurotransmitter release and uptake to synaptic connections are modulated.

Traumatic Brain Injury, Peripheral Neuropathy and Hormones

When we talk about injuries to the nervous system, be it the brain and spinal cord, which is called the central nervous system (CNS), or all of the nerves that control movement and organ function in the body, the peripheral nervous system (PNS), there are two categories of injuries, those that develop acutely, post trauma, or those that develop chronically because of some metabolic dysfunction. In the case of the former, traumatic brain injuries (TBI) or  traumatic nerve injuries, the research points to progesterone for repair and regrowth. In the case of the later, where injuries develop as a result of internal and often chronic dysfunction, such as diabetic neuropathy, multiple sclerosis and other diseases affecting nerve fibers and myelin, less is known about progesterone and the thyroid hormone triiodothyronine (T3) is implicated, more strongly.

What is Myelin and How Does it Impact Neuropathy?

Myelin is the insulation that protects the axons of the neuron (in the brain) or nerve (in the body) to allow rapid conduction or messaging across the brain or through the body. Recall the axon is the part of the neuron/nerve that sends messages to other neurons/nerves, to other tissues, like muscle, or to organs like the heart and the liver. The dendrites receive messages and the nucleus processes messages. Myelin is like the plastic coating around the electrical wiring in your house. If the coating is too thick, conduction is blocked. If the coating is frayed or too thin, electrical sparks fly everywhere. Frayed myelin around axons is one of the mechanisms of neuropathic pain. Myelinated axons in the brain look white and therefore are called white matter. Whereas the grey matter, is where the nuclei of the brain reside. White matter in the brain consists of the oligodendrocytes – the type of cell that forms the myelin sheathing around axons. Myelin in the body, around the peripheral nerves, is made from cells called Schwann cells.

Progesterone, Myelination and the Nervous System

In the 1990s, Etienne-Emil Baulieu and colleagues recognized a role for progesterone (and other hormones) in central nervous system myelination. Over the next two decades, researchers uncovered the possible mechanisms and delineated more clearly for whom and in what types of injury progesterone seems most helpful. From studies of neurons (CNS) nerve cells (PNS), we now know that progesterone is key for myelination and neuron/nerve regrowth, at least in the acute stages. Progesterone stimulates myelination both directly by acting on oligodendrocytes and indirectly via actions on the neurons and the astrocytes that then message the oligodendrocytes to produce more myelin. Similarly in the PNS, progesterone aids in the remyelination and re-growth of nerve fibers, via the Schwann cells and via progesterone receptors located in what are called the dorsal root ganglia (DRG), the sensory neurons that carry information from the periphery to the brain. Whether in the CNS or the PNS, timing and length of progesterone administration are critical.

Animal Research – Progesterone, Nerve Injury and Neuropathy

The animal research has been mixed, but taken together, the results seem dependent upon the type of injury, the timing of the treatment and the methods of assessment. When treatment is begun early enough and extended long enough (this varies) and when the measure is neuropathic pain versus other potential outcomes (such as morphological changes to the nerve), there seems to be a favorable response. In rodents, single dose treatment does not seem to work, neither does treatment that is initiated too late after the injury or ended prematurely, though these criteria vary from study to study.

For example, using an induced model of diabetic neuropathy, researchers from Italy found that diabetes markedly reduced progesterone concentrations in male rodents within three months (females were not tested). This was the only study I could find that measured progesterone concentrations relative to treatment and outcomes. Chronic treatment (one month) with progesterone or one of its derivatives restored nerve function, increased key components of myelin production and reduced pain. Similarly, an induced model of trigeminal pain in male rodents found when progesterone was initiated early and at a high enough dosage, it tempered the experience of pain while increasing myelin producing proteins. Lower dosages did not work.

From Animals to Humans: Traumatic Brain Injury and Neuropathy

The research with animals, male rodents specifically, shows that progesterone treatment works best if given early enough, for long enough, and at high enough dosages. With acute or induced injuries under experimental conditions, early treatment is much easier than in real life where neuropathic pain develops much more gradually and often goes undiagnosed and untreated for some time. Would progesterone work in humans and would it work for chronic, well established neuropathy? The answers to those questions are not clear because the human research on progesterone and myelin focuses on acute injury, like the traumatic brain injuries. The human research also suffers from short duration dosing, includes mostly males, and without exception fails to address endogenous progesterone concentrations either pre or post treatment. Nevertheless, there are some indications that progesterone therapy may work.

Progesterone and TBI – Human Studies

In a smaller, single center open trial and two larger, double-blind, placebo-controlled, human trials, progesterone therapy was administered to individuals with severe traumatic brain injuries (Glasgow coma scale <8). In each case, the progesterone group did better, showed reduced morbidity rates than the placebo groups.

In the first study, 26 cases were treated with progesterone and 20 controls with placebo. At both 10 days and three months post injury and treatment, the progesterone treated group improved significantly more than the control group (abstract only).

In a second study, 159 patients, arriving to the treatment facility just eight hours post traumatic brain injury were randomized to receive either intramuscular injections of progesterone (82) or placebo at 1.0 mg/kg via intramuscular injection and then once per 12 hours for 5 consecutive days. Both intake neurological functioning and post treatment functioning were assessed and compared using a number of measures. Follow up assessment was conducted at 3 and 6 months post injury/treatment. The results were positive, albeit small. The progesterone treated group improved significantly across all measures showing consistently larger improvements compared to the placebo group. It should be noted that only 44 of the total subject population was female, 24 in the placebo group and 20 in the progesterone group. No analysis by sex was conducted and so it is not clear whether progesterone therapy works equally well in males and females.

In the third study, called ProTECT, a similar double-blind, placebo controlled, randomized methodology was used. Here, however, the randomization was 4:1 and favored progesterone treatment, whereas in the study cited above, the progesterone and placebo randomization was 1:1. Progesterone was given via IV for three days. The ProTECT study researchers found that patients in the progesterone had a lower 30-day mortality rate than controls (rate ratio 0.43; 95% confidence interval 0.18 to 0.99). While those who suffered more severe injuries had relatively poor outcomes at the follow up tests 30 days post injury, despite the treatment, and those who suffered only moderate traumatic brain injury and received progesterone were more likely to have a moderate to good outcome than those randomized to placebo (abstract only).

Two additional trials are on-going, hoping to test progesterone on thousands of patients: the ProTECT-III and SynAPSe studies.

Translating the TBI Research for Use with Neuropathy

What does improvement post TBI tell us about treating neuropathic pain from demyelination disorders? It is not clear, because even though researchers know that progesterone promotes myelination, the human research has focused narrowly on injuries where demyelination occurs but also where other factors are also involved in the outcome. We know from animal and cell culture research that progesterone attenuates the cascade of events that occur post TBI or post nerve injury via multiple mechanisms, inducing myelin regrowth is only one of those mechanisms. Progesterone reduces swelling of both vasogenic and cytotoxic sorts. It has anti-oxidant properties, upregulating enzymes that increase free radical elimination. Progesterone inhibits inflammation, stabilizes mitochondria, reduces neural excitoxicity and can limit apoptosis. Finally, progesterone promotes myelination. All factors that should point to consistent improvement in TBI and neuropathic pain syndromes, but the research is limited and mixed. Why?

The primary reason for mixed results is study design, almost all are short duration. Hormones are long acting molecules and the shorter duration may not be sufficient to generate the response, particularly when the injuries are severe or longstanding. Longer treatment regimes are likely in order.

Another reason for mixed results is the one-size-fits-all approach. None of the human studies and few of the animal studies, investigates why progesterone works in some subjects and not others. Almost all of the studies are predominantly male, rodent and human alike. None have investigated whether being female has anything to do with efficacy. None of the human studies measured circulating concentrations of progesterone, either pre-, during, or post-treatment and so there is no way to tell if those who responded had higher circulating concentrations or if improvement was contingent upon reaching a certain concentration.

Perhaps even more importantly, is the fact that progesterone, like any hormone, works within a vast and compensatory network of other hormones. The reductionist approach that utilizes a single hormone treatment protocol, while ignoring the potential cross-talk with other hormones and other variables is a consistent flaw these and other research protocols. Again, hormone measurement, progesterone and its metabolites, in addition to other key hormones, is imperative if one is to determine therapeutic efficacy.

I Have Peripheral Neuropathy, Should I Try Progesterone?

Progesterone therapy is generally safe, but as with everything there are risks. Women have been using it for generations in its bio-identical form to mitigate menstrual and menopausal symptoms. Since it is fat soluble, transdermal (skin) absorption is possible and progesterone creams have become popular. Some physicians prefer micronized progesterone, a pill form that reduces the molecule so it more easily passes through the liver without degradation. The pill form, and to a much lesser degree, transdermal progesterone, cause sedation and should be taken at night. Micronized progesterone has been shown to increase free thyroxine (T4) as well. For some women, and presumably men too, a gain of function mutation on the mineralocorticoid receptor can evoke very high blood pressure with any increase in progesterone concentrations (luteal phase of the menstrual cycle and during pregnancy especially). Although there are dosing references for progesterone relative to menstrual or menopausal therapy, the dosing is individualized and often includes the replacement of other hormones along with progesterone. Salivary hormone testing is used to monitor and hormone doses are adjusted regularly. Progesterone is also used predominantly for women. No such dosing considerations exist for men that I am aware of. Likewise, for peripheral neuropathy there are no references from which to design a treatment protocol and so it would be prudent to work with a functional medicine specialist, familiar with hormone management, to develop and monitor the course of treatment.

My Two Cents

I suspect, if progesterone therapy works for peripheral neuropathy, it will require a much longer term treatment period than is currently tested in the human trials. I suspect also, it will be difficult to ascertain whether it is the sole contributor to improvements in neuropathy symptoms, as neuropathy is a multi-factorial process that ought to be treated as such. Nevertheless, if you suffer from neuropathy and can find a physician to work with that is familiar with hormones and the research, progesterone therapy might provide a viable option, among other options like stabilizing thyroid hormones and supporting mitochondrial function.

Postscript

This article was first published February 19, 2014. Since then, a few more studies and review articles have been published and continue to support the role of progesterone in myelin regeneration, although the data are mixed. From a 2020 article.

Indeed, PROG and its metabolites modulate the expression of myelin proteins of the PNS, such as myelin basic protein (MBP), myelin proteolipid protein, glycoprotein zero (P0) and peripheral myelin protein (PMP22) as well as myelin formation [6,8,9,20,63,64]. In particular, the expression of P0 in the sciatic nerve of adult male rats, as well as that in Schwann cell culture, is increased by treatment with PROG, DHP or THP.

…Data here reported support the concept that neuroactive steroids, synthetic ligands acting on their receptors or inducing their synthesis, may improve PN symptoms, including neuropathic pain and consequently may represent an interesting possible therapeutic strategy. In addition, based on the sexual dimorphism of neuroactive steroids as well as of PN here discussed, a gender specific treatment based on these compounds may be also proposed.

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This article was published originally on February 19, 2014. 

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Urological and Sexual Symptoms in Male Thiamine Deficiency

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male urological symptoms with thiamine deficiency

I’m a 29-year-old male who has experienced a vast umbrella of odd symptoms over the last three years, including several urological and sexual capacity symptoms. Only a few months ago did I discover the relevance of thiamine in all of my issues. All of my problems began at the age of 27 years old. I was drinking three to seven cups of coffee per weekday and binge drinking alcohol one to two nights on most weekends. Despite this, I was and am still a very fit, muscular, and lean individual. If I were to describe all of my health problems to a stranger, they’d be very surprised to hear that I was dealing with such things given my healthy appearance.

Urological Symptoms and Reduced Sexual Capacity

The seemingly random downward spiral in my health began in October 2019. I remember being alarmed as I started to feel some odd urological symptoms. I felt numbness and burning in my penis, pain with ejaculation, erectile dysfunction, altered sense of ejaculation, and more. As you can imagine, as a 27-year-old male who is still in his reproductive years this was very troubling.

I went to a urologist and without doing any testing, they told me I had prostatitis. I was convinced for the longest time that I had something called Chronic Pelvic Pain Syndrome (CPPS), which is a poorly understood condition as well. I had all of the lab work that one would get done including an STI screening, hormonal panel, CBC, etc. I had no STIs, my testosterone was north of 800 ng/dl and all my other health markers were very well in range. On paper, I looked extremely healthy.

Gastrointestinal Problems

At the same exact time that I developed urological symptoms, I started to experience some very odd gastrointestinal symptoms as well. I’d experience extremely high levels of abdominal distention even after eating the smallest portion of food. I’ve always been into fitness and counting my calories therefore I knew it wasn’t because I was eating too much food. I’d also find myself constantly needing to burp, had reflux and I felt like food was just sitting in my stomach. I sort of ignored the GI symptoms a bit because the urological ones were so much more at the forefront of my brain.

Fatigue, Brain Fog, and Muscle Fasciculations

Three months later, I started to develop extreme levels of fatigue. A feeling of being “tired behind my eyes” and having no motivation to do anything. Just focusing on a task or even socializing with people became extremely difficult. Around this time, I also developed muscle fasciculations throughout my entire body seemingly at random. They weren’t painful, but just very odd. We’ve all experienced the occasional eyelid twitch, but this was way different.

Other Odd Symptoms

Other symptoms I’d experienced during the last three years included a hand tremor, feeling more “clumsy” than normal, anxiety, depression, SIBO, joint pain, muscle pains, random tingling and burning sensations. I had one panic attack, developed laryngopharyngeal reflux, and more.

My symptoms would wax and wane seemingly at random. I remember I tried cutting out alcohol and any form of caffeine for three months thinking that would help. Although it didn’t hurt, it didn’t completely resolve any of my issues. I also tried water fasting for three days and going gluten-free for a month.

Discovering Thiamine

Throughout the last three years, I’ve learned an exceptional amount about health, longevity, supplementation, etc. At one point, I became extremely fascinated by the process of methylation and was trying to see how various genetic polymorphisms may be playing into my issues (MTHFR in particular.). I knew I didn’t just have prostatitis or CPPS because it made no sense to me that all of a sudden all these different systems of my body were negatively affected (neurological, gastrointestinal, urological).

Then randomly, one day I stumbled upon one of Elliot Overton’s videos on thiamine when browsing Reddit. I must say that at this point I had never heard of anyone discussing thiamine. All of the information regarding B vitamins online was generally focused on B9 and B12. I binge-watched most of Elliot’s videos regarding thiamine in the course of a day. So many things started to make sense and I finally felt like I potentially had an explanation for all of my odd symptoms. I ordered TTFD fairly shortly after that.

The Path to Recovery

Of course, me being me I didn’t go “low and slow”. I started with a dose of 200 mg TTFD per day. On the second day of 200 mg TTFD, I remember feeling human again. It was as if someone gave me Adderall. I had an abundance of mental energy, I felt incredibly sharp, focused, relaxed and my ability to socialize with people improved tremendously. When I would walk around, I felt “connected” to people again. I don’t know how else to describe it. There was no need for my typical coffee when feeling this way.

On top of this, I noticed that my libido and erectile quality had massively improved. I was able to get aroused incredibly easily without any manual stimulation. I also noticed that the muscle fasciculations had reduced tremendously in frequency and were far less noticeable. This fell in line with the hypothesis of all these health issues being interrelated.

Unfortunately, this limitless pill feeling didn’t last. I noticed that despite the tremendous improvement experienced in those two days, my symptoms would constantly fluctuate. I remember I had some GI disturbances when I continued the 200 mg TTFD dose.

This is where I decided to become extremely detailed in my supplementation log. I’m highly analytical in nature and therefore of course I developed a spreadsheet where I would log my intake of all supplemental forms of B vitamins and what quantity I was taking. I would make notes regarding how I felt each day, my libido, the quality of my sleep, and anything else that may be relevant. I started digging more into Elliot’s videos, learning about the paradoxical effect, what each symptom may mean, etc.

At this moment, this is still a puzzle I’m trying to figure out. There are times in my supplementation with TTFD that I feel like I’m truly on the “limitless pill”. I’m a completely different person and it’s apparent to everyone around me. Things that would normally seem like a big deal were no longer a big deal.

One big breakthrough that I did have was that I realized that I may have gone too hard too fast with the TTFD. I was able to achieve the same level of success after bringing the dosage back down to 50-100 mg. I’ve also experimented with some different forms of thiamine including Sulbutiamine and Benfotiamine, although I’m not sure I’d say I’ve responded as well to those forms.

Diet, Medications, and Exercise

Although I eliminated foods with gluten for a period, I observed no noticeable change when I removed it from my diet. So I am back to eating breads and grains. If I had to give a rough macronutrient breakdown, I’d say my diet consists of approximately 150 g protein, 70 g fat, 300 g carbohydrates. This varies a lot day to day. I don’t go as far as tracking my macronutrients these days but I think this is a decent estimate. I definitely grew up on white rice and probably a generally higher carbohydrate diet. I wouldn’t say my carbohydrate sources are the healthiest, mostly bread and white rice.

I have really tried to minimize caffeine and alcohol intake. I may drink two to four cups of coffee per week max. I would like to eliminate it entirely because I feel like it does nothing but mask my symptoms and I know that genetically I have a SNP that causes me to be a slow metabolizer of caffeine. I am also trying to abstain from alcohol but it’s difficult and that definitely fluctuates. I’d say generally two nights per week I have 2-3 drinks for a total of 4-6 drinks.

I take no medications except Cialis on occasion.

I work out 3-4 days per week. It consists of a moderate volume of lifting weights and 20-45 minutes of low-moderate intensity cardio each time.

Every now and then I’ll take some BCAAs that have some sodium, potassium and a little bit of B6 as Pyridoxine HCl in each scoop. I only just started taking a whey protein supplement for the first time in ages. Maybe a scoop per day.

These are the supplements I have been taking.

  • B Complex: Originally started with Thorne’s Basic B and switched to Thiavite.
  • TTFD – 100 mg per day
  • Vitamin C: 500 mg as Ascorbic Acid/ 75 mg citrus bioflavonoids per day.
  • Vitamin D: I used to take more but lately only 10,000 – 15,000 IU per week. I live in Florida.
  • NAC: 500 mg – 1000 mg: I’ve cycled this off and on. I heard that sluggishness and unrefreshing sleep can be due to low glutathione levels and that this could help. I’ve also heard it’s good for your liver health, which is why I originally started taking it.
  • Magnesium Bisglycinate: 300 – 450 mg
  • Creatine: 5 grams
  • EPA: 4 grams
  • Seed Probiotic

Current Status and Remaining Issues

My current symptoms wax and wane and are as follows: fatigue, unrefreshing sleep, low libido, variable erectile quality, neuropathy (burning feet and numbness in my forearm) and muscle fasciculations. My GI-related issues are pretty much gone.

I feel like I’m on the cusp of figuring this out but it’s a bit tricky to get everything in the right balance, especially with a lack of testing. When I look back on my life, I definitely think there’s some genetic aspect to this considering I can’t even remember when my brain felt as good as it did during those first few days of TTFD. Not to mention some of those lifestyle factors like excessive coffee consumption and weekend alcohol binges.

Just thought I would share in case this could help anyone else out there. Would also love to know if anyone has any advice.

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, and like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

Image by Darko Djurin from Pixabay.

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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.

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.

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This article was published originally on November 4, 2015. 

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Dysautonomia and Hypoxia

Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the

Rapidly Deteriorating Health With Thiamine Deficiency

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thiamine deficiency

In May 2020, I experienced my first symptoms with what I now believe to be thiamine deficiency (beriberi). I believe other nutrient deficiencies played a role as well. This was preceded by an especially difficult several months that included a marital separation and possible COVID infection. In addition, I experienced a mild head injury during this time when my son and I accidentally collided while picking up toys together. I have a history of traumatic brain injury, so am susceptible to post-concussive syndrome from mild head trauma.

It was these factors that precipitated the downward health spiral that first began in May 2020 when I was 38 years old. Prior to this time in life, I felt my health to be good. I had gone through some very challenging mental health struggles in the past, a TBI and post-concussive syndrome, as well as a few other issues related to physical health, but for the most part, I would have considered myself to be a fit, healthy, and resilient person. I consumed a paleo diet, which I thought very nutritionally dense, and I exercised regularly. However, looking back on my history suggests risks for thiamine deficiency. Here are some factors that are part of my overall health history:

  • Five pregnancies and nine years of breastfeeding with very little multivitamin supplementation
  • Former short-term fruitarian and vegan diets for purposes of detoxification
  • Former sporadic heavy binge drinking from age 15 to 33
  • Former tobacco smoker from age 15 to 33
  • Consumed extreme amounts of candy as a child
  • Overdosed on pills three times between ages 15 and 17. The third overdose involved Serzone, which has a warning for liver damage
  • Was prescribed antibiotics at least 75 times from age 5 to 33 for chronic UTIs and bronchitis
  • Prior health problems: chronic urinary tract and kidney infections as a child and young adult, chronic bronchitis as a child, candida overgrowth, digestive problems, insomnia, anxiety, depression, PTSD, and depersonalization disorder

In May, the combination of stressors, along with likely longstanding nutrient deficiencies, precipitated a rapid downward spiral leading to multiple hospitalizations, and ultimately, what I believe was severe thiamine deficiency. At its worst, I believe I was headed toward Wernicke’s encephalopathy and heart failure. Since the best physicians could offer was Ativan, antidepressants, and a presumed multiple sclerosis diagnosis (despite a lack of evidence), it was up to me to save myself, particularly because I am a parent to five children. Through extensive internet research, I learned about thiamine deficiency and began to treat myself. This is my story.

Rapidly Disintegrating Nerve Function

The first symptom I remember experiencing was a strange tingling in the center of my chest upon standing. The next symptom was flank pain. I thought perhaps I had a kidney stone and made an appointment with my primary care. During this time, I was also intensely tired in a way I’d never been before, very pale, anxious, uncharacteristically irritable, shaky, short of breath, thirsty, lost weight, and became sweaty at random times.

At the appointment with my primary care, it was decided I would get an ultrasound of my kidneys to check for kidney stones. I didn’t make it to the ultrasound appointment because that same day I stood up after a nap and experienced sudden debilitating chest pain that felt like I was having a heart attack. It started in the area of my heart and moved to my left arm and up to the left side of my neck. I called an ambulance and was taken to the emergency room. They ruled out a heart attack and proceeded with the kidney ultrasound after I shared with them the other strange symptoms I’d been experiencing. Nothing of significance was found on the ultrasound, and I was sent home.

Shortly after that incident, I started experiencing numbness in my legs at random times during the day and night, as if they’d fallen asleep. I went into the ER again after a particularly intense experience of numbness where I felt uneasy about even standing to walk. Again, nothing was found, and I was sent home. My arms began to go numb at night while in bed, in addition to my legs. I’d wake up to this numbness, and shortly thereafter I could feel the numb sensation in my head as well.

I began to experience gastroparesis, and my intestinal motility seemed frozen at times but then would go into overdrive during the night, requiring urgent bowel movements in the middle of the night, which was not normal for me. At the same time, I could feel the sudden rapid digestive motility, I could also feel the blood flow dropping from my brain. As soon as I’d have a bowel movement, the blood flow would return to my brain. These sensations were all so strange and unnerving and unlike anything I’d previously experienced in life.

Loss of Consciousness, Compromised Speech, and Vision Changes

I went to an acupuncture appointment and shared with the practitioner what was happening. She treated me for yin deficiency. That night I woke to use the bathroom, and on the way back to my bedroom, I nearly lost consciousness for the first time. It was a terrifying experience. My ability to speak was compromised, and I tried to communicate to my daughter what was happening, but my voice was in slow motion. My vision was growing tunnel-like and dark. I thought I was having a stroke. My daughter gave me my phone, and I called an ambulance and was able to very slowly articulate what was happening as I lay on the floor, wondering if I was going to die. I was taken on a stretcher to the ER, and the diagnosis from that trip was that I’d had a panic attack. I was given Ativan and sent home. I knew that a panic attack was not the correct explanation, although I was indeed in a state of panic over my current health. I felt very strange, with strange sensations throughout my body and brain, severe anxiety, erratic heartbeats, and tachycardia.

Things grew progressively worse over the next couple days, and my mother drove me to a better hospital four hours away to hopefully get answers. By the time we arrived, I could not walk due to the total body numbness. I was given a neurological exam and had no reflexes in my knees, ankles, and feet. I was then given two bags of IV saline and felt relatively normal a few hours later. Many labs were done, but no nutrient levels were checked. I was kept overnight and examined by a neurologist, but I wasn’t experiencing symptoms during the exam. It was found that my blood sugar was abnormally low during the night (65), and I was told to improve my nutrition and sent home with no real answers.

Was it B12 Deficiency?

I started taking a B complex and multivitamin and tried to eat as healthy as possible, but during the following weeks, I continued to experience near syncope, dizziness, cardiac and GI issues, strange body sensations, and severe anxiety. I’d have pockets of time where I felt relatively normal, but symptoms always returned, and night numbness was a regular occurrence. I often felt ataxic, like I was about to lose my balance or fall. My hearing seemed to change, and my right eyelid began to twitch relentlessly. Nerve pain began in my joint junctions and felt like sparking, electrical, stinging sensations. Over the course of several days, these nerve pains began to affect the base of my spine and slowly moved up my spine to my head. It was a very painful and frightening experience.

When researching symptoms, I came across information about B12 deficiency and wondered if that is what I was dealing with, so I asked my naturopath if he would prescribe methylcobalamin that I could inject at home, and I began daily B12 injections. The nerve pain resolved after a few weeks, which was a tremendous relief. As a result of this resolution, I believed a B12 deficiency to be at the root of my problems. I continued with B12 injections after the nerve pain healed but dropped down to once weekly injections.

Another Hit to My System

Shortly after the nerve pain resolved, I got very sick with a Campylobacter infection. It was strange because no one else in my family got sick, and we’d all been eating the same meals. I went to the ER after several days of relentless diarrhea and high fever. I was given fluids and my stool was tested, which revealed the Campylobacter bacteria, and I was prescribed azithromycin. In hindsight, I wish I’d not taken the antibiotic because I believe it made my condition worse.

After the antibiotic, I felt like I was in a permanent state of semi-consciousness. I felt hypoxic, like I was being asphyxiated. When I’d start to fall asleep, I’d wake up with a jolt because it felt as though I were falling and losing blood flow to my brain. I had constant high-pitched ringing in my ears. Life became a total nightmare. My arms and legs were swirling with strange sensations I’d never felt before – paresthesias and cramping muscles. My heart was in a near constant state of palpitations with alternating bradycardia and tachycardia. When I’d roll from one side to the other in bed or stand up, my heart rate would go from 40s and 50s to 120s and 130s. It felt like my heart was constantly pounding, no matter if the rate was slow or fast. The sound was audible to me day and night, and the pounding seemed to shake my entire body. Sometimes it felt like my heart would stop for an abnormally long amount of time, then sluggishly start thumping again. I would wake up in extreme pain on whichever side I slept on. I recall using my finger oximeter one night and getting a reading of 84% oxygenation.

Maybe Multiple Sclerosis?

During this time, several doctors suggested I might have Multiple Sclerosis (MS). I had an MRI of my brain that showed no lesions, so MS was ruled out. I was eventually diagnosed with POTS by the medical community. I researched POTS and saw that extra salt was often helpful for minimizing dizziness, so I started adding salt and electrolytes to my water. It did seem to help some, so I began drinking about a gallon of water a day with 2-3 extra teaspoons of Celtic or Pink Himalayan salt and added electrolytes.

In late September 2020, my POTS symptoms resolved. My heart had normalized, and I was no longer dizzy or experiencing near syncope, but I was left with “stocking and glove” peripheral neuropathy. I had numbness from my feet up to my calves and numbness in my hands and forearms. I was relieved that the POTS symptoms were gone and felt I could tolerate the numbness and paresthesias. I still felt very weak and struggled with bacterial infections in my ears and sinuses as well as cold intolerance.

Discovering Thiamine Deficiency

Life continued this way until early November, when I decided to try R-Lipoic acid for the peripheral neuropathy and occasional spinal pain and tingling that periodically occurred. This was a devastating mistake. I ingested the first capsule in the morning and second in the evening, and within an hour of the second capsule, nerves all over my body felt like they were on fire. The only thing I’d changed that day was the lipoic acid, so I started researching contraindications to lipoic acid online and found that thiamine deficiency was a contraindication. Lipoic acid and thiamine work in tandem in the Krebs cycle, so by adding one with a deficiency of the other, it creates a draw on an already almost empty tank. In one study, when thiamine deficient rats were administered alpha lipoic acid, it created a toxic reaction. Unknowingly, I’d taken a supplement that made my situation go from difficult to much worse.

I then looked up thiamine deficiency symptoms and recognized my experience immediately in beriberi disease. I found the website, Hormones Matter, run by Dr. Derrick Lonsdale and Dr. Chandler Marrs. I began reading through the information and stories, and my belief that thiamine deficiency was the root of my problems grew stronger. Dr. Lonsdale suggests using a type of thiamine called Allithiamine (thiamine tetrahydrofurfuryl disulfide), as it crosses the blood brain barrier superior to other forms of thiamine. I ordered a bottle and took a large dose of thiamine hydrochloride I had on hand before going to bed.

I didn’t sleep well that night. My nervous system felt like it had been severely damaged. I was shaking, my heart was once again beating erratically with tachycardia upon movement. The nerve pain was intense and spread throughout my entire body. The next day, I went for a short walk and nearly blacked out. The muscles in my legs were painfully cramping. I had no energy. I couldn’t even read. I went to bed that night feeling like I had a head injury.

Each day was progressively worse. I was taking thiamine hydrochloride and benfotiamine every couple of hours, but it didn’t seem to be stopping the downward spiral of symptoms. I felt like I was going to collapse. My brain was not functioning well. I was nauseous and had severe GI distress. All the symptoms I had experienced before, in addition to many new symptoms, manifested again in rapid succession. I went into the ER and attempted to explain that I believed I had a severe thiamine deficiency, hoping I would be given IV thiamine, but I was only handed a thiamine tablet, given some IV fluids and sent home.

Five days went by, and the Allithiamine arrived in the mail. By this point, I was vomiting, could barely walk, and felt like I had a traumatic brain injury. I took one 50 mg capsule and felt relief of the extreme brain injury sensations within half an hour. Encouraged, I continued to take a 50 mg capsule each time I would start to decline. The nerve pain lessened, I stopped vomiting, and my heart rate somewhat normalized, but the most profound effect of the Allithiamine was in reducing the intense brain injury sensation.

I’ve experimented with dosage and arrived at 100 mg every two waking hours being the most effective for keeping most symptoms at bay. In addition to the 100 mg of Allithiamine, I also take 150 mg benfotiamine and 50 mg magnesium glycinate every two hours, a daily high dose B complex, multivitamin, phosphatidylcholine, ubiquinol, digestive enzymes, probiotics, and fish oil. Five weeks out from taking lipoic acid, I still experience constant moderate nerve pains all over my body, problems with bacteria (eye infections, ear pain, sinus infections, sore throat), mild tachycardia upon sudden movement, pounding heart, random sweating, high fasting blood glucose (between 110 and 120), shakiness, dizziness, anxiety, weakness, and exercise and cold intolerance. The Allithiamine and benfotiamine have improved my brain function, nerve pain and paresthesias (from severe to moderate), digestion, and my ability to sleep, and I’m hopeful that with time I’ll see more improvements.

Recovering But Disillusioned With Modern Medicine

I believe the work of Dr. Chandler Marrs and Dr. Derrick Lonsdale and supplementing with Allithiamine saved my life. I believe I was headed toward Wernicke’s encephalopathy or high output heart failure before taking Allithiamine. My quality of life is currently very poor, but I have hope that recovery from beriberi and mitochondrial damage is possible. Some damage may be permanent, but I see small improvement each day, which indicates to me that more improvement is possible.

I wish so much I’d found the Hormones Matter website earlier in the course of my disease, as I’m certain things could have been more easily reversed. I hope that others might benefit from my story and avoid the horrendous decline that I experienced. Just by taking such a simple nutrient as vitamin B1, so many devastating health consequence can be avoided. Why don’t more doctors have awareness of this?

I am disillusioned with the medical community in not identifying my illness despite dozens of trips to the ER with comprehensive symptom lists in hand and visits to internists, cardiologists, and neurologists with detailed descriptions of my ailments. No one ever checked my nutrient status beyond vitamin D, iron, and zinc levels, and B12 and folate at my request. I was treated as though I had an anxiety disorder and offered anxiety medication and antidepressants.

How is it that in 2020, the only thing that comes to mind for the medical community when presented with complex neurological symptoms is MS? Time and time again, I was told I likely had MS, but my MRI clearly showed I did not. Beriberi is a well-documented condition that’s been known for hundreds of years, yet the medical community doesn’t consider it other than Wernicke’s encephalopathy in alcoholics. I hope this can change. Awareness needs to grow. I know there must be many others who have experienced similar symptoms to my own and sought help. We deserve better medical care in what is supposed to be among the most technologically advanced countries in the world. Until and unless things change, websites like Hormones Matter serve as beacons of hope. I am profoundly grateful to the work of Dr. Chandler Marrs and Dr. Derrick Lonsdale.

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. 

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Dysautonomia and Hypoxia

Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the

Longstanding Thiamine Deficiency Ignored By Doctors

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Thiamine deficiency isn't all in your head

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

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

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

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

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

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

My Silent Demise: Unrecognized Thiamine Deficiency

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

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

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

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

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

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

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

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

Again, I adamantly refused meds without learning the cause.

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

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

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

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

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

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

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

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

A Possible Family History of Latent Thiamine Issues

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

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

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

The Path to Recovery

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

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

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

Drugs Don’t Solve Vitamin Deficiencies

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

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

We Need Your Help

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

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

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neuropathy thiamine biotin MS

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.

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. 

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The Truth About Salt

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Angela A Stanton,Ph.D.

When we salt our food, we rarely think of salt as a crucial aspect of our physiology. In particular, we think it has absolutely nothing to do with anything other than taste and we certainly do not think of hormones. In this short post, I would like to clarify a few myths about salt and salt types and hint at their importance and hormonal connection.

The Myths of Designer Salts

Myth #1 sea salt versus table salt. There are hundreds of posts on the Internet about the benefits of sea salt over table salt. I would like everyone to know that there is only one salt on planet earth: sea salt. The fact that it may be called table salt simply suggests that some time ago it was clearly understood by all that all salt came from the sea. There was no need to place the word “sea” in front of salt; we all knew what it was. Somehow we have forgotten that salt comes from the sea. Now many designer salts have showed up with the word “sea” in front of the word salt and sell for much more than table salt. Don’t be fooled: all salts come from the sea! Preferences, of course, may mean you pick a designer salt over table salt, but I would like to make sure you know that in terms of salt, they are the same for the body.

You may ask: how can they be the same for the body if one contains all kinds of other elements as well as pure salt itself. The answer is very simple. In the body, salt molecules (NaCl) break down into ions (Na+ and Cl-) and only these two ions participate in what is called voltage activated sodium pumps (Nav1.1-1.9) where 1.1 to 1.9 indicates that there are 9 such pumps and Nav stands for voltage activated sodium pump. Thus, for the body only ions matter. Na+ is inside the cell and is positively charged. Cl- is outside the cell and is negatively charged. The two create the voltage necessary for the cell to function. Some of these pumps also have additional functions—such as sending pain message when a pump opens and does not close properly. The influx of Na+ and Cl- can cause the signal of pain to go off causing chronic pain. Much is yet to be understood by the function of salt but the one thing we already know: salt is NaCl and no additional organic matter matters.

Myth #2 refers to rock salt that comes from mountains like the Himalayas in various colors. They make beautiful lamps but in reality they are sea salts that have fossilized as the tectonic plates have shifted and lifted the Himalayans out from under the sea. Why are they pink or orange and very colorful in general? Because as the mountains were lifted, pressure increased on the salt deposits and the weight of the mountain pressing heat and metals through the salt created fossilized salt with various metals trapped in the salt itself. There is nothing wrong with eating fossilized rock salt except that by the nature of the fossilization process of high heat, pressure, and the many metals, a large percentage of these “minerals” entrapped in the salt are actually radioactive metals. Again, it is a taste question whether you prefer Himalayan or other salt but know what you are getting.

Myth #3 is Celtic and similar sea salts of various colors that are collected from clay pools and evaporated such that each sea salt crystal has little cavities of entrapped water with “minerals.” I see many lists of minerals for various sea salts but few of us actually consider where those minerals come from. I know we all love to eat sea food, fish, shellfish, and sea weeds as well. The mineral deposits in designer sea salts come from the debris of these sea animals, including their excrement and dead bodies. There is nothing wrong with eating fish poo and dead fish as long as you know that your choice of salt contains it. Some of these salts are proud to also include a bit of clay, and hence, the moisture must be kept else you will need a hammer and chisel to break the salt up. So, much of the charm about designer salts is trickery and harmless misinformation that takes advantage of those who are not aware.

The truth: salt, by chemical composition Sodium-Chloride (Na+, Cl-) is only these two elements combined, as discussed above. Our bodies use these chemicals only in ionic form. Salt is part of the baby’s amniotic fluid in our bodies (not Himalayan salt, and not various colored sea salts; just simple Na+ Cl-). This standard chemical element constitutes a very large part of the over 70% saline brine of our bodies. We are made of salt water. When we visit the emergency room with any illness, the most often used first step – the needle with a clear liquid dripped into our vein – is also saline water electrolyte. Electrolytes contain other elements to complete the full list of micro and macro nutrients of the 70% brine.

Other Minerals in Salt

What about the so called “minerals” that are in the designer salts? Do we need them?

  • Magnesium is a very important element that provides a key such that the cells can open at all given the proper electrical environment. Magnesium also provides crucial nutrient for the mitochondria (little bacteria in every single cell of our body that converts the food we eat to energy packets our cells can use). You get more magnesium out of a bite of food (just about any food) than from an entire box of designer salt.
  • Calcium is needed for high voltage channels where the neurotransmitters are released.
  • Potassium is needed to keep the balance of hydration in the cell and outside of the cell to ensure that the cell is not overly hydrated (potassium is a diuretic).
  • Phosphates. We also need phosphates and other elements and of course a ton of water, but the elements in designer salt sold as essential mineral are minuscule and meaningless.
  • Iodine. Another important factor is iodine. Designer salts do not contain iodine. In the US, the government has gone through great trouble placing iodine into our salt to eradicate goiter, a disease of the thyroid. Without adequate iodine our thyroid is not able to produce the right amount of hormone to keep our brain healthy. Recall also, in Japan after the nuclear plant released all that radiation, the first item sold out throughout the country was iodine. Iodine acts like a sponge, soaking up many toxins from our body to be able to eliminate them. Radioactivity is one of those things iodine can help clear from our bodies.

Salt and Hormones

So the question then is: what does salt have to do with our hormones? Does it matter? Indeed, it does. Those who have read the migraine series 3-part posts know that the most critical element in preventing and treating migraines is salt. Every single neuron in our brain has several voltage-gated sodium pumps (sodium-potassium pumps) to generate voltage. Without such voltage the neurons are not able to manufacture and release their neurotransmitters-hormones in the body. Thus, restricting salt in your diet retards the hormone manufacturing of your body. In previous articles, I showed how studies show that low salt diets are harmful even for those with preexisting heart conditions and hypertension. Salt does not increase blood pressure, provided that salt is consumed with sufficient amount of water, along with potassium and the other minerals and nutrients, I listed above.

Sodium retains water thereby hydrating the cells. Sodium chloride maintains the polarity differences between the inside and the outside of the cell membrane to control the electrical activity, which then open the pumps. Having enough salt in your brain makes the difference between having a headache/migraine or not. What if it also helps prevent other diseases of the brain? There are suggestions that fibromyalgia and neuropathy may be connected to one of the Nav pumps. I wonder if other conditions such as bipolar disorder, anxiety disorder, and even depression could be, at least partly, caused by an inappropriate level of sodium in the brain?

Possible Role for Sodium – Potassium Pumps in Disease

Let’s investigate one of the voltage activated sodium pumps. The one we seem to know most about so far: Nav1.7.  According to recent research, this particular pump has a critical role in chronic pain dampening. Experiments on various poisonous animals—including the Chinese red-headed centipede and the snake black mamba—show that their venom seems to selectively choose this particular pump to dampen the pain associated with some types of chronic pain. The pain signals need not be located in any one particular location of the body, but are relayed by the brain as hormones release for the pain message. People with neuropathy, such as Type 2 Diabetes or those who have been been floxed (suffered an adverse reaction to a fluoroquinolone antibiotics) are very familiar with this pain. Nothing seems to help with this type of pain except a very few types of strong drugs of the brain, some (like Gabapentin) inhibit nearly all activities in the body in near-full-force. The drugs of the brain are systemic whereas the venom is capable of acting on only one sodium-potassium pump, the Nav1.7.  Perhaps, in the future, this finding can be applied to reduce neuropathic pain without global nervous system dampening.

My Two Cents

I suspect most ailments of the central nervous system that include a hyper-sensitivity for pain will become a subject of sodium pump malfunction research. There are also indications that there is a switch in the connection of the peripheral nervous system to the spine, and thereby the central nervous system, where there should be a relay station to either inhibit or amplify the pain. Apparently, at this relay station the switch is flipped backwards and what should be inhibiting actually amplifies. Pain experienced from these crossed wires is called allodyna. I suspect we will be hearing much about this term in the future and how it connects to various sodium pump malfunctions that today we do not yet understand.

Sources:

Pain Scientific American December 2014; p:62-67

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A New March Madness – Endometriosis Awareness Month

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This March I am celebrating a different kind of madness.  It has nothing to do with college basketball; nor is it related to four leaf clovers, egg shaped candy or seder plates.  No, this March is for reproductive health education and raising awareness about endometriosis. There is nothing nice about endometriosis, even the word is cumbersome to say.  This March, we need to talk about endometriosis and reproductive health and we are going to talk about it; because the state of reproductive care surrounding endometriosis is not OK and it’s not going to get better until more people know about endometriosis and the facts surrounding it.

It is estimated that 1 out of every 10 women has endometriosis.  Endometriosis is a secondary autoimmune disease that occurs when the endometrium (the lining of the uterus) grows outside of the uterus.  Common places for this tissue growth is outside of the uterus, on the fallopian tubes, ovaries, bladder, within the pelvic cavity, on the pelvic floor, and on the bowels.  In extremely rare cases endometriosis can be found growing up towards and on the liver, lungs, brain and on the central nervous system.  These growths respond to the menstrual cycle the same way that the lining of the uterus does.  Each month, the lining builds up, breaks down and then sheds (aka ‘your period’).

When a woman gets her period the broken down lining exits the body as menstrual blood through the vagina.  When a woman has endometriosis, the tissue and blood from the endometrial growths found outside of the uterus have no way of leaving the body.  This results in internal bleeding and inflammation; both of which can cause chronic pain, infertility, scar tissue formation, adhesions and bladder and bowel complications.  Women with endometriosis also suffer from higher rates of allergies, yeast infections, asthma, chronic fatigue, fibromyalgia, other autoimmune diseases (such as hypothyroidism and lupus and others) and increased rates of ovarian cancer, non-Hodgkin’s lymphoma and brain cancer.

There is no cure for endometriosis and treatments leave a lot to be desired.  Common treatments include oral contraceptives, GnRH agonists, progesterone therapies, surgery and hysterectomy.  Since endometriosis usually appears during the reproductive years, hysterectomy is not a welcomed option and yet is commonly prescribed.  Surgery does not cure endometriosis, in many cases the growths reappear within five years. Hysterectomy does not cure endometriosis, with 40% of women see a reoccurrence of their symptoms.  There is no cure for endometriosis.

This March we need to raise awareness.  It’s not a comfortable topic but that is no reason for millions of women to suffer in silence with no known cure.  The discomfort society feels in talking openly about menstruation or uteri or vaginas is no reason to deny any woman the right to proper reproductive care.  1 in 10 women have endometriosis. These women are your friends, neighbors, sisters, co-workers, lovers, girlfriends, cousins, aunts, nieces, mothers, and fellow humans.  It takes an average of 7 years to get a proper diagnosis and even longer to find an effective treatment plan (if any).  This is about proper reproductive care, about millions of women who are embarrassed to talk about painful periods, about millions of women who suffer in silence.  It needs to stop.

This is not a call to arms but a call to uterus(es). This month lets promote reproductive care and raise awareness for endometriosis. Ask me about my uterus, ask those you care about, about their uterus.  Yes, it sounds strange, but how else are we to start the discussion and break the stigma against talking about reproductive illness; especially if we can’t even say uterus or vagina without snickering or feeling as embarrassed as a third grader would.  Please help us raise awareness this March; share this article, share your story, start a conversation, ask a loved one about their uterus and break the silence!

 

 

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