dementia

Thiamine Deficiency: A Slow Road to Dementia

Published on
10813 views
thiamine deficiency dementia

 

‘Jo, you’ll be relieved to hear the tests are all normal.’

I’d heard this line so many times, and it wasn’t reassuring. Each time it became less likely that I had an illness that could be defined, diagnosed, and consequently cured, or even treated. If there was nothing wrong with me, why did I feel so awful? I had been gradually deteriorating over months, perhaps longer.

Fatigue and Other Seemingly Innocuous Symptoms

It’s difficult to say when I first felt unwell. One of the initial symptoms was terrific fatigue – struggling to find the energy to carry on each day at work. I was taking longer and more frequent tea breaks and relying on sugar to give me the buzz to carry on. Of course, it didn’t help that I didn’t sleep well. I would fall into a deep sleep early evening and then wake feeling strangely on edge with a racing heart, unable to sleep for most of the night. Even if I could sleep, it didn’t make me feel any better.

There were several other symptoms, which I could explain away, but one odd symptom was muscle twitches or fasciculations. These were worse when I was tired or had been more active. I also had dodgy guts – more about this later.

Even though I was exhausted I could continue working, being a mother to our four children – albeit a rather terrible one that repeatedly fell asleep in the middle of bedtime stories, until I developed brain fog. I felt like my thinking was occurring at less than half the usual speed. I struggled to hold a conversation, as this required listening, interpreting the other person’s words, formulating an answer, and talking. I would have to really concentrate to think about anything. I would forget things unless I wrote them down, which just meant I had unfinished lists scattered everywhere.

After falling on the ward where I had been working as a doctor, I finally acknowledged that I was sick, even if there was nothing apparently wrong with me. Once I stopped working, I deteriorated further, such that I was unable to recognize people and even places.

A Slow Road to Dementia

This was over 10 years ago. Clearly, I’ve improved since then. I’ve written a book to try to characterize my symptoms, explain what caused them, and why it was difficult to make a diagnosis. This seems even more pertinent since a lot of the symptoms I suffered with then resemble long Covid now.

My main concern was that I had developed dementia. I had many of the features: I struggled to remember recent events, I had problems following conversations, I was forgetting the names of friends and even commonly used objects, and I was repeating myself and having problems with thinking and reasoning. I also had difficulty recognizing where I was — this is visuospatial disorientation — a key marker of dementia.

Since the medical profession seemed to have no idea how to treat me I decided to try to work it out for myself. What choice did I have? Away from work, I had time to slowly read through medical papers, whilst I rested. I recognized that my symptoms improved after taking antibiotics for a gum infection. Any exertion made me markedly worse, but not immediately afterward, it would be the following day and last for several days. I improved if I rested. My other symptoms included pains in my hands and feet. I thought this was arthritis initially, but when I developed pins and needles and subsequently numbness, I realized this was a peripheral neuropathy – a problem with the sensory nerves in my extremities.

Some months earlier a close colleague had told me I was thiamine deficient, mainly because I had lost a lot of weight. I was taken aback, assuming he thought my diet was poor, or that I was drinking alcohol. I hadn’t drunk any alcohol for years as it made me feel rough after a few sips. I investigated thiamine deficiency and found that it causes loss of sensation as well as loss of balance; I already knew it affected memory from treating alcoholics under my care.

My friend kindly agreed to try high-dose intravenous thiamine on the ward. Neither of us really thought it would work, but it was worth a shot. I was astounded when after a few minutes of the infusion I started to be able to think clearer and even the pains in my hands and feet disappeared. I practically skipped off the ward to buy oral thiamine and dose up. Sadly, thiamine tablets didn’t work and two days later I was back on the unit begging for more shots. This thrice-weekly dosing of thiamine infusions continued for months.

The Gut Connection

I trained in Gastroenterology and General Medicine. They say doctors make the worst patients. For as long as I could remember I had suffered from intermittent severe central abdominal pains, which usually occurred after eating quickly on an empty stomach. According to my mother, I had been a colicky baby and had also returned to the hospital as a new baby with uncontrollable vomiting. Nothing abnormal was found.

In fact, not all the tests I had were normal. After several second opinions, I had a few abnormal tests. I had a CT scan of my abdomen, which showed that I had gut malrotation. The severe pains I had experienced throughout life were due to small bowel volvulus – twisting. I learned that if I stopped eating and lay down on my back the pain would gradually subside. Each time my guts twisted scar tissue formed adhesions, slowing down my gut movements.

My guts had been noticeably abnormal for many years. I had noisy guts and passed very loose, frequent motions. I don’t know many slim 20-year-olds who suffered from severe gastro-esophageal reflux as I did. As this progressed, I developed recurrent chest infections and required multiple courses of antibiotics. Eventually, I worked out that I was aspirating gut contents into my lungs each night, and I stopped eating in the evening and propped myself up with many pillows. All sorted – no more chest infections – no more antibiotics.

One of the other abnormal tests was an incredibly low vitamin D. Through late-night searches of anything vaguely relevant and my gastroenterology knowledge I worked out that a low vitamin D occurred in bacterial overgrowth. This made sense. I had developed bacterial overgrowth in my small intestines — the part of the gut responsible for the absorption of nutrients from food.

Small intestinal bacterial overgrowth or SIBO is due to an excess of bacteria in the small intestines. There are many risk factors including sluggish guts from adhesions, previous surgery, medications that slow the gut, but also multiple courses of antibiotics, poor immune system, and use of drugs that block acid production in the stomach, as well as pancreatitis. I’m sure that a diet high in sugar didn’t help.

I had another test specifically looking for bacterial overgrowth, which the nurse (a colleague I’d worked with many times) and I interpreted as abnormal. The consultant I saw thought the machine must have broken. This was frustrating; after so many normal tests to have a wildly abnormal test attributed to faulty equipment. I decided it was better to treat the patient (me) rather than a dubious test result. After starting antibiotics, I no longer needed the thiamine infusions. The diarrhea also improved.

I worked out that I had bacterial overgrowth from mal-rotated guts, obstructed from adhesions, which improved with antibiotics and were eventually treated with corrective surgery. I also had severe vitamin D deficiency, which was corrected with injections, and thiamine deficiency, which I subsequently managed with a fat-soluble thiamine analogue — benfotiamine. I found a paper online reporting thiamine deficiency in extremely obese patients who had undergone surgery on their small intestines to aid weight loss. Many of these patients had thiamine deficiency; they also had high folate, which was thought to be a marker of bacterial overgrowth. Oral thiamine had no effect on their thiamine levels, but after taking antibiotics the patients’ thiamine returned to normal. Interestingly, my folate was high.

What was less well known was that some bacteria produce an enzyme called thiaminase, which destroys thiamine. I can only assume that I had these kinds of bacteria in my gut. Interestingly these bacterial enzymes do not destroy benfotiamine.

I followed up on my theory of the underlying cause of dementia: that too many bacteria, producing a lot of thiaminase enzyme, destroy the thiamine in our food rendering us thiamine deficient. I found out that thiamine is essential for all living things, and it is necessary for the release of energy from food, particularly sugar or glucose. The brain only uses glucose as an energy supply. There are reports of low thiamine levels in the brain in patients who have died of dementia. Glucose metabolism in the brain is never normal in dementia. Benfotiamine has been shown to improve mild cognitive impairment. I speculated that this was the cause of my brain fog.

Thiamine Deficiency: The Missed Diagnosis

Why was it so difficult to make a diagnosis? I believe there are several reasons. Firstly, thiamine levels are rarely tested in the UK. Even though I had worked in the NHS for over 20 years I had never requested a thiamine test. Secondly, thiamine deficiency is known to present in widely differing ways. This is like many of the mysterious syndromes — a constellation of recognizable symptoms and signs with largely normal tests: irritable bowel syndrome, fibromyalgia, etc., and also long Covid. Thirdly, I wasn’t listened to. I’m not sure whether this is because I’m female, but I became extremely sick before anyone really tried to help, and even then I was reliant on friends I have in the medical profession.

I’m remarkably well now. I regained my memory and ability to think, although it probably took a couple of years. My guts still aren’t completely normal, but bacterial overgrowth is often a chronic condition. I still take supplements and I’m careful with my diet, avoiding sugar and alcohol. My diet is quite restrictive, but it’s worth it. I wouldn’t want to go back to how I was.

#1
The Missing Link: A Memoir

15 customer reviews

The Missing Link: A Memoir*

by Jo Dixon




 Price: $ 7.81

Buy now at Amazon*

Price incl. VAT., Excl. Shipping

Last updated on December 28, 2023 at 6:07 pm – Image source: Amazon Affiliate Program. All statements without guarantee.

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. 

Photo by Katie Moum on Unsplash.

This article was published originally on June 30, 2022. 

Related posts:

atomic imprint- chronic illnessAtomic Imprint: A Legacy of Chronic Illness It all comes down to energyIt All Comes Down to Energy Thiamine and sugarSugar Intake and Thiamine thiamine mosquitosAre You Attractive? Connections Between Low Thiamine and Mosquito Bites

You might be interested in

Thiamine Deficiency Gaining Recognition: New Book

Published on
10103 views
new thiamine book

In the 5 years since Dr. Lonsdale and I published our book: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition (and 50 years since Dr. Lonsdale first began working with thiamine) recognition of the role of thiamine in health and disease have increased steadily year over year. Sales of the book double each year. Admittedly, the numbers were low and remain low in comparison to other popular topics, but the increase in awareness is heartening. Unfortunately, much of this awareness has not reached the medical profession. We regularly see reports in the medical literature boasting recognition of ‘rare’ cases of thiamine deficiency diseases like beriberi and Wernicke’s. If only physicians knew how common these conditions were and that they are only rare because we are not looking. Insufficient thiamine is Hiding in Plain Sight.

A New Book

In 2020, a UK physician by the name of Jo Dixon published a new book on thiamine deficiency, a personal account of her declining health, her discovery of thiamine, and her efforts to get treatment and spread the word. The book, called The Missing Link in Dementia, A Memoir, documents her journey. Unfortunately, she neither mentions thiamine in the title, the description, or even in the text until halfway through. One would not know the book is about thiamine until one reads it or unless it is recommended, so I will recommend it here. This would be a great starter book for someone beginning their health journey.

She has a second book listed on Amazon, Swimming in Circles that I have not read, but I suspect it details thiamine deficiency in fish in other animal populations.

While I would have preferred her to mention thiamine deficiency in the title or introduction, I found the book quite telling of the lengths one has to go to uncover this deficiency, even as a physician. Her case, unfortunately, is highly typical of what we see in patients everywhere. She had longstanding bowel dysfunction, which limited her ability to eat and maintain nutritional status. She led a busy life as a physician and mother of four children, which put pressure on thiamine stability. Even so, she functioned quite well for a long time. It wasn’t until her health took a severe turn for the worse that thiamine deficiency was recognized. Like others who develop issues with thiamine, she was forced to diagnose herself. No other physician, and she saw many, could provide any answers to her declining health. She had to figure it out herself. She was also forced to treat herself. Fortunately for her, she convinced a physician friend to provide IV thiamine, a protocol that was not accepted by her hospital and one she could not readily provide to other patients when she identified their deficiencies.

All of this is typical. We believe that thiamine deficiency was solved and thus any cases that do appear must be rare (to a tee, most case reports include ‘rare’ in the title or introduction). In reality, they are only rare because we do not look for them. We believe falsely that thiamine deficiency emerges acutely, and while it does in some cases, mostly it sits in the background, quietly and insidiously destroying one’s health. We have cases of high functioning individuals whose health begins to decline and whose thiamine levels are tested as low and should merit treatment but ignored for years as not being pertinent. And those are the lucky ones. Most physicians refuse to test for thiamine.

Thiamine deficiency is easily treatable if recognized early. It becomes more complicated as the years pass, and it is impossible if we never bother to look.

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. 

Photo by Alif Caesar Rizqi Pratama on Unsplash.

Related posts:

recovering from thiamine deficiencyRecovering From Suspected Thiamine Deficiency

You might be interested in

Genetic Thiamine Deficiency Ravaged My Family

Published on
5110 views
Modern thiamine deficiency - foot drop

My Father’s Decline

In 2015, my 72-year-old Dad, a daredevil who raced motorcycles and piloted planes he built himself, started losing the ability to walk. His legs would give out from under him without warning. He thought it was a back injury compressing nerves, and he spent months going to the chiropractor hoping adjustments would fix him. But his legs only continued to grow weaker, eventually becoming so numb he couldn’t feel them. Within a year, he was stuck on the couch, barely able to drag himself to the bathroom. Numerous doctor visits provided no answers. He was eventually accused of “drug-seeking” and refused to let us take him to any more doctors. He continued to deteriorate, his legs swelling up like balloons. He became incontinent, and couldn’t stop peeing on himself. He required constant visits by me and my sisters to clean him up and put food within his reach. It was clear he was dying without any medical diagnosis or even real curiosity from his doctors. I eventually moved him in with me, but his disability overwhelmed me. He couldn’t even roll over on his own because his arms were now weak and numb, too. I had my husband help me load him into the car and take him to the emergency room.

Once there, doctors told me my father’s bladder was unable to void on its own (neurogenic bladder), and urine had been backing up into his kidneys for who knew how long. He now had a severe kidney infection, as well as a septic blood infection. He likely would have died within a matter of days, the doctor said. They put a catheter in him and gave him IV antibiotics. He now had permanently damaged kidneys and a new diagnosis of congestive heart failure, with his heart working at only 30 percent of normal. They put a pacemaker in him to keep his heart going. But, despite all manner of tests, none of the doctors could figure out why his bladder could no longer empty, nor why his legs had stopped working. On his sixth day there, a team of neurologists gathered at the foot of his bed and hesitantly suggested that the cause could be some spinal stenosis they could detect in his neck. “It would be an unusual presentation for injury there to impact his legs more than his arms, but perhaps it’s worth trying surgery to correct it.” My father asked if it would help him regain the ability to walk; he dearly wanted to be able to fly his plane again. They said they couldn’t predict, the body was mysterious, who knew what the outcome would be?

My father went through neck surgery to repair the stenosis, followed by weeks in a rehab center. Then I brought him home. For the next eight months, he stabilized to a degree, and slowly regained upper body function. Still, because of his ankle drop and emaciated muscles, he could not walk without a walker and custom-built braces. Nor did he regain the ability to pee on his own; he now had to catheter himself five times a day to void his urine. I remained unconvinced that relatively minor spinal stenosis of the neck had caused him such physical wreckage.

Two Sisters With the Same Deficiency

In the meantime, we learned my youngest sister had been diagnosed with dementia, although the neurologist said he couldn’t pinpoint what “type.” She was only 51 years old. It was upsetting and scary to me, because for a long while I had been dealing with strange mental symptoms of my own. For years, I had been experiencing plenty of tingling and numbness in my legs, but that felt a minor nuisance compared to what I called “episodes” where my mind seemed to not be perceiving things right. Everything around me felt unreal. These episodes were increasing, yet I’d been so distracted by my father’s medical drama that I didn’t pay much attention. Then, not long after I got my Dad moved to an assisted living facility, I woke up feeling as if I was trapped in some kind of drugged state, like an LSD trip gone wrong, accompanied by heart-pounding panic attacks that seemed never to end. My husband took me to the ER. They said my blood work was all fine, told me I likely had an anxiety disorder and sent me home with a prescription for anxiety medication. Over the next few months, the feeling of unreality never went away. I felt like I existed in some kind of bubble, with a thick glass wall between me and the world, with the constant anxious question of “Is this real?” I was also starting to walk strangely, staggering unexpectedly. I was going numb from the knees down, and my arms were suddenly numb from the elbows down to my fingers. I had to hold on to the wall in the shower so I wouldn’t fall over. It was terrifying to feel so unsafe in my own mind and body, and several times I thought of ending my own life.

Three months into this agonizing state, it became worse, my mind went completely sideways; everything swam around me, and I felt I couldn’t form words. I was sure I’d experienced a stroke. Another trip to the ER. While there, I confessed I was a frequent alcohol drinker, so the doctor ordered a CT scan, looking for Wernicke’s Encephalopathy, he said. But my brain looked fine on the scan. Doctor visit after doctor visit, test after test, I got no answers beyond a case of hyperthyroidism that responded quickly to medication, but the resolution of which gave me no relief from my symptoms.

Discovering Thiamine and Another Sister Develops Symptoms

Of course, I was on the Internet constantly, trying to find a reason for what was happening to me. After my second ER visit, I typed in the word “Wernicke’s” into a search engine, alongside the list of my symptoms, and found an article by Dr. Derrick Lonsdale on the Hormones Matter site, an article which talked about thiamine deficiency, Wernicke’s and modern-day beriberi. My heart raced as I read such a close description of my symptoms. I quickly read through his book co-written with Chandler Marrs on thiamine deficiency, and immediately started swallowing thiamine pills. But as predicted by Dr. Lonsdale, I experienced the vitamin “paradox” of worsening symptoms and had to step back, divide up pills, and increase the dosage very slowly.

I also ordered another book Dr. Lonsdale mentioned, published in 1965, about beriberi in early 20th century Japan. Inside were many photos of beriberi victims, one Japanese soldier’s photo captioned with “the emaciation and characteristic ankle drop of beriberi.” I was stunned to see the soldier’s legs looked exactly like my father’s. I also found descriptions of sufferers being unable to urinate, a problem I’d never found on Internet lists of thiamine deficiency symptoms. The book also talked about “wet beriberi,” which damages the heart, just as my father’s heart was now damaged. Finally, an answer! There was no doubt in my mind that my dad had somehow developed beriberi.

I started giving extra thiamine to him as well, although he’d been taking some in the B-complex his doctor had prescribed to him in the hospital for anemia. (Could the extra thiamine in that daily pill have been the reason he was able to stabilize after his neck surgery?) At his next doctor visit, I took the photos of my dad alongside beriberi victims and asked if this could be what happened to him. She said, “Hm, interesting,” and ordered a lab test to determine his thiamine levels. I warned her I had been giving him thiamine for weeks, so the test would likely come out normal. Which of course, it did, and she thus dismissed the idea he might have had beriberi. I couldn’t understand why, after seeing those striking photos, she wasn’t curious to investigate more.

Meanwhile, I took my sister with dementia, who had been complaining of numbness in her hands and arms for months, to a lab to get her thiamine levels checked, too. The results came back normal. But I handed her a bottle of benfotiamine anyway and asked her to start taking it. She said she would but later confessed she threw the bottle in the trash. “I don’t like taking pills,” she said. I wished she would, but I didn’t press. After all, my halting efforts at taking more thiamine hadn’t led to any kind of big improvement for me. I was still struggling along in a bubble of unreality and numbness. I eventually took seriously Dr. Lonsdale’s advice to go beyond vitamin pills and get B-1 injections. I found a naturopathic doctor willing to give me daily thiamine shots for two weeks. Again, I felt no dramatic difference, which made me doubt that I had a thiamine issue after all. But I suppose it did seem some of the numbness in my legs was improving. I could at least stand on my own in the shower again. So, I kept taking daily benfotiamine and getting the occasional B-complex shot with thiamine in it.

Slowly, over the next two years, I noticed my mental state improving and the numbness in my limbs finally resolving. And my father, having gone through several bottles of benfotiamine, started getting some sensation back in his legs. But he believed his doctor that it could not be beriberi that took him down, and he waved away more extra thiamine, although he was still getting it from his daily B-complex. Eventually, another sister came to visit and told me how scared she was because her legs had started going numb. I gave her all the thiamine I had and begged her to take it, and a few months later she called me, grateful the numbness has gone away. She now takes benfotiamine every day.

Tragically, my sister with dementia went into a memory care home where she would only eat the junk food and sugary carbohydrates served to her, a diet which I now understand depletes thiamine very quickly. As she was not allowed to swallow any pill not prescribed by a doctor, and her blood levels of thiamine had been measured as “normal,” she was not prescribed thiamine. She declined rapidly, and soon started asking me the same question I had so often asked myself, “Is this real?” Like our father, she stopped being able to walk or otherwise control her limbs. Also, like our father, she stopped being able to urinate on her own and had to be catheterized.  This past January, she died a truly horrific death from what the doctor called “complications of dementia.” She was 53 years old.

A Probable Genetic Cause

I am now convinced that there is an inheritable problem with thiamine transport in my family and that we require much higher levels of thiamine than the rest of the population to function normally. I cannot prove it without the help of doctors who will take seriously such a possibility, and even if I could find such doctors, how could they prove it? What tests would tell us that? Even after all that me and my father and siblings have been through, my certainty can waver. After all, it took many months of persistent thiamine intake for me to return to anything close to normal, so how do I know I wouldn’t have improved without it? I can’t know for sure. But, I have found that if I get distracted by life and neglect taking thiamine for several weeks, my hands start to go numb again, and my primary mental symptom of unreality starts to creep back. I also notice that if I take thiamine with strict regularity, I feel so much better.

Today, I am haunted by the possibility that many others might have a similar genetic problem in handling thiamine, and could be going through similar desperate declines as my family experienced, without ever knowing that a simple vitamin pill could resolve it. All because of a calamitous blind spot in the medical system. Imagine all the human misery that could be avoided, not to mention medical costs saved, if more doctors would consider the possibility that beriberi can still strike. I will be forever grateful for the tireless work of Dr. Lonsdale and the Hormones Matter site; I believe the information I learned there literally saved my life. I hope my story helps others in the same boat to see themselves and be able to save themselves as well.

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. 

Related posts:

thiamine deficiencyRapidly Deteriorating Health With Thiamine Deficiency Familial Beriberi - genetic thiamine deficiencyFamilial Beriberi: Discovering Lifelong, Genetic, Thiamine Deficiency recovering from thiamine deficiencyRecovering From Suspected Thiamine Deficiency

You might be interested in

dysautonomia thiamine deficiency

Dysautonomia and Hypoxia

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

Dementia and Thiamine Deficiency

Published on
8322 views
dementia thiamine

In this post I will try to indicate how you might detect cognitive changes in a loved one and how you might help defer the onset of severe neurological disease. Every person developing dementia goes through mild cognitive impairment first. A given symptom might be short-term memory loss, difficulty in finding a particular word or forgetting well-known procedures. We expect such changes in people in their nineties, but if they develop in the fifties, you can suspect that this is the beginning of dementia that is a disease, not normal aging.

What Do We Know About Dementia?

A study published in 2017 reviewed the observational studies examining associations between non-genetic factors and dementia. A total of 76 unique associations were examined, of which seven presented convincing evidence. They found an association with use of benzodiazepines (common drugs for mental disease), depression at any age, late-life depression and infrequency of social contacts for all types of dementia. Late-life depression and type  2 diabetes were associated with onset of Alzheimer’s disease (AD). Emotional stress causes brain function that consumes energy.

A review assessed the effect of the drug metformin (used in the treatment of type 2 diabetes) on the risk, progression and severity of AD and other forms of dementia, as well as any measures of cognitive performance or impairment. A case of encephalopathy (brain disease) occurred in a patient receiving metformin who was in end-stage diabetic renal failure. The drug was withheld and signs and symptoms quickly resolved. The authors hypothesized that metformin induced thiamine deficiency (TD), based only on their use of brain imaging that has a characteristic pattern caused by TD. Although metformin has become a drug of choice for the treatment of type 2 diabetes, some patients may not receive it “owing to the risk of lactic acidosis (increased concentration of lactic acid in blood or urine)”, a significant finding in critically ill patients who often respond to thiamine administration . Diabetic patients taking metformin may be predisposed to thiamine deficiency that  is common in diabetes anyway . There is epidemiological evidence linking type 2 diabetes and its related conditions (obesity, insulin resistance, metabolic syndrome) to AD and it has recently been proposed that AD can be considered as “type 3 diabetes” because of disturbed glucose metabolism in that disease .

Mental Versus Physical Disease

It is probably absurd to separate the body from the brain. As has been said on this website many times, the body is composed of between 70 and 100 trillion cells, all of which have individual responsibility. I have used the analogy of a symphony orchestra where the brain is the conductor and the body organs are like banks of instruments that have to work together. The cells in each organ can be compared to the instrumentalists. They all know what to do but must work together “to play the symphony of health” under “the baton” of the “brain conductor”. Hence, for example, the immune system is an extremely complex union of mental and physical, requiring the brain, the nervous system and a variety of cells that carry out function. Assuming that the genetically determined genome”blueprint” is perfect (without mistakes in the DNA) all the cellular machinery requires is energy and that comes from an enormously complex list of nutrients.

Resulting from a great deal of personal experience and the genius of Hans Selye, I have concluded, like him, that energy metabolism is the focal point of health and disease. Selye developed the idea of what he called the “diseases of adaptation”. He coined the phrase the “General Adaptation Syndrome (GAS) in which he described the processes by which an animal adapts to physical and mental impositions of stressors. A stressor is any form of threat encountered  by us on a day-to-day basis. It may be mental (a divorce) or physical (infection, trauma). He concluded that energy was required to drive the GAS (the ability of the brain/body orchestra to face the stress and adapt to it). One of  Selye’s students was able to support this idea by producing the GAS in an experimentally induced thiamine deficient animal. The remarkable thing about this work was that in Selye’s time, little was known about energy metabolism. Today, the biochemistry is well outlined, if not complete, and thiamine stands out as a vitally important component. In continuing the analogy of the orchestra, I have nominated it as “the leader” (the chief violinist in an orchestra).

The Demands of an Active Brain

By far and away the best example of an energy defect in human disease is that of thiamine deficiency beriberi. Because energy deficiency is the underlying cause, it can imitate virtually any collection of symptoms that are regarded as those of a specific disease in the present medical model. Also, because it has many “psychological” symptoms, a long morbidity (continuation of symptoms) and a low mortality, it is dismissed as trivial. Since the brain and heart are the most energy consuming organs, it would be an obvious conclusion that a well endowed functional brain (genius) might be more at nutritional  risk than someone less well endowed. I turned to the medical histories of three historical characters, all of whom were acknowledged geniuses. Their health problems have been debated without any conclusions. It was their similarity that appeared to me to be so striking.

Charles Darwin

His medical history is discussed online. Apparently he suffered repeatedly throughout life, suggesting “genetic risk”. His symptoms included chest pain, heart palpitations, stomach upsets, headaches, malaise, vertigo, dizziness, muscle spasms, tremors, vomiting, cramps, bloating and fatigue, all described in beriberi. He was treated by a Dr. James Gully, whose therapy included “a strict diet” that was reported to give Darwin “improvement in his symptoms”. In September 1849 his symptoms increased, apparently “during the excitement of a British Association for the Advancement of Science”. Excitement is a brain perception whose function elevates the brain from a resting state and requires increased energy to adapt. Between the ages of 56 and 57 symptoms were reportedly continuous and the text described “copious and very pallid urine”. Cellular energy is dependent on an efficient consumption of oxygen (oxidation) and the yellow pigment that gives urine its characteristic color is known as urochrome, an oxidation product of hemoglobin. It suggests that the pallid urine may well have been an indicator of decreased oxidative function. Perhaps we can hypothesize that the exacerbation of symptoms related to virtually any form of stress may well have been from a combination of dietary deficiency and genetic risk.

Mozart

The medical history of this genius is less clear online than that of Darwin. He suffered poor health throughout life, again suggesting genetic risk. Between 1789 and 1790, the symptoms described were weakness, headaches, fainting and hyperactivity and he reportedly had many falls. A left temporal fracture was described in his skull, examined after his death, suggesting a fall injury. Also, it was reported that “drinking was a well-known weakness of Mozart”. The association of alcohol with thiamine deficiency is well documented. It produces functional changes  in the automatic brain controls of the autonomic  nervous system  that might not necessarily result in loss of intellectual function, at least in the early stages.

Beethoven

His medical history is also less clear but apart from his well known deafness, the text reported repeated diarrhea, abdominal pain, migraine, rheumatism, nosebleeds and he died in delirium at the age of 56.

Of course, I am well aware of the multiple theories to explain the medical problems of these three geniuses. My point is that the workload exercises the brain and its function requires energy. It seems reasonable to suggest that the brain of a genius requires more energy than one less well endowed. Furthermore the passion that goes into the work often makes diet a secondary issue that is frequently neglected by such individuals. In the case of Mozart, the depletion of thiamine by alcohol would also have a deleterious effect on energy metabolism.

Neurodegenerative Disease and Thiamine

We know that thiamine metabolism is involved in the pathology of Alzheimer’s and Parkinson’s diseases. This has been shown in many papers published in the medical literature. An Italian doctor by the name of Costantini has published a number of manuscripts using high-dose thiamine in no less than seven different disease conditions, most of which are described as neurodegenerative diseases. Obviously, this is extremely offensive to the present medical model that believes each disease has a separate cause demanding specific treatment for each. If we look at the biochemistry of the human body, think of its complexity, its extraordinary dependence on a combination of genetic integrity, nutrition and lifestyle, it becomes easier to understand how a single molecule (thiamine) can be so vital. It stands at the gateway of the biochemical machinery that synthesizes energy in the form of ATP.

What is Energy?

Let us take a very simple analogy, that of rolling a stone up a hill. The point is that energy is consumed by overcoming the force of gravity trying to keep the stone at the bottom of the hill. We are imbuing it with what Newton called “potential energy”. When it gets to the top of the hill a simple push can cause it to roll down the hill and this would be referred to as “kinetic” energy. Although the principles in the human body are exactly the same, the mechanism is widely different. An electric force rolls electrons up an electronic gradient that converts ADP to ATP (the top of the electronic hill). ATP is a chemical that stores energy and is sometimes called “the energy currency”. Natural food contains all the ingredients that provide us with fuel. But it also contains vitamins and essential minerals that enable our cells to turn the calorie bearing part of the food into chemical energy. The chemical energy has to be transduced to electrical energy, so the body can be defined as an electrochemical “machine”.

Dr. Marrs and I have long been concerned that concentration on many artificial foods, particularly those concerned with sugar in all its different forms, results in manifestations of disease that are being constantly overlooked and misdiagnosed. We have hypothesized that the symptoms experienced in the early stages of this kind of malnutrition are multitudinous and do not fit into our categories of so-called organic disease. Often attributed to psychosomatic causes, and the prevailing inability to recognize its true underlying mechanisms, has led to frequent doctor shopping by people that have genuine disability. They go from specialist to specialist, all of whom have resolutely decided that vitamin deficiency in America is a thing of the past.

What can you do?

First of all, recognize that dietary mayhem, particularly in children, is common. This results in loss of cellular energy that has its main relevance in the energy consuming brain. Chronic fatigue is perhaps the commonest symptom, but heart palpitations, headache, cold and heat intolerance and other functional symptoms may occur. The peculiarity of behavior observed in someone is because of distorted brain function that can vary enormously in the way it is expressed. I would suggest that if a loved one in his fifties begins to show the signs of aging discussed above, the first thing to do is remove sugar from the diet. Books have been written directing us toward a healthy diet but our pleasure loving brains have become addicted to sweet taste since the earliest beginnings of life. Therefore, because nobody objects to taking pills for their health, appropriate supplements can restore the balance between calories and vitamins. The most under appreciated vitamin (thiamine) may actually be the most important of all of them. However, if we look at the history of the treatment of beriberi, it took huge doses of vitamin B1 (thiamine) for months to restore health. A dose of 100 mg of thiamine hydrochloride, together with a similar dose of magnesium and a multivitamin might be better than all the pharmaceuticals in creation. There is abundant evidence to suggest that neglect of these functional symptoms may gradually lead to biochemical changes that are irreversible and we then call it a neurodegenerative disease.

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.

 

Image credit: Gerd Altmann from Pixabay

Related posts:

thiamine and cancerA Role for Thiamine Deficiency in Cancer

You might be interested in

Uterus and Ovaries: Fountain of Youth

Published on
7893 views
uterus ovaries fountain of youth

Numerous studies have shown a strong correlation between removal of both ovaries / bilateral oophorectomy (castration) and accelerated aging as measured by an increased risk of chronic health conditions. Hysterectomy / uterus removal with preservation of both ovaries is also associated with some of these chronic conditions. These include heart disease, stroke, metabolic syndrome, osteoporosis, hip fracture, lung cancer, colorectal cancer, dementia, Parkinsonism, impaired cognition and memory, mood disorders, sleep disorders, adverse skin and body composition changes, adverse ocular changes including glaucoma, impaired sexual function, more severe hot flushes and urogenital atrophy. Wow, that’s quite a list!

Ovaries: Health Powerhouses

This 2016 article titled “Study: Remove ovaries, age faster” sums up the findings of Mayo Clinic researchers proving yet again the harmful and unethical practice of ovary removal. The study found that ovary removal (oophorectomy) is associated with a higher incidence of 18 chronic conditions and should be discontinued in women who are not at high risk for ovarian cancer. Although this study cites the increase in chronic conditions in women who undergo oophorectomy before age 46, other studies have shown that oophorectomy even after menopause does more harm than good. Here is one that showed that to be true up to age 75.

The ovaries have both reproductive and endocrine functions as detailed in this International Menopause Society article. After menopause, the ovaries produce mostly androgens, some of which are converted into estrogen. Testosterone levels are more than 40% lower in women without ovaries compared to intact women. Women without their uterus likewise have lower levels but not as low as women without ovaries per this article. Estrogen therapy mitigates some but not all of the increased health risks of oophorectomy. But estrogen further reduces androgen levels increasing risk of osteoporosis and fracture. Nothing can replace the lifelong functions of the ovaries (and uterus).

The Uterus / Ovaries / Tubes Connection

The harms of ovary removal would also apply to ovarian failure that commonly occurs after hysterectomy and some other medical treatments. As previously cited, women who have had a hysterectomy have lower levels of testosterone. According to this 1986 publication, 39% of these women showed signs of ovarian failure. This study showed a nearly 2-fold increased risk of ovarian failure when both ovaries were preserved and nearly 3-fold when one was preserved. This likely explains the increased risk of heart disease and metabolic conditions as shown by multiple studies including this recent Mayo Clinic one. However, per this 1982 study, the uterus itself protects women from heart disease via the uterine substance prostacyclin. Loss of bone density is another harm of hysterectomy as shown by multiple studies such as this one.

Removal of even one ovary (unilateral oophorectomy) without hysterectomy is also harmful. Studies out of the Mayo Clinic showed increased risks of cognitive impairment or dementia and parkinsonism. Colorectal cancer is another increased risk according to this Chinese study and this Swedish one.

The Fallopian tubes appear to impair ovarian function to some degree as evidenced by Post Tubal Ligation / Sterilization Syndrome. This study shows an increase in Follicle Stimulating Hormone (FSH) after tube removal (salpingectomy).

Ovarian impairment after hysterectomy or salpingectomy is thought to be the mechanism of the reduced risk of ovarian cancer which is already rare.

The Uterus: Anatomy, Sex, Cancer Prevention

Hysterectomy is associated with other harms besides impaired ovarian / endocrine function. The uterus and its ligaments / pelvic support structures are essential for pelvic organ integrity as well as skeletal integrity. The effects on these structures and functions are detailed here and here. This article shows the many hysterectomized women lamenting their “broken bodies” – changes to their figures, back, hip and midsection pain, pelvic pain, bladder and bowel issues, and effects of severed nerves and blood vessels.

The uterus and associated nerves and blood vessels play a key role in sexuality and vibrancy. You can hear the desperation in women’s comments about the devastating sexual losses and feelings of emotional emptiness.

There is an increased risk of renal cell, thyroid, and colorectal cancers after hysterectomy. How ironic when cancer fear tactics are commonly used to market hysterectomy and/or oophorectomy.

Adhesions that commonly form after these surgeries can cause serious problems especially in the long term. Surgical complications – nerve injuries, bladder, bowel and ureter injuries, vaginal cuff dehiscence, a too short vagina, infections, hemorrhage – are more common than indicated by gynecologists.

Although “The Miraculous Uterus” article fails to mention the anatomical harms, it is otherwise “spot on.” It talks about the “ovarian conservation scam” and that “passion, love, ecstasy, the emotional essence that drives human achievement, forever after elude them.” This explains why “there’s no effective outrage against the barbarism of hysterectomy.”

Compelling Evidence of Harm

Clearly, there is compelling medical evidence that both hysterectomy and oophorectomy are destructive surgeries. Unfortunately, some hysterectomy forums censor negative posts giving a slanted view of the life shattering effects. Here is a sampling of women’s experiences on the Gyn Reform site.

The medical literature on the harms of these surgeries dates back over a century. Listed below are a small number of the numerous publications (minus the ovarian failure studies cited above). The Gyn Reform website has a fairly comprehensive list of resources on oophorectomy. Its Ovaries for Life sister site provides a good overview of the lifelong importance of our ovaries.

1912 – The Physiological Influence of Ovarian Secretion

1914 – Nervous and Mental Disturbances following Castration in Women

1958 – The controversial ovary

1973 – Osteoporosis after Oophorectomy for Non-malignant Disease in Premenopausal Women

“Oophorectomy before the age of 45 years was found to be associated with a significantly increased prevalence of osteoporosis within three to six years of operation.”

1974 – Endocrine Function of the Postmenopausal Ovary: Concentration of Androgens and Estrogens in Ovarian and Peripheral Vein Blood

1978 – The emotional and psychosexual aspects of hysterectomy

1981 – Premenopausal hysterectomy and cardiovascular disease

1981 – Sexual response after hysterectomy-oophorectomy: Recent studies and reconsideration of psychogenesis

1981 – The role of estrogen and oophorectomy in immune synovitis

1982 – Prostacyclin from the uterus and woman’s cardiovascular advantage

1989 – The effects of simple hysterectomy on vesicourethral function

“The results show that simple hysterectomy is associated with a significant incidence of post-operative vesicourethral dysfunction and that there is an identifiable neurological abnormality incurred at operation which is pertinent to the subsequent disordered voiding.”

1990 – Effects of bilateral oophorectomy on lipoprotein metabolism

1994 – The climacteric ovary as a functional gonadotropin-driven androgen-producing gland

1996 – Urinary incontinence in older women: who is at risk? Study of Osteoporotic Fractures Research Group

“Urinary incontinence is a common problem in older women, more common than most chronic medical conditions. Of the associated factors that are preventable or modifiable, obesity and hysterectomy may have the greatest impact on the prevalence of daily incontinence.”

1997 – Bladder, bowel and sexual function after hysterectomy for benign conditions

1998 – Ovaries, androgens and the menopause: practical applications

1998 – Impairment of basal forebrain cholinergic neurons associated with aging and long-term loss of ovarian function

1998 – Influence of bilateral oophorectomy upon lipid metabolism

1999 – Estrogen and movement disorders

2000 – The hypothalamic-pituitary-adrenal and gonadal axes in rheumatoid arthritis

2000 – Risk of myocardial infarction after oophorectomy and hysterectomy

2000 – Hysterectomy, Oophorectomy, and Endogenous Sex Hormone Levels in Older Women: The Rancho Bernardo Study

2005 – Ovarian conservation at the time of hysterectomy for benign disease

“Ovarian conservation until age 65 benefits long-term survival…. There is sustained, but decreasing, benefit until the age of 75, when excess mortality for oophorectomy is less than 1%.”

2007 – Ovarian conservation at the time of hysterectomy for benign disease

“Approximately 78% of women between the ages of 45 and 64 years have prophylactic oophorectomy when hysterectomy is performed for benign disease…. Therefore, the decision to perform prophylactic oophorectomy should be approached with great caution for the majority of women who are at low risk of developing ovarian cancer.”

2009 – Ovarian conservation at the time of hysterectomy and long-term health outcomes in the nurses’ health study

“In no analysis or age group was oophorectomy associated with increased survival.”

2010 – Current indications and role of surgery in the management of sigmoid diverticulitis

“A previous history of hysterectomy is a valuable clinical clue to the correct diagnosis as colovaginal and colovesical fistulas are rare in females with their uterus in place, as the uterus becomes a screen interposed between the inflamed colon and the bladder and vagina.”

2012 – Oophorectomy for whom and at what age? Primum non nocere

2016 – Study: Remove ovaries, age faster

2017 – Cardiovascular and metabolic morbidity after hysterectomy with ovarian conservation: a cohort study

A Harmful Practice That Won’t Die

Ovary removal / castration was introduced by Robert Battey in 1872 and “was practised widely for several decades….. Better insight into female physiology and ovarian function finally pushed the sinister operation of Robert Battey from the scene.” This publication refers to Battey’s operation as “barbaric.”

Despite the long-standing and compelling evidence of harm, these surgeries continue at alarming rates. Publications are misleading in that they report inpatient surgeries despite the large majority being outpatient (70% in 2014). This 2008 article reported that oophorectomies “more than doubled in frequency since the 1960’s.” According to results of a FOIA request by Ovaries for Life, there are over 700,000 oophorectomies every year despite there being only ~22,000 cases of ovarian cancer. Hysterectomy figures obtained by Ovaries for Life are also shocking at 830,000 in light of less than 70,000 cases of endometrial and cervical cancers.

Many media reports have questioned the high rate of these surgeries since gynecologic cancers are rare. The oldest one I could find was dated 1969. I found about three articles per decade in the mainstream media since then. According to the Athena Institute, half of U.S. medical schools in 1986 “had changed their suggestions and were now recommending a reconsideration of the common practice of ovariectomy.” Evidently, that never took hold.

Congress held two hearings on hysterectomy, one in 1976 and one in 1993. The 1993 transcripts state that the hysterectomy rate increased 250% in women ages 15 to 24 and 186% in ages 25 to 34 from 1965 to 1984! Despite these shocking statistics, it appears that no action was taken after either hearing.

According to this “Reassessing Hysterectomy” article, the Agency for Healthcare Research and Quality sponsored research and conferences on the overuse of hysterectomy in the 1990’s. This article is packed with information on the prevalence and harms of hysterectomy and oophorectomy as well as alternative treatment options. Yet, the high rate of hysterectomy has continued such that 45% of women will end up having one. Citing 2006 data, the oophorectomy rate was 73% of the hysterectomy rate.

How to End the Harm?

I’ve been researching this subject for over 10 years and sharing my experience and knowledge on various websites. It’s shocking how many women are misled and deceived into these surgeries. Age doesn’t seem to matter; younger and younger women are undergoing these surgeries. This appears to be the biggest surgical racket and women’s healthcare con as discussed here.

There are a number of issues that perpetuate the gross overuse of these harmful surgeries. These include:

  1. These surgeries and “forever after” care are very lucrative.
  2. The public has been led to believe that the female organs are disposable after childbearing is complete.
  3. Medical education and decades of practice have made these surgeries “a standard of care.”
  4. Informed consent is seriously lacking.
  5. Gynecology consent forms are open ended giving surgeons “carte blanche” to remove organs unnecessarily.
  6. We still live in a climate of gender disparity / male dominance.

As you can see from the list of publications above, some study authors have called out the practice of ovary removal as unethical. Numerous professional societies have issued guidelines discouraging its use in most women. But most have been silent on the overuse of hysterectomy despite its many harms.

Why has our government not stepped in to address this egregious harm? Women who have contacted their legislators have been met with indifference. Gyn Reform reported on their experiences with legislators and other authorities who can effect change. The non-profit HERS Foundation has been educating women and advocating for informed consent legislation since the 1980’s.

Why do insurance companies approve so many of these surgeries that are rarely necessary? Not only are the surgeries themselves expensive, treatments for the chronic after effects are costly. Reining in unnecessary treatments especially those that cause lifelong harm would go a long way towards making healthcare more affordable.

Why has Graduate Medical Education (GME) not changed their surgical requirements to favor organ preservation? Each resident must do at least 70 hysterectomies but there is no requirement for myomectomy (fibroid removal). Residents don’t need to do any cystectomies (cyst removals) either which is partly why so many women lose ovaries for benign ovarian cysts. Here are the GME ob/gyn requirements.

A popular mantra at Tufts in the 1970’s – “There’s no room in the tomb for the womb” – reflects this culture of the disposable uterus and gynecologists’ obsession with its removal. Insurance reimbursement rates are also to blame as they incentivize hysterectomy and oophorectomy over myomectomy and cystectomy. In many cases, medical management versus surgery is the appropriate course. The “Reassessing Hysterectomy” article cited above lists a number of treatment options for gynecologic problems. Revamping reimbursement rates to strongly favor organ preservation should eventually force GME to change their requirements. But how do we make that happen?

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. 

Lucas Cranach the Elder, Public domain, via Wikimedia Commons

Related posts:

hysterectomy secret - figure changesHysterectomy’s Best Kept Secret: Figure Changes hysterectomy heart diseaseHysterectomy: Bad for the Heart and Much More dexamethasone pregnancyIs Prenatal Dexamethasone Safe: The Baby Makers’ Hubris lupron keto dietLupron, Brain Function, and the Keto Diet

You might be interested in