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The Analgesic Effects of B Vitamins

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back pain and b vitamins

It appears that high doses of vitamins B1, B6 and B12, administered separately or in combination, can alleviate acute pain by potentiating the analgesic effect of non-opioid analgesics such as diclofenac (an NSAID), sold under various trade names. These facts were published in a German paper. In addition, a randomized, double-blind, controlled clinical study was reported in 378 patients with lumbago. The term lumbago is a relatively old one and it is now often referred to as “back strain”.

The patients were divided into two groups, half of them receiving diclofenac together with very large doses of vitamins B1, B6 and B12. The other half received only diclofenac . The investigators concluded that the addition of the B vitamins did indeed enhance the analgesic effect of the drug. The primary mechanism for the anti-inflammatory, anti-pyretic and analgesic action of diclofenac is thought to be by a biochemical mechanism that is well known in the body and described in the paper.

When I read this, I became aware that the mechanism they were describing was the same mechanism that has been described for one of the actions of thiamine tetrahydrofurfuryl disulfide (TTFD, Allithiamine, Lipothiamine) a thiamine derivative that I have mentioned a number of times in posts on this website. When I further researched the mechanisms of action of diclofenac, I read that “diclofenac also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis”. Could it be that the drug has an effect on mitochondrial DNA in people using it to relieve their pain? If so, this would be a serious indictment on its use.

Mitochondrial DNA

We now have reason to believe that our mitochondria (cellular energy producing organelles) have evolved from an original bacterium millions of years ago, and we now know that they have their own genes. These genes, inherited only from the mother, are completely separate from the cellular genes that we inherit from both parents. They are vitally important in the function of mitochondria that are responsible for synthesizing ATP, the energy currency used by the body. The interesting thing is that mitochondrial DNA is like bacterial DNA, has a different conformation from that of cellular DNA, and could be expected to be sensitive to the “DNA related bacteriostatic activity” reported to be one of the effects of diclofenac.

Side Effects of Diclofenac

There are 50 side effects of diclofenac recorded online. It may surprise you to know that 20 of the symptoms reported as side effects are identical to those that are well known in relationship to the thiamine (vitamin B1) deficiency disease, beriberi. Since thiamine is vital to the normal function of mitochondria, perhaps it suggests why three members of the vitamin B complex enhance the analgesic effect of the drug by protecting the patient from harm. This would enable it to be used with reduced dose, thus obviating the possible appearance of side effects.

Side Effects of Pharmaceuticals

It is always wise for a patient who is taking a drug to know what the potential side effects are. With this story of diclofenac, I was reminded of a drug that was produced in the 1930s in order to stimulate weight reduction. The chemical name is dinitrophenol (DNP). The side effects were so severe and occasionally caused sudden death, so it was withdrawn in 1938. Its present use is in experimental research in animals because it inhibits mitochondrial function and enables the researcher to study energy metabolism. Believe it or not, DNP is still available for weight reduction. There is no doubt that it works but it certainly offends  the Hippocratic oath accepted by all physicians, “thou shalt do no harm”.

Genetic Susceptibility

We simply do not know the genetically determined susceptibility of an individual in the use of a foreign agent prescribed to relieve a given symptom. The body always recognizes a “foreigner” and sets about breaking it down and getting it out of the body as quickly as possible. If a vitamin is used in a much larger dose than merely replacing it as an essential nutrient, it may be thought of as a drug. This is really a new concept in medicine and has not yet reached the collective psyche of medical practice. Perhaps the body recognizes the huge dose, but uses what it needs and excretes the excess. The trouble with that is that the present concept is that vitamin replacement is thought to be confined to the tiny doses found in natural food that are required by a healthy individual. No thought has been given to the fact that a vitamin may have to be used in order to stimulate and restore the decayed effectiveness of the enzyme to which it must bind. It is as though the roles of the enzyme and the vitamin are reversed. In a sense, the enzyme becomes cofactor to its requisite vitamin rather than the normal enzyme/cofactor relationship.

Energy Metabolism is the Core Issue

What seems to be emerging from all this is that failure of energy metabolism, coupled with genetic risk and the imposition of individual life stresses, provides us with a new medical model for disease. Besides killing the “enemy”, the bacteria, viruses or cancer cells safely, the only real treatment possible is an educated use of nutritional components to coerce damaged cellular systems back into a state of functional efficiency. Healing takes energy and only the body knows how to do that. We should give it every possible assistance. There is much evidence that even cancer cells become maverick because of devious energy metabolism.

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

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Diabetes and Thiamine: A Novel Treatment Opportunity

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diabetes and thiamine

Underlying all diabetic conditions is poor sugar control or hyperglycemia. Hyperglycemia can be due to a lack of insulin as in Type 1 diabetes or insulin resistance as in Type 2 diabetes. In either case, the corresponding diabetic complications that evolve over time in many diabetics, the cardiovascular disease, retinopathy, peripheral nerve and vascular damage, represent the effects of sustained hyperglycemia. Until recently, the mechanisms by which diabetic vascular damage developed eluded researchers. Although multiple, seemingly discrete biomarkers had been identified, no single, unifying mechanism was understood. It turns out that diabetics, both Type 1 and Type 2, are severely deficient in thiamine or vitamin B1 and that thiamine is required for glucose control at the cell level. Why is thiamine deficient in diabetics and how does thiamine manage glucose control? The answers to those questions highlight the importance of micronutrients in basic cellular functioning, particularly mitochondrial functioning, and the role of excessive sugar in disease.

Thiamine

Thiamine (thiamin) or vitamin B1 is an essential nutrient for all living organisms. The body cannot synthesize thiamine by itself and so it must be obtained from diet. Thiamine is present in yeast, pork, fish, various nuts, peas, asparagus, squash and grains (unprocessed) and because of the severity of the illnesses that thiamine deficiency evokes, many processed foods have been fortified with thiamine. Nevertheless, thiamine deficiencies thought resolved by modern nutritional technologies, are emerging once again. Modern thiamine deficits appear to be caused by diets of highly processed, carbohydrate and fat laden foods, exposures to thiamine blocking factors such as alcohol and those found in many medications (fluoroquinolones, possibly others) and vaccines (Gardasil, possibly others), environmental toxicants and some foods. Thiamine deficiency is also common after bariatric surgery and in disease processes like AIDS and cancer. Over the course of our research, thiamine deficiency has been observed in previously healthy, young, non-alcoholic patients, post medication or vaccine, along with symptoms of dysautonomia.

Thiamine Deficiency Symptoms

Thiamine deficiency at its worst is linked to severe decrements neurological functioning, like Wernicke’s Encephalopathy that include noticeable ataxic and gait disturbances (loss of voluntary control of muscle movements, balance and walking difficulties), aphasias (language comprehension and/or production difficulties), and if it persists, Korsakoff’s Syndrome (severe memory deficits, confabulations and psychosis). Early on though and as the deficiency is evolving, thiamine deficiency presents much like the mitochondrial disease that it is – with the myriad of seemingly unrelated symptoms, that are not typically attributed to thiamine deficiency, such as fatigue and excessive sleeping, hair loss, cardiac dysregulation,  GI disturbances such as gastroparesis and others, autonomic instability, demyelinating syndromes and hormone irregularities, especially thyroid, but also reproductive hormones. In diabetics, thiamine deficiency may present as ketoacidosis, lactic acidosis, hyperglycemia and persistent encephalopathy. Thiamine deficiency attacks the mitochondria. Mitochondrial dysfunction presents diversely. In fact, with mitochondrial dysfunction, symptoms are as varied as the individuals who experience them. Diabetes, may be just one more phenotype of among many.

Thiamine Deficits in Diabetes

With diabetes, thiamine deficiencies are common, though likely under-recognized. Diabetics are susceptible to thiamine deficiencies mediated by diet and exposures like most of the Western world, but also have added risk factors associated with the disease itself. In diabetics, kidney function is altered which decreases thiamine reabsorption while increasing thiamine excretion. In some people, diabetic and non-diabetic alike, thiamine deficiency can be exacerbated even further by a mutation in the thiamine transporter protein that brings thiamine into the cells.

How thiamine deficient are diabetics? One study found that in comparison to non-diabetics, individuals with Type 1 and Type 2 diabetes had 75% and 64% less thiamine, respectively. Think about this for a moment. If diabetes predisposes individuals to thiamine deficiency without any other intervening factors, imagine what happens when diabetics are nutritionally thiamine deficient, exposed to the myriad of environmentally or medically thiamine-depleting substances currently on the market, or worse yet, carry the thiamine transporter mutation. Alone, but especially in combination, thiamine deficiency diseases, many of which align with diabetes-related complications, could be magnified exponentially. The remarkable thing about this new research is that treatment is easy, it requires only dietary changes and high dose thiamine therapy alongside normal diabetes interventions. (Although one suspects with Type 2 diabetes at least, dietary changes and thiamine supplements could replace other medications entirely). Backing up a bit though, let us look at the research and mechanisms by which thiamine moderates sugar exposure at the cell level and how thiamine modifies those processes.

The Hyperglycemic Cascades

Under normal conditions, with appropriate dietary nutrients and physiological concentrations glucose, dietary sugars are converted to ATP in the mitochondria. The byproduct of that reaction is the production of free radicals also known as oxidative stress or reactive oxygen species (ROS). ROS are neither good nor bad, but too much or too little ROS wreaks havoc on cellular functioning. The cells can clear the ROS and manage oxidative stress via activating antioxidizing pathways and shuttling the excess glucose to secondary, even tertiary processing paths. However, under conditions of chronic hyperglycemia, mediated by diet or diabetes, the conversion of glucose to ATP becomes dysregulated, the production of ROS become insurmountable and a cascade of ill-effects are set in motion.

Too much ROS cause the mitochondria to produce high concentrations of an enzyme called superoxide dismutase (SOD) in the endothelial cells of both the small and large blood vessels. SOD is a powerful antioxidant, however, like everything else, too much for too long causes problems. Superoxide then upregulates the five known chemical pathways that alone and together perturb vascular homeostasis and cause the diabetic injuries that have become commonplace. Technically speaking, hyperglycemia causes:

  1. Increased activation of the polyol pathway
  2. Increased intracellular formation of advanced glycation end products (AGEs)
  3. Increased AGE receptor expression and ligands
  4. Upregulated protein kinase C (PKC)
  5. Enhanced hexosamine pathway activity

In non-technical terms, elevated concentrations of circulating glucose increase the production of ROS and superoxide, but also, and as a compensatory survival reaction to maintain cellular health, secondary and tertiary glucose processing pathways come online. These backup pathways are not nearly as efficient and so produce additional, negative metabolic byproducts which can damage blood vessels if not cleared. The body is capable of clearing these byproducts, but only when the reactions are short term and the nutrient substrates feeding those reactions are present. If, however, the nutrients are deficient and/or the hyperglycemia is chronic, or both, those clearance mechanisms are insufficient to remove the toxins. The toxic byproducts build up and diabetic vascular diseases ensue.

High Dose Thiamine Therapy and Diabetes

Over the last decade or so, researchers have found that thiamine normalizes each of these five aberrant processes activated by sustained hyperglycemia and implicated in diabetic vascular complications. High dose thiamine (300mg/day) reduces the biochemical stress of hyperglycemia human subjects. Additionally, thiamine can prevent and/or offset incipient vascular damage in diabetic patients. Finally, in rodent models of Type 1 diabetes, thiamine transporters have been identified and emerging research shows that thiamine moderates pancreatic insulin secretion significantly. In rats fed a thiamine deficient diet, glycolysis (sugar processing and conversion to ATP by mitochondria) was inhibited by 41%, utilization of fatty acids (secondary energy processing pathway) declined by 61% in just 30 days and insulin production diminished by 14%. The connection between pancreatic downregulation of fatty acid utilization and thiamine is particularly interesting considering the recent discovery of a thiamine dependent enzyme in fatty acid regulation, the HACL1.

Diabetes and Modern Medicine

Diabetes and the destruction it causes affects every cell, tissue and organ system in the body. As such, some researchers have postulated that diabetes represents a model for the paradigm shift in modern medicine. If diabetes is the model for chronic, multi-system illness that marks modernity, then thiamine, and likely other nutrients, are the markers by which the new model of medicine must be drawn. Diabetes is, at its root a mitochondrial disorder. Whether diabetes is inherited, as in Type 1 or induced environmentally as in Type 2, diabetes exemplifies how we convert food to fuel to power cellular functions. When that food is deficient in vital nutrients, the power conversion processes adapt for survival. The compensatory actions have consequences, especially when sustained beyond their capacity to meet the needs of the body. Disease erupts, first gradually then explosively.

Consider the implications of thiamine deficiency, a single micronutrient available in food, on cellular health, and indeed, physical health. In addition its role in mitochondrial functioning, thiamine controls sugar metabolism through multiple pathways. Inefficient sugar metabolism leads to disease. Thiamine also regulates the metabolism of fatty acids and provides the necessary substrates for the neurotransmitters acetylcholine and GABA. Thiamine, much like other critical nutrients, is not only absent from the largely processed diets of modernity, but at every turn, can be depleted by medications and environmental toxicants. Against the backdrop of nutrient depleted and damaged mitochondria, accommodating  medications, vaccines and environmental toxicants that also damage mitochondria, increase oxidative stress and further deplete critical nutrients, it is no wonder we are living sicker and dying younger than ever before. The depletion of critical nutrients is causing disease; diseases no medication can treat.

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

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This article was published previously on Hormones Matter in August 2014.

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Maternal Vitamin B: From Periconception and Beyond

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Chandler Marrs

A wise midwife recently told me that in 1960’s the B vitamins were part and parcel of a healthy pregnancy, not just folate (vitamin B9), that we stress now, but the entire complex of B vitamins, including: thiamine (vitamin B1), riboflavin (vitamin B2), niacin (vitamin B3), pantothenic acid (vitamin B5), pyridoxine (vitamin B6), biotin (B7), folate (B9) and the cobalamins (vitamin B12). Thiamine (also referred to as thiamin) was viewed as critical for maternal and fetal health and used within the midwifery community to ensure not only a healthy pregnancy, but a healthy postpartum. In many non-industrialized regions, thiamine is still supplemented for maternal and fetal health and maternal thiamine deficiencies are still recognized as critical impediments to health. Not so in the Western, industrialized world. Here, most resources and education seem set on prenatal folate; so much that it is difficult to escape folic acid supplementation in everyday foods.  Despite heavy fortification and regular use of prenatal vitamins, we see increasing evidence of nutrient deficiencies in pregnant mamas and most especially, in their children. Some of these deficiencies are visibly obvious, as least to those who look, such as the increased incidence of neural tube defects in children of women who are low in vitamin B12, but sufficient, even abundant in folate or B9. While other deficits are not so obvious, at least not immediately.

Maternal vitamin B status is important to the pregnancy at hand but also for the child’s long term health, as many of the B vitamins are capable of activating or deactivating gene programs in the children. Maternal vitamin B deficiencies can induce long-term epigenetic changes in the children, and likely, grandchildren. Maternal (and probably paternal too) vitamin B deficiencies silence genes in their off-spring that significantly increase the risk of insulin resistance, high blood pressure and a host of metabolic disorders through adulthood. Nutrition, in addition to its vital role as a source of energy for our cells, is the guidepost for DNA activation and inactivation. The balance of nutrients tell our cells how to function or not function, as the case may be. This information is carried from parents to offspring, across generations. It is this genetic control derived from lifestyle and nutrients that forms the basis of health for our children, and so it becomes something as parents we must pay attention to.

The B Vitamins are Important for Mom’s Health

For the moms, latent deficiencies in core nutrients will become unmasked with the increasing energy demands of pregnancy as many nutrients are shuttled preferentially toward placental and fetal needs, depleting maternal stores. Following delivery, the demands of lactation will further deplete maternal nutrient status and depending upon the vitamin in question, adversely affect her health and/or her child’s health.  Reports link maternal thiamine deficiency to hyperemesis gravidarum – severe vomiting across the pregnancy, in some instances leading to a full blown Wernicke’s Encephalopathy. Maternal vitamin B12 deficiency is linked to an increased risk of developing preeclampsia, intra-uterine growth retardation, preterm labor, but also, low vitamin B12 puts mom at risk for developing a myriad of neurocognitive, neuromuscular and psychiatric symptoms associated with B12 deficiencies both during pregnancy and postpartum.

How Prevalent is Maternal Vitamin B Deficiency?

Since there are few reference ranges for vitamin status during pregnancy, with most ranges based upon non-pregnant women, and since much of the research in nutrition is conducted in non-industrialized, poorer countries, it is difficult to assess how many outwardly healthy, western women carry nutritional deficiencies into pregnancy and postpartum. A 2002 study reported the vitamin profile in 563 pregnant New Jersey women at different points across the pregnancy. They found a trend towards too much folate, riboflavin, biotin and pantothenate (vitamin B5) and too little niacin, thiamin, vitamins A, B6, B12, suggesting that prenatal vitamins neither appropriately nor sufficiently address maternal nutrient demands.

A study of healthy pregnant women in Spain found that 32-68% of the women tested were deficient in thiamine, riboflavin or pyridoxine. Interestingly, the severity of deficiency correlated with oral contraceptive use, specifically with the length of oral contraceptive washout period prior to becoming pregnant. That is, when the woman became pregnant shortly after stopping oral contraceptives, she was more likely to exhibit a vitamin deficiency than if she had to waited to become pregnant and allowed her body to readjust to the non-oral contraceptive state. Additionally, the researchers found that if the woman was deficient in one of these nutrients, she was more likely to be deficient in each of them. Although not measured in this study, we know from other studies that many medications, including oral contraceptives, metformin and statins, decrease vitamin B12 significantly.

These reports, combined with the current trends in obesity, type 2 diabetes and the inherent nutritional shortcomings in the Western diet, suggest that it is likely that nutritional deficits and even nutritional imbalances are more common than are recognized.

Maternal Vitamin B Status Before Pregnancy Affects Health of the Male Offspring

A study carried out in sheep found clear evidence linking maternal vitamin B9 and B12 status pre-conception to the health the male offspring later in life. This particular study compared the offspring from sheep fed a nutritionally normal diet to those fed a slightly deficient diet, but one that was still within accepted nutritional parameters, from eight weeks before conception, throughout the pregnancy and six days postpartum. While the pregnancy proceeded normally in both groups and both male and female offspring appeared normal and healthy at birth, continued monitoring across the lifespan of the sheep, showed remarkable changes in the health of the adult males conceived on the nutritionally deficient diets. These males were heavier, had significantly disrupted immune function, impaired glucose metabolism and increased blood pressure, than the females and in comparison to the offspring whose moms had more nutritionally sound diets. This slight change, towards the lower end of what is considered a nutritionally normal diet, had significant influence on long term health in the male offspring. This study also identified clear epigenetic markers in the offspring conceived with dietary deficiency.

Maternal Vitamin B Status, Breast Milk and Infant Health

Maternal vitamin demands do not end postpartum. Lactation increases the demand for maternal nutrients. Deficits in maternal vitamin status impacts infant health and development as well as maternal health and recovery. It should be clear that maternal vitamin deficiencies negatively affect maternal health. Even so, there has been some contention regarding the relationship between maternal vitamin status, fetal development, the quality of breast milk and subsequent infant health and development.

A review of studies assessing vitamin status in breast milk found widespread deficiency, with levels below what is considered adequate intake for proper infant development in most of the samples. The B vitamins (thiamine, riboflavin, B6, B12 and choline) were particularly inadequate.

What was particularly interesting about this study is that researchers found that nutrient deficiencies affect maternal health more so than infant health. Nutrients can be categorized into two groups, those that respond favorably to maternal supplementation with higher milk concentrations (Group 1) and those that do not (Group 2). Group 1 nutrients included thiamine, riboflavin, B6, B12, choline, retinol, vitamin A, vitamin D, selenium and iodine. These nutrietns are secreted into breast milk and depleted rapidly in breast milk when maternal nutrient status is low. Deficiencies in these nutrients can be supplemented and passed on through the breast milk. In this way, maternal nutrient status directly affects the quality of the milk. Group 2 nutrients (folate, calcium, iron, copper and zinc), on the other hand, do not respond as well to supplementation. Breast milk concentrations of these nutrients remain relatively unchanged by maternal status, even when maternal status is declining. Supplementation with Group 2 nutrients affects maternal health more so than infant health.

Take Away

Fetal and infant health and development can be severely impaired by maternal nutrient deficiencies during pregnancy and during breastfeeding. The period across which maternal nutrient status affects the health of her offspring should be extended to well before conception. The B vitamins are especially important to proper development and long term health and appear to regulate genetic expression via epigenetic mechanisms. Recognizing and treating the potential nutritional deficiencies in modern, western diets, may go a long way towards reducing maternal illness while improving fetal, infant, child and adult health for generations. A growing body of evidence, and indeed, common sense suggest that while vitamin B9 or folate is critically important to maternal and fetal health, deficiencies in the remaining B vitamins and other nutrients may be equally important.

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The Paradox of Modern Vitamin Deficiency, Disease, and Therapy

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calorie rich versus nutrient rich

In order to understand why this article is about “paradox”, the concept of vitamin therapy must be appreciated. Hence, the explanation of the title is deferred to the end. Although vitamin deficiency disease is believed by most physicians to be only of historical interest, this is simply not true. When we think of a vitamin deficiency disease, we envision an individual living in a third world country where starvation is common. Such an individual is imagined as being skeletal, whereas an obese person is considered to be well fed with vitamin enriched foods. For this reason, common diseases, some of which are associated with obesity, are rarely, if ever, seen as potentially vitamin deficient.

The Calorie Rich and Nutrient Sparse Modern Diet

Our food is made up of two different components, the caloric and the non-caloric nutrients.  When we ingest high calorie foods (e.g. a doughnut) without even a vestige of non-caloric nutrients, we refer to this as “empty” or “naked” calories.  For our food to be processed into energy that enables the body and brain cells to function, there must be a ratio of the calorie bearing component to that of the non-caloric nutrients.  When we load the calories together with an insufficiency of non-caloric nutrients, we alter this ratio and produce a relative vitamin deficiency.  The trouble with this is that it does not result in the formation of the classic vitamin deficiency diseases as recorded in the medical literature. There is a gradual impairment of function, resulting in many different symptoms. Because modern medicine seeks to make a diagnosis by the use of imaging techniques and laboratory data and because of the physician’s mindset, if the tests used are normal, the possibility of a relative vitamin deficiency is ignored.

The Brain as a Chemical Machine

We have two different nervous systems. One is called “voluntary” that enables us to do things by will-power.  This is initiated and controlled by the upper brain, the part of the brain that thinks. The other system is known as the autonomic nervous system (ANS).  This is initiated and controlled by the lower part of the brain, the limbic system and brainstem.  This system is controlled automatically.  Although it collaborates with the other system, it is not normally under voluntary control. The limbic system and brainstem are highly sensitive to oxygen deficiency, but since the oxygen is useless without the non-caloric nutrients, their absence would produce the same kind of phenomena as oxygen deficiency. Thiamine (vitamin B1) has been found to be of extreme importance as a member of the non-caloric nutrients. The brain, and particularly the limbic system and brainstem, is highly sensitive to its deficiency.

Since the ANS is automatic, we are forced to think of the limbic system and brainstem as a computer.  For example, when it is hot, you start to sweat.  Evaporation of the sweat from the skin produces cooling of the body, representing an adaptive response to environmental hot temperature. When it is cold, you may start to shiver. This produces heat in the muscles and represents an adaptive response to environmental low temperature. If you are confronted by danger, the computer will initiate a fight- or- flight reflex.  This is a potential lifesaving reflex.  It is designed for short term use, consumes a vast amount of energy and prepares you to kill the enemy or flee from the danger.  Any one of these reflexes may be modified by the thinking brain. For example the lower brain, also known as the reptilian system, initiates the urge to copulate.  It is modified by the upper brain to “make love”.  The reptilian system, working by itself, can convert us into savages. There is an obvious problem here because our ancestors were faced with the dangers of short term physical stress associated with survival.  In the modern world the kind of stress that we face is very different for the most part.  We have to contend with traffic, paying bills, business deadlines and pink slips. The energy consumption, however is enormous, continues for a long time and it is hardly surprising that it is associated with fatigue, an early sign of energy depletion. It has been shown in experimental work that thiamine deficiency causes extensive damage to mitochondria, the organelles that are responsible for producing cellular energy.

Autonomic Function

The autonomic nervous system, controlled by the lower brain, uses two different channels of neurological communication with the body. One is known as the sympathetic system and the other is the parasympathetic. There are also a bunch of glands called the endocrine system that deals with the brain-controlled release of hormones.

We can think of the sympathetic branch of the ANS as the action system. It governs the fight-or-flight reflex for personal survival and the relatively primitive copulation mechanisms for the survival of the species. It accelerates the heart to pump more blood through the body.  It opens the bronchial tubes so that the lungs may get more oxygen. It sends more blood to the muscles so that you can run faster and the sensation of fear is a normal part of the reflex. When the danger is over and survival has been accomplished, the sympathetic channel is withdrawn and the parasympathetic goes into action. Now in safety and under its influence, body functions such as sleep and bowel action can take place.  That is why I refer to the parasympathetic as the “rest and be thankful system”.

Dysautonomia, Dysfunctional Oxidation and Disparate Symptoms 

When there is mild to moderate loss of efficiency in oxidation in the limbic system and/or brainstem they become excitable. This is most easily accomplished by ingesting a high calorie diet that is reflected in relative vitamin deficiency.  The sympathetic action system is turned on and this can be thought of as a logical reaction from a design point of view.  For example, if you were sleeping in a room that was gradually filling with carbon dioxide, the gradual loss of efficiency in oxidation would be lifesaving by waking you up and enabling you to exit the room. In the waking state, this normal survival reflex would be abnormal.

High calorie malnutrition, by upsetting the calorie/vitamin ratio, causes the ANS to become dysfunctional. Its normal functions are grossly exaggerated and reflexes go into action without there being any necessity for them. Panic attacks are merely fragmented fight-or-flight reflexes.  A racing heart (tachycardia) may start without obvious cause.  Aches and pains may be initiated for no observable reason. Affected children often complain of aching pain in the legs at night. Unexplained chest and abdominal pain are both common. This is because the sensory system is exaggerated. One can think of it as the body trying to send messages to the brain as a warning system.

Nausea and vomiting are both extremely common and are usually considered to be a gastrointestinal problem rather than something going on in the brain. Irritable bowel syndrome (IBS) is caused by messages being conveyed through the nervous system of the bowel, increasing peristalsis (the wave-like motion of the intestine) and often leading to breakdown of the bowel itself, resulting in colitis.  Of course, the trouble may be in the organ itself but when all the tests show that “nothing is wrong”, the symptoms are referred to as psychosomatic. The patient is often told that it is “all in your head”.

Emotional instability seems to be more in keeping with psychosomatic disease because emotional reactions are initiated automatically in the limbic system and thiamine deficient people are almost always emotionally unstable. A woman patient had been crying night and day for three weeks for no observable reason. A course of intravenously administered vitamins revealed a normal and highly intelligent person.  Intravenously administered vitamins are often necessary for serious disease because the required concentrations cannot be reached, taking them by mouth only.

The Vitamin Therapy Paradox

The body is basically a chemical machine.  But instead of cogwheels and levers, all the functions are manipulated through enzymes that, in order to function efficiently, require chemicals called “cofactors”. Vitamins are those essential cofactors to the enzymes.  If a person has been mildly to moderately deficient in a given vitamin or vitamins for a long time without the deficiency being recognized, the enzyme that depends on the vitamin for its action appears to become less efficient in that action.  A high concentration of the vitamin is required for a long time in order to induce its functional recovery.

Although the reason is unknown, doctors who use nutritional therapy with vitamins have observed that the symptoms become worse initially.  Because patients expect to improve when a doctor does something to them and because drugs have well-known side effects, it is automatically assumed by the patient that this worsening is a side effect of the vitamins. If the therapy is continued, there is a gradual disappearance of those symptoms and overall improvement in the patient’s well being. Unless the patient is warned of this possibility he or she would be inclined to stop using the treatment, claiming that vitamins have dangerous side effects and never getting the benefit that would accrue from later treatment.  This is the opposite effect that the patient expects. This is the paradox of vitamin therapy. 

If we view dysautonomia as an imbalance in the functions of the ANS and the vitamin therapy as assisting the functional recovery by stimulating energy synthesis, we can view this initial paradoxical as the early return of the stronger arm of the ANS before the weaker arm catches up, thus worsening an existing imbalance. However, this is mere speculation. I did not learn of the “paradox” until I actually started using mega dose vitamins to treat patients.

The Paradox and Thiamine

In this series of posts, we are particularly concerned with energy metabolism and the place that thiamine holds in that vital mechanism.  It is, of course, true that worsening of serious symptoms is a fact that has to be contended with and vitamin therapy should be under the care of a knowledgeable physician. The earlier the symptoms of thiamine deficiency are recognized, the easier it is to abolish them. The longer they are present the more serious will be the problem of paradox and a clinical response will also be much delayed and may be incomplete.

Beriberi and Thiamine Deficiency

I will illustrate from the early history of beriberi when thiamine deficiency was found to be its cause.  Many of the patients had the disease for some time before thiamine was administered, so the danger of paradox was increased. It was found that if the blood sugar was initially normal, the patient recovered quickly. If the blood sugar was high, the recovery was slow.  If the blood sugar was low, the patient seldom recovered.  In the world of today, an abnormal concentration of glucose in the blood would make few doctors, if any, think of thiamine deficiency as a potential cause. It is no accident that diabetes and thiamine metabolism are connected. Education of the doctor and patient are both absolutely essential. I believe that the ghastly effects of Gardasil, and perhaps some other medication reactions covered on Hormones Matter, can only be understood by thinking of the body as a biochemical machine and that the only avenue of escape is through the skilled use of non caloric nutrients.

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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Post Gardasil POTS and Thiamine Deficiency

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Autonomic nervous system

On July 8th 2013, I received an e-mail from a mother of a 17-year old daughter who had received Gardasil vaccination in 2008 resulting in a severe reaction. Two weeks after the second injection she began to experience a “flu-like” episode that continued for about a week and was followed by facial swelling, streptococcal infection, double ear infection and a diagnosis of mononucleosis. It was initially concluded that this was coincidental, not due to the vaccination. From then on she suffered from Postural Orthostatic Tachycardia Syndrome ( POTS), severe edema and “digestion issues which have been constant since”. POTS is a multi-symptomatic disease of the lower brain that affects many aspects of brain/body control mechanisms. She reported that “30,000 girls (and some boys) have been affected by the vaccine” and of those of which she was aware,“ the majority have POTS and trouble metabolizing sugar and carbs”.

Because of the persistent edema and digestive problems, my informant had done her own research and concluded that her daughter’s symptoms were due to thiamine (vitamin B1) deficiency. She found my name in connection with this subject and requested my help. There is a blood test, known as erythrocyte (red cells) transketolase that is specific for identifying thiamine deficiency, so I suggested that this be done. It was strongly positive, proving TD. This led to the test being done on another Gardasil affected girl and this was also strongly positive.  Most of the affected girls known to her had POTS. Some had mitral valve prolapse (MVP).  About twenty five percent of POTS patients are disabled.  The symptoms often follow a virus infection. It is one of many conditions classified as dysautonomia and this includes beriberi, long known to be due to thiamine deficiency.

Dysautonomia, often associated with MVP, affects the lower brain controls of both branches of the autonomic (automatic) nervous system (ANS) that enable our adaptation to the constant changes in environment. For example, one branch, known as the sympathetic system, accelerates the heart and the other, called the parasympathetic, slows it. We sweat when it is hot and shiver when it is cold, both automatically initiated by the sympathetic branch of the ANS.

In the early stages of beriberi the ANS is unbalanced, so that either the sympathetic or parasympathetic, normally working in synchrony, dominates the reaction, adversely affecting blood pressure, pulse rate and many other adaptive mechanisms, like POTS.  It can be seen that the patient with POTS or beriberi is essentially maladapted and is unable to adjust bodily systems to meet environmental changes. Edema (swelling in parts of the body), a cardinal feature of beriberi, supported a diagnosis of thiamine deficiency in this mother’s daughter. Also, Gardasil is a yeast vaccine and an enzyme called thiaminase, whose action destroys thiamine, is known to be in the yeast. Thiaminase disease has been reported in Japan in association with dietary thiamine deficiency.

We know from the history of beriberi that exposure to the stress of ultraviolet light (sunlight) sometimes “triggers” the first symptoms of the disease when thiamine deficiency is marginal, but not severe enough to cause symptoms. Other stress factors (virus, inoculation, injury) can do the same. In effect, diet may cause an individual to be in a state of marginal vitamin deficiency. A mental or physical stress factor automatically induces a need for energy to meet this stress. If cellular energy is insufficient to drive the  mechanisms by which an adaptive adjustment is required, it results in a maladaptive response.

The lower brain, where the ANS control mechanisms are situated, is particularly sensitive to thiamine deficiency, equivalent to a mild to moderate degree of oxygen deprivation. The commonest cause of thiamine deficiency in industrial nations is alcohol, but it is also known that sugar consumption will increase the need for thiamine. Beriberi has recently been reported in Japan in seventeen adolescents consuming carbonated soft drinks. The social life of adolescents may thus increase the risk from an inoculation that might otherwise be less threatening.

The statistics on sugar ingestion (150 pounds per person per year) suggests that marginal TD is common. The report of a “difficulty in metabolizing sugar and carbs” may be highly relevant. One of the questions asked by parents of the affected girls known to my informant is why did the vaccine seem to “pick off” the most intelligent and athletic individuals. The answer must be that the higher the IQ, the more is cellular energy required by the brain. Sugar, even at social levels of consumption, may be a greater risk for them.

It is important to understand that there are multiple factors that have to be taken into account in solving the cause of this disaster. The “fitness” of the individual implies her adaptive ability in biochemical terms, not her athletic or student prowess. Dietary indiscretion may or may not enter the equation and depends on individual sensitivity to food substances as well as the ratio of calories to the necessary vitamins for their processing in the body. The stress factor, the case in discussion being Gardasil, may be more or less stressful in its own right, perhaps related to batch number or commercial process. Lastly the genetics of an individual always enters the equation. These three factors, Genetics, Stress and Nutrition can be seen as three interlocking circles, all of which overlap at the center. Each circle must be evaluated in its contribution to the ensuing result.

Publications and resources from Dr. Lonsdale:

  1. A Review of the Biochemistry, Metabolism and Clinical Benefits of Thiamin(e) and Its Derivatives
  2. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: A pilot study.
  3. Thiamine
  4. Asymmetric functional dysautonomia and the role of thiamine.
  5. Exaggerated autonomic asymmetry: a clue to nutrient deficiency dysautonomia.
  6. Oxygen – the Spark of Life. Dr. Lonsdale’s blog.

Resources for Understanding Thiamine Deficiency

Molecular Mechanism of Thiamine Utilization

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