thiamine deficiency pregnancy

Are Pregnant Women Getting Enough Thiamine?

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thiamine pregnancy

If the last 80 years of research is any indication, the answer is no, pregnant women are not getting enough thiamine to have healthy and uncomplicated pregnancies. Although the research is sparse, almost every study published since 1940, regardless of country, regardless of food fortification/enrichment programs, and sometimes, in spite of prenatal vitamins, consistently shows deficiency in at least 20% of the women tested and sometimes in as many as 60%. While testing methods, trimester, and diet account for some of the variance, the high degree of congruence amongst these studies demonstrates a glaring misunderstanding of thiamine needs during pregnancy.

Much of this misunderstanding emanates from the original assumptions used to guide research and establish recommended values; assumptions that have since become codified into general practice despite ample contradictory evidence. As the first in a series of papers to build a case for increasing thiamine intake during pregnancy, this article will review the assumptions and research associated with thiamine recommendations for pregnancy.

Origins of the RDA

In the US, the recommended dietary allowance (RDA) for thiamine intake during pregnancy is 1.4 mg. In other countries the dietary reference intake (DRI) ranges from 1.3-1.5mg per day. RDA values are set at amounts proposed to prevent deficiency symptoms in approximately 97% of healthy populations and DRI is recent term used to represent all quantitative estimates of nutrient values and is proposed for dietary planning for healthy people. It largely mirrors the RDA.

RDA values evolved from dietary recommendations developed during World War I and the great depression. Originally, recommendations focused on ensuring sufficient protein and caloric intake (3000 kcal) for active service men. In 1939, two women, Hazel Stiebeling and Esther Phipard, expanded those recommendations to include thiamine and riboflavin. Their original estimates suggested 460 international units (IU) or 1.39mg for healthy adults but added the caveat:

The allowance of a margin of 50% above the average minimum for normal maintenance can now be given the clear definition it has always needed. It is an estimate intended to cover individual variations of minimal nutritional need among apparently normal people. . . .

In 1941, the National Research Council (NRC) recommended 516IU/1.55mg for active males. Ultimately, however, 1.2mg was adopted. This was based upon observational governmental surveys, and through committee showing that for healthy 70kg/154lb active males doing muscular work, 1.2mg of thiamine daily was enough to stave off symptoms of beriberi in 97% of this healthy population. While one might realistically consider the dynamic aspect of each of these variables, e.g. the health of the individual, caloric intake, body weight, and/or activity level might change, recommendations for daily intake became fixed and have remained so ever since. These recommendations appeared to disregard Steibeling’s recommendations, the NRC recommendations and contemporaneous findings arguing that while 1.2mg prevented observable manifestations of deficiency, 1-5-2.0mg per day was associated with better overall health.

In planning diets for adults, allowances may well be set two or three times as high as the minimum required to prevent beriberi. This would mean a level of intake of from 1.5 to 2.0 milligrams of thiamin (500 to 666 International Units) for a 70-kilogram adult or about 20 International Units per 100 calorie.

From those reports, it was then assumed that based upon changes in mass and a perceived reduction in activity levels, non-pregnant women required only 1.1mg daily. There was no research, nor has there been any research since to confirm this assumption. From the National Academy of Sciences report published in 1998, the report upon which the NIH currently bases its recommendations:

Studies were not found that directly compare the thiamin[e] requirements for males and females. A small (10 percent) difference in the average thiamin[e] requirements of men and women is assumed on the basis of mean differences in body size and energy utilization.

Based upon additional assumptions of increased energetic demand and mass, the RDA for pregnancy was set to 1.4mg per day. Once again, there was no research to back this up. Even so, these numbers have remained unchanged for 80 years.

Each decade or so, panels in the US and elsewhere, reconvene to assess nutrient intake and re-evaluate nutrient recommendations, and with each report, the same few studies published between 40-80 years ago provide the rational for maintaining the status quo. From the European Food Safety Authority (EFSA) report in 2016, a report that reviews work from other agencies worldwide:

The Panel considers that the available data on the relationship between thiamin[e] intake and biomarkers of thiamin[e] status in pregnancy cannot be used for deriving DRVs (dietary recommended values) for thiamin[e] in pregnancy. There are no data on the relationships between thiamin[e] intake and biomarkers of thiamin[e] status in lactating women.

Notably, the most commonly cited study used to justify current values across all agency reports, was conducted in 1979 and involved 7 healthy men.

In general, no matter the country or panel, justification for thiamine requirements in women and during pregnancy involves only a few studies, many of which do not include women, pregnant or otherwise.

Returning to the EFSA for a moment, after discussing all of the early research upon which these values were based, panel members performed an additional comprehensive search for more recently published studies though 2016. A few were mentioned, but the conclusion remained:

The Panel considers that available data on thiamin[e] intake and health outcomes are either limited or inconsistent and cannot be used for deriving DRVs for thiamin[e].

Although there have only been a few studies across the decades that show women require more thiamine to sustain a healthy pregnancy, none have swayed governmental recommendations. Among them, a study conducted at Harvard from 1943 looked at thiamine metabolism and excretion in pregnant versus non-pregnant women. Researchers concluded that pregnant women required 3x the amount of thiamine to reach peak excretion compared to non-pregnant women. Peak excretion studies provided supporting data to justify current recommended values for healthy male adults. They do not consider health variables, but rather the rate at which the largest amount of thiamine is excreted relative to intake. Deficient individuals show no increase in excretion without high doses, usually by injection. The 1979 study of 7 healthy men mentioned above was a peak excretion study.

In accordance with the increased thiamine demand, it is interesting to note that during World War II, reports from a health station in Oslo, Norway, recommended 4mg of thiamine per day for pregnant women and up to 9mg from brewer’s yeast or synthetic thiamine, when available. In doing so, and despite the stressors of war and limited food availability, maternal and infant morbidity and mortality was remarkably low; lower than what one would expect and certainly lower than modern rates of the same complications.

Thiamine Intake and Nutritional Surveys

Based on nutritional surveys conducted in the US and elsewhere, population-wide deficits in thiamine are considered rare. Supporting this conclusion, US nutrition surveys dating back to 1955, show that the average intake for all but the poorest 10% of the population was 1.5mg. These numbers were based upon something called an equivalent nutrition unit, which was calculated using the thiamine intake of 25 year old males. Presumably, it was normalized for everyone else but there are no data as such. From the 1977-78 report onward, values were reported by age and sex. There were still no data for pregnant women, however. The intake for boys and men ranged between 1.4-1.8, while those for girls and women, with exception of girls ages 9-11 (1.3mg), hovered just over a milligram. The numbers were similar for men in the 1987 report, while women increased their intake to around 1.1-1.3mg depending on the age group. In the 1994 reports, women were solidly in the 1.3 range. Reports can be found here.

The most recent  National Health and Nutrition Examination Survey (NHANES) conducted between conducted from 2013-2016, found that for non-pregnant women between the ages of 20-30, the average daily dietary intake of thiamine was 1.4 mg/day, suggesting that many women consume sufficient thiamine should they become pregnant. A NHANES survey conducted between 2001-2014 included pregnant women (n=1003) and appears to support this claim. Based upon a single 24-hour recall of food intake, only 10% of respondents were determined to be at risk for deficiency. From foods alone, the average intake was 1.8mg and from foods plus supplements the average was 3.6 mg.

Overall and despite the lack of actual data on thiamine intake during pregnancy, nutritional surveys from 1955 onward suggest that based upon intake alone, thiamine deficiency across the population should be rare. As discussed frequently on this website, and below, it is not.

Deficiency During Pregnancy

Over the years, there have been very few studies published on thiamine during pregnancy in developed countries. Most of the research has been focused on undeveloped regions with food insecurity where thiamine deficiency is endemic. Nevertheless, among the studies that have actually measured thiamine, the results are clear. Thiamine deficiency during pregnancy is quite common. Conservatively and based upon the most recent US studies, ~20% of pregnant women are likely to be deficient at some point during the pregnancy. Across all studies, however, the numbers may go as high as 60%. Below is a listing of studies conducted that include presumed healthy women.

There were a few studies during this time period that were unable to detect deficiency. These included:

  • Thiamine and riboflavin intakes and excretions during pregnancy (1950) – US: 15* women on a regular diet; 1.3mg oral thiamine was given for 7 days and urinary excretion measured. Excretion paralleled intake (high intake, more excreted), except in women consuming less that <1mg of thiamine daily, where excretion increased 2-3X over non-pregnant women. This was in contrast to the 1943 cited above that found 2-3X increase globally but methodology, dosage, and delivery route (injected versus oral), were also different. *Five women were excluded due to excessively low caloric intake, so the sample size was technically only 10 despite claim. Moreover, low caloric intake could be considered either cause or consequence of low thiamine.
  • Longitudinal vitamin and homocysteine levels in normal pregnancy (2001) – Netherlands: cohort of 225 women tracked before conception, during pregnancy, and postpartum from 1987-90. Data displayed via scatterplot with no statistics provided and no discussion of deficiency. While roughly 30-40 data points fall below deficiency values across all time points, it is impossible to know how many within-subject measurements those data represent.

Conclusion

Despite a longstanding belief that pregnant women require only 1.4mg thiamine per day, the research confirming this number is severely lacking. Similarly, the oft repeated assertions that thiamine deficiency is rare during pregnancy is also in conflict with the data. Although the research is sparse, the conclusions are clear. Not only is it likely that far more women are deficient than is recognized by population-based data, but the very nature of the RDA assumptions may be called into question. While one can accommodate potential errors and misunderstandings about nutrient intake that might have swayed recommendations in the early days of vitamin research, the underlying assumptions that women are simply small men and that changes of pregnancy can be represented solely by a change in mass, seems a far stretch of the imagination, especially by today’s standards. And yet, that is the state of vitamin research.

Since medical decisions, then as now, are made based upon these assumptions, it behooves us to challenge them. What if these assumptions are as wrong as they appear? What if the research on deficiency during pregnancy, as sparse as it is, is actually correct? And what if we are missing an opportunity to help women have healthier, complication free pregnancies simply by increasing the intake of this and other nutrients? Would not it be worth it to reassess what we thought we knew about pregnancy and nutrition through the lens of what we now know about bioenergetics and metabolism?

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Notes on Thiamine and Pre-Eclampsia: The Sugar Connection

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If you have read any of the articles on this website or anything relative to modern thiamine deficiency, you are aware of the connection between sugar consumption and thiamine deficiency. The more sugar, in any form, that one consumes, the more thiamine one needs to process it. This is because thiamine is the rate-limiting step in the metabolism of glucose into ATP. This pathway can be overwhelmed easily by the high sugar and low nutrient content of modern foods. The mismatch becomes particularly evident during pregnancy, where increased energetic demands may lead to insufficient thiamine independently of sugar intake if one is not careful, but also may be compounded by sugar intake. A study published in 1969 looking at thiamine and pre-eclampsia elegantly illustrates this point. Pre-eclamptic women, it appears, have a problem with sugar metabolism and the logjam is insufficient thiamine.

Pre-eclampsia

Pre-eclampsia, which affects up to 6% of all pregnancies, is marked by dangerously high blood pressure, edema, proteinuria with kidney damage and potentially damage to other organs. There is a high risk of stroke and other serious, even fatal complications, for the mom. For the fetus, because of the impaired functioning of the placenta, placental abruption is possible along with growth restriction and pre-term birth. There are few useful treatments, beyond bedrest and early delivery, but even then mom’s health may continue to be at risk. Postpartum spikes in blood pressure, called postpartum pre-eclampsia, affect up to 27% of women. As bad as these numbers are, they are likely even worse, given that most women are seen in the emergency rooms where the association with pregnancy is not regularly tabulated.

Metabolic Disturbances, Thiamine, and Pre-eclampsia

Pre-eclampsia has long been associated with metabolic derangements leading to poor energy metabolism of the placenta and mom alike. Although some have considered the role of thiamine in pre-eclampsia, the research has been mixed, generally decades old involving non-Western populations where food insecurity and not excess drives deficiency. In all, the research is sparse at best.

Although this particular study is older, its unique design merits discussion. Specifically, it shows that the activity of a thiamine-dependent enzyme that is responsible for a key aspect of the metabolism of glucose into ATP is impaired or overwhelmed in women with pre-eclampsia. This impairment then, leads to both maternal and placental energy deficits, which in turn, result in poor maternal kidney and cardio-metabolic function and all of the negative sequelae associated with pre-eclampsia.

Depending upon the severity of the impairment though, the problems with thiamine and subsequently glucose metabolism may not be noticeable unless challenged. That is, early on in the disease process, despite symptoms of pre-eclampsia, the metabolic dysfunction associated with insufficient thiamine are hidden with typical testing. It is not until the patient either faces a metabolic challenge, such as the one devised by the study below, and/or the disease has progressed sufficiently in severity that the thiamine issues may be detected.

Study Details

Backing up just a bit, let us look at this study more closely. Here, three groups of pregnant women were recruited: a healthy control group, a mild pre-eclampsia group (BP >160/100, plus edema and albuminuria) and a hospitalized eclampsia group. Instead of measuring thiamine directly, which has a high rate of false negatives, the researchers devised a challenge test wherein blood pyruvic acid concentrations were measured fasted and then 30 minutes following the administrations of dextrose.

Recall, thiamine is required for pyruvate dehydrogenase (PDH), the gatekeeper enzyme within the mitochondria, responsible for taking pyruvate (derived from glucose) and converting it into acetyl CoA, so that after a series of reactions, ATP can be produced. This pathway is called oxidative phosphorylation or OXPHOS, because the reactions require oxygen. With OXPHOS and sufficient thiamine, for every molecule of glucose, the mitochondria synthesize 30-38 units of ATP. This is compared to only 2 units of ATP produced via glycolysis, the intracellular pathway that converts glucose into pyruvate.

Pyruvate or in this case, pyruvic acid, is inversely associated with thiamine concentrations such that when thiamine is sufficient, pyruvic acid concentrations are low, even in response to the ingestion of sugars. When thiamine is low, however, pyruvic acid skyrockets. This means that a higher than expected pyruvic acid in response to the ingestion of dietary carbs or in this case dextrose, would indicate a logjam at the PDH, likely associated with low thiamine. Since the PDH enzyme also utilizes riboflavin and lipoic acid, it is possible that these nutrients may also be involved. Similarly, if any of these nutrients are severely low or this enzyme is more completely overwhelmed, we would expect to see elevated pyruvic acid even when fasted and even higher concentrations after the dextrose challenge. And that is exactly what these researchers found.

Compared to the healthy group, fasting pyruvic was similar but increased significantly after the dextrose challenge in the less severe pre-eclampsia group. For the hospitalized eclampsia group, however, both fasting and challenge pyruvic concentrations were elevated significantly. The healthy range for pyruvic acid is .5mg-1mg. Pyruvic concentrations in pre-eclampsia fell within the range while fasted but their numbers shot up, in some cases over 2mg. The average was 1.62 (SD .4). For the hospitalized group, pyruvic was elevated both when fasted (r=1.05mg) but especially with the dextrose challenge (r=1.93mg, SD .26).

Whoa.

Let’s put this in context. We use sugars (and fats, but that is another story) to make ATP. ATP is the energy currency produced by the mitochondria and used by all of the cells to do the things they need to do. Not enough ATP means not enough energy. Imagine trying to grow a new organ like the placenta and a new human without sufficient ATP. It just will not work out very well. Something will have to give. In this case, maternal kidney and heart function suffer. Both require huge amounts of ATP.

Getting pyruvate though PDH is the rate-limiting step. If the PDH does not have its cofactor nutrients, it will not work well and if it is not working, not much else will either. I should note that there are several other thiamine dependent enzymes in this and other pathways that control the metabolism of fats and proteins as well.

So, if pyruvate cannot get into the mitochondria and be worked on by the PDH, not only will ATP production decline and pyruvic build up at the gates of the mitochondria, but in an effort to rid the body of the excess pyruvate, some of it will be transported to another enzyme called lactate dehydrogenase or LDH. LDH and PDH work together to generate back up energy by converting pyruvate to lactate and back again. If one is healthy, lactate can be used as a fuel source and fed back into the mitochondria but only if one has sufficient thiamine to run the PDH. If thiamine is lacking, all of that pyruvate and lactate build up and that is what we see here. The PDH is not working well and so concentrations of pyruvic acid and likely lactic acid, though not measured, increased especially in the presence of a dextrose challenge and as the disease processes progresses in severity.

Final Thoughts

What this study tells us is that there is problem in this pathway that may not be readily apparent biochemically unless stressed appropriately, in this case, with dextrose but I imagine any high carbohydrate diet might produce the same reaction. And since, thiamine is involved in other metabolic pathways, I suspect had the researchers devised challenges to test them as well, we would likely have seen a similar pattern. While this study looked at pregnant women specifically, this pattern holds across all populations. The body adapts for as long as it can, but the chinks in the system are there. We simply do measure them appropriately in the early stages of disease – with challenge tests.

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Notes On Thiamine Status During Pregnancy

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Currently, I am researching thiamine status during pregnancy for a series of articles to be published by the newly formed Thiamine Advocacy Foundation. Over the next few months, I will be publishing snippets of that research, and of course, when the project is finished, I will let everyone know and provide links to the articles. Today, I want to discuss a study published in 1980 about thiamine deficiency in pregnant and non-pregnant women.

For this study, the thiamine status of 60, presumably healthy, pregnant women was assessed across multiple times points (second trimester, third trimester, and in the immediate postpartum. Not all women completed all assessments. Food diaries were collected for three days preceding each test time to identify thiamine intake and a lifestyle survey to assess contraceptive use, smoking and alcohol history was given. Samples and diaries from 20 non-pregnant women were collected as well.

To determine thiamine status the erythrocyte transketolase test with thiamine pyrophosphate activation was used. This is among the reasons I found this study useful. It is only one of only a few studies of this population using the transketolase test. Recall from Dr. Lonsdale’s discussion Understanding the Labs (and here), the transketolase test is arguably a more accurate measure of thiamine status than plasma, serum, and some measures using whole blood.

Using the transketolase test, researchers found that 30% of the non-pregnant women were deficient in thiamine as were 28-39% of the pregnant/postpartum women depending upon the phase of pregnancy. Importantly, not all women were deficient at all test times. This means that the deficiencies likely waxed and waned relative to other variables like intake and stressors. Intake was considered sufficient in all but 10 of the women and for those 10 women it was only minimally below the RDA. Additionally, the researchers reported that previous oral contraceptive use had no apparent effect on thiamine status during pregnancy but that there was a trend for an increased risk of deficiency with previous pregnancies.

While this was a small study, the percentage of women who are deficient in thiamine is striking, especially the non-pregnant controls. If thiamine is deficient before pregnancy, the risk of severe health issues across pregnancy increases. Here though, none of the women who were deficient in thiamine displayed the classical symptoms of thiamine deficiency, although details were lacking. Moreover, all of the women delivered presumably healthy children, or at least healthy weight children, as other parameters were not measured. Again, this finding is important because it suggests that either 1) what we expect to see with deficiency during pregnancy is not completely accurate, 2) that the persistence or chronicity of the deficiency matters, and/or 3) that it is not simply a deficiency in thiamine that causes some of the more severe complications of thiamine deficiency during pregnancy.

I have written previously about the mismatch between classically defined symptoms of thiamine deficiency and what we are more likely to see with modern diets and stressors. I suspect this applies to pregnancy as well. I have also written about how thiamine status is likely to change relative to intake and demand. Rodent studies have shown that the typical neurological symptoms of deficiency do not appear until there is 80% decline of thiamine stores. Since we store a little over two weeks of thiamine, one would have to completely eliminate intake for more than a week before those symptoms might emerge, and even then, it might be a while before they were recognized. This is certainly a factor with hyperemesis gravidarum, the severe vomiting that some women experience during pregnancy but perhaps not in non-HG related pregnancies.

It is important to note, however, HG and thiamine deficiency go hand in hand. Thiamine deficiency, along with other deficiencies, may trigger HG (think gastrointestinal beriberi) in the first place, and once the vomiting begins, will easily deplete thiamine stores. None of the women in the current study developed HG, however, or other complications, so that leads me to believe, that we need additional triggers and we need persistent or chronic thiamine deficiency before noticeable complications arise.

In this study, all we have are indications of deficiency at specific points in time. We have no evidence of how long those deficiencies were present or whether other variables were somehow buffering maternal and fetal health such that the typical complications associated with thiamine deficiency were not observed. Even so, a finding that upwards of 30% of a test population of women, both non-pregnant and pregnant thiamine deficient speaks to how common this deficiency may be and how close to the precipice of more severe health issues a percentage of the population resides. Although observable changes in health were not reported or perhaps even recognized in this report, knowing what we know about thiamine’s role in energy metabolism, it is not unlikely that there were many negative metabolic patterns brewing just below the surface.

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It All Comes Down to Energy

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It all comes down to energy

The Threat Around Us

Animals, including Homo Sapiens, survive in an essentially toxic environment, surrounded by microorganisms, potential poisons, the risk of trauma, and adverse weather conditions. Evolutionary development has equipped us with complex machinery that provides defensive mechanisms when any one of these factors has to be faced. Before the discovery of microorganisms, medical treatment had no rhyme or reason, but killing the microorganisms became the methodology. The research concentrated on ways and means of “killing the enemy”, the bacteria, the virus, the cancer cell. The discovery of penicillin reinforced this approach. We are now facing a period of potential impotence because of bacterial resistance, failure of attempts to kill viruses, and the resistance to chemotherapeutic agents in cancer. Louis Pasteur is purported to have said on his deathbed, “I was wrong, it is the terrain that matters”, meaning body defenses.

Hans Selye, whose research into how animals defend themselves when attacked by any form of stress, led to his description of the General Adaptation Syndrome (GAS). He recognized the necessity of energy in initiating the GAS and its failure in an animal that succumbed to stress. He labeled human disease as “the diseases of adaptation”. In Selye’s time, there was little information about energy metabolism but today, its details are fairly well-known. The suggestion of a new approach depends on the fact that our defenses are metabolic in character and require an increase in energy production over and above that required for homeostasis. If the GAS applies to human physiology and that we are facing the “diseases of adaptation”, it is hypothesized that research should be applied to methods by which energy metabolism can be stimulated and mobilized to meet the stress.

Energy Deficiency, Defective Immunity, and COVID-19

There is evidence that energy deficiency applies to each of the diseases described here. It may be the unrecognized cause of defective immunity in Covid-19 disease. Although in coronavirus disease the clinical manifestations are mainly respiratory, major cardiac complications are being reported involving hypoxia, hypotension, enhanced inflammatory status, and arrhythmic events that are not uncommon. Past pandemics have demonstrated that diverse types of neuropsychiatric symptoms, such as encephalopathy, mood changes, psychosis, neuromuscular dysfunction, or demyelinating processes may accompany acute viral infections or may follow infection by weeks, months, or longer in viral recovered patients. Electrocardiographic changes have been reported in Covid-19 patients. The authors suggest that it may be attributed to hypoxia as one possibility. Because the total body stores of thiamine are low, acute metabolic stress can initiate deficiency. Thiamine deficiency has a clinical expression similar to that observed in hypoxic stress and the authors referred to it as pseudo-hypoxia. It is therefore not surprising that defective energy metabolism can express itself clinically in many different ways.

The present medical model regards each disease as having a separate cause, but the large variety of symptoms induced by thiamine deficiency suggest the ubiquitous nature of energy deficiency as a cause in common. Obesity, a reflection of high calorie malnutrition, has been published as a risk factor for patients admitted to intensive care with Covid-19. Thiamine deficiency was reported in 15.5-29% of obese patients seeking bariatric surgery. Hannah Ferenchick M.D. an emergency room physician commented online that many of her patients with Covid-19 had what she called “silent hypoxemia”. These patients had an arterial oxygen saturation of only 85% but “looked comfortable” and their chest x-rays “looked more like edema”  It has long been known that patients with beriberi had low arterial oxygen and a high venous oxygen saturation. All that would be needed to support the hypothesis of thiamine deficiency in some Covid victims would be finding a high venous oxygen saturation at the same time as a low arterial saturation. Also, edema is a very important sign of beriberi, and thiamine deficiency has been noted in critical illness.

Disrupted Autonomic Function

There have been many articles in medical journals describing dysautonomia, mysteriously in association with a named disease, but with no suggestion that the dysautonomia is part of that disease. More recently, there is increasing evidence that dysautonomia is a feature of chronic fatigue syndrome (CFS), manifested primarily as disordered regulation of cardiovascular responses to stress. Manipulating the autonomic nervous system (ANS) may be effective in the treatment of CFS. Dysautonomia is also a characteristic of thiamine deficiency. Patients with Parkinson’s disease begin to lose weight several years before diagnosis and a study was undertaken to investigate this association with the ANS. Costantini and associates have shown that high dose thiamine treatment improves the symptoms of Parkinson’s disease, although the plasma thiamine concentration was normal. They have also shown that high dose thiamine treatment decreases fatigue in inflammatory bowel disease, Hashimoto’s disease, after stroke, and multiple sclerosis. As already noted, it is also an important consideration in critically ill patients.

Multiple System Atrophy is a devastating and fatal neurodegenerative disorder. The clinical presentation is highly variable and autonomic failure is one of its most common problems. Dysautonomia was found to be a clinical entity in Ehlers-Danlos syndrome, a musculoskeletal disease, and this syndrome frequently coexists with Postural Orthostatic Tachycardia Syndrome (POTS), a disease that is included in the group of diseases under the heading of dysautonomia. Some cases of POTS have been reported to be thiamine deficient. This common condition often involves chronic unexplained symptoms such as inappropriate fast heart rate, chronic fatigue, dizziness, or unexplained “spells” in otherwise healthy young individuals. Many of these patients have gastrointestinal or bladder disorders, chronic headaches, fibromyalgia, and sleep disturbances. Anxiety and depression are relatively common. Not surprisingly the many symptoms are often unrecognized for what they represent and the patient may have a diagnosis of psychosomatic disease.

Immune-Mediated Inflammatory Diseases (IMIDs) is a descriptive term coined for a group of conditions that share common inflammatory pathways and for which there is no definite etiology. These diseases affect the elderly most severely with many of the patients having two or more IMIDs. They include type I diabetes, obesity, hypertension, chronic pulmonary disease, coronary heart disease, inflammatory bowel disease, rheumatoid arthritis, Sjogren’s syndrome, systemic lupus, psoriasis, psoriatic arthritis, and multiple sclerosis. The recent recognition of small fiber neuropathy in a large subgroup of fibromyalgia patients reinforces the dysautonomia-neuropathic hypothesis and validates fibromyalgia pain. These new findings support the disease as a primary neurological entity.

Energy Deficiency During Pregnancy: The Cause of Many Complications

Irwin emphasized the energy requirements of pregnancy in which the maternal diet and genetics have to be capable of producing energy for both mother and fetus. He found that preventive megadose thiamine, started in the third trimester, completely prevented all the common complications of pregnancy. Hyperemesis gravidarum is the most common cause of hospitalization during the first half of pregnancy and is second only to preterm labor for hospitalization in pregnancy overall. This disease has been associated with Wernicke’s encephalopathy, well known to be due to brain thiamine deficiency. The traditional explanation is that vomiting is the cause, but since vomiting is a symptom of thiamine deficiency, it could just as easily be the cause rather than the effect. In spite of the fact that migraines are one of the major problems seen by primary care physicians, many patients do not obtain appropriate diagnoses or treatment. Migraine occurs in about 18% of women and is often aggravated by hormonal shifts. A complex neurological disorder involving multiple brain areas that regulate autonomic, affective, cognitive, and sensory functions, it occurs also in pregnancy. Features of the migraine attack that are indicative of altered autonomic function include nausea, vomiting, diarrhea, polyuria, eyelid edema, conjunctival injection, lacrimation, nasal congestion, and ptosis.

The Proteopathies: Disorders Involving Critical Enzymes

The earliest and perhaps best example of an interaction between nutrition and dementia is related to thiamine. Multiple similarities exist between classical thiamine deficiency and Alzheimer’s disease (AD), in that both are associated with cognitive deficits and reductions in brain glucose metabolism. Thiamine-dependent enzymes are critical components of glucose metabolism that are reduced in the brains of AD patients. Senile plaques and neurofibrillary tangles are the principal histopathological marks of AD and other proteopathies. The essential constituents of these lesions are structurally abnormal variants of normally generated proteins (enzymes). The crucial event in the development of transmissible spongiform encephalopathies is the conformational change of a host-encoded membrane protein into a disease associated, fibril forming isoform. A huge number of proteins that occur in the body have to be folded into a specific shape in order to become functional. When this folding process is inhibited, the respective protein is referred to as being mis-folded, nonfunctional, and causatively related to a disease process. These diseases are termed proteopathies and there are at least 50 different conditions in which the mechanism is importantly related to a mis-folded protein. Energy is required for this folding process. Because of their reported relationship with thiamine, it has been hypothesized that mis-folding might be related to its deficiency on an energy deficiency basis.

It All Comes Down to Energy

A hypothesis has been presented that the overlap of symptoms in different disease conditions represents cellular energy failure, particularly in the brain. If this should prove to be true, the present medical model would become outdated. An attack by bacteria, viruses or an oncogene might be referred to as “the enemy”. The defensive action, organized and controlled by the brain, may be thought of as “a declaration of war” and the illness that follows the evidence that “a war is being fought”. This concept is completely compatible with the research reported by Selye. It underlines his concept that human diseases are “the diseases of adaptation”, dependent on energy for a successful outcome in a “war” between an attacking agent and the complex defensive actions of the body. Killing the enemy is a valid approach to treatment if it can be done safely. Unfortunately, the side effects of most medications sometimes makes things worse and that is offensive to the Hippocratic Oath. We badly need to create an approach to research that explores ways and means of supporting and stimulating the normal mechanisms of defense.

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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 originally on May 11, 2020.

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Heart Problems, Pregnancy, and Nutrient Deficiency

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pregnancy heart complications thiamine

In the Wall Street Journal, August 14, 2018, Your Health, written by Sumathi Reddy, recorded the case of a 34-year-old pregnant woman who went to the hospital with shortness of breath and dizziness. Doctors decided that they were “pregnancy-related symptoms and nothing to be overly concerned about”. The column goes on to say that eight weeks after her daughter was born she experienced terrible stomach pains, orthopnea (severe breathing difficulty when lying down) and chest pains. At the emergency room, she was diagnosed with peripartum cardiomyopathy, noted  as “a type of heart failure related to pregnancy”. Reddy continues: “the rates of heart-related problems in women before and after childbirth have increased in the US., a problem that some experts think may be contributing to a rise in the country’s maternal mortality rate. It has been reported that the number of women having heart attacks before, during and after deliveries increased by 25% from 2002 through 2013. Around 4.5% of women who had heart attacks died”.

This is truly an appalling statistic, begging for an explanation as soon as possible. I believe that such an explanation is possible. With the necessary clinical knowledge, thiamine deficient beriberi would certainly enter into the potential diagnosis. The combination of “shortness of  breath and dizziness”  as an initial guide to its consideration, together with the later onset of “terrible stomach and chest pain” associated with heart failure 8 weeks after parturition in the case of that 34-year old pregnant woman, should have given  rise to its consideration. The trouble with this description is that it is not pathognomonic (uniquely indicative) of beriberi, a diagnosis that the medical profession refuses to recognize as a possibility in America.

What needs to be understood is that pregnancy is an enormous metabolic stress. The mother has to feed herself and her offspring, requiring a vast amount of cellular energy, not only to meet her own maintenance, but to support the rapid growth of her fetus. The enormous variety of complications in pregnancy can only be explained by a failure to produce sufficient energy to meet the metabolic demand. The diet in America, together with possible and undiagnosed genetic risk, does not always meet that goal. A common problem is known as hyperemesis gravidarum (severe pregnancy vomiting), a thiamine deficiency complication that can result in the much more serious thiamine deficiency brain disease known as Wernicke encephalopathy. So let us look at the evidence to support thiamine deficiency as a cause of pregnancy complications..

Thiamine Treatment of Severe Pregnancy Toxemia

In 2013 I received a letter from a retired American specialist in OB/GYN, John B. Irwin M.D., together with a book that he had written with the intriguing title “The Natural Way to a Trouble-Free Pregnancy” with subtitle “The Toxemia/Thiamine Connection“. He was desperate in trying to locate a physician who could subject his work to further research. His many attempts had fallen on deaf ears. He hoped that I could promulgate his work. In retirement he had hired himself out to the government of the Commonwealth of the Northern Mariana Islands to try to improve upon their system of obstetrical care.  He had attended an introductory meeting with a group of island doctors who were all American board-certified in their specialties. They introduced him to a woman who, at 36 weeks of gestation was essentially moribund with severe preeclampsia (advanced pregnancy toxemia), severe gestational cardiomyopathy (pregnancy heart failure), and with some premature separation of the placenta. Recognizing that the patient had the thiamine deficiency disease beriberi and in spite of the massive skepticism of the assembled doctors, he told them that he was going to make her well with mega-thiamine. He treated her with 100 mg of thiamine daily, reporting that she was physiologically well in six days. She delivered a 3 lbs. 12 oz. infant with a normal Apgar score

Yes, I know how many will react to this. They will say that “this patient was on a tropical island where beriberi was much more likely. This could not happen in America where the science of nutrition is so well known and where all the foods are enriched with vitamins”.

Thiamine Deficiency and Pregnancy Complications

Because of this case, Dr. Irwin started the clinic patients on prophylactic thiamine, beginning in the second trimester. Over a period of 25 years, during his retirement, he had found that it prevented the development of every type of toxemia completely, including eclampsia, preeclampsia, intra-uterine growth retardation, premature delivery, fetal death, premature rupture of membranes, placenta previa and gestational diabetes. In short, he had found that this simple non-toxic administration of megadose thiamine had virtually abolished all the common complications of pregnancy. It is important to recognize that he had spent his professional lifetime before retirement in Connecticut, attempting to bring healthy babies into the world. He was conversant with all the complications of pregnancy, for which he had previously known the absence of adequate treatment. He wondered whether the island doctors had failed to recognize beriberi, or whether toxemias of pregnancy were merely a manifestation of thiamine deficiency.

In his book, Dr. Irwin reports that

“the daily 100 mg thiamine tablet has been given to over 1000 unselected prenatals so far, starting in the second and third trimesters. More than 450 cases were conducted in Saipan of the Mariana Islands, over 600 in Waterbury Connecticut after his return from Saipan and 15 selected high risk cases with a collaborator in Adelaide, Australia. There have been no adverse reactions to thiamine. The expected and predictable number of toxemia patients in this group would be well over 150, but the actual occurrence was zero. This was an almost unbelievably favorable response. Modern science has not been able to do what thiamine has done for my patients. I have treated pregnancy-induced heart failure patients who were very close to heart failure death. They returned to normal, and continued their pregnancies to a normal conclusion at term. Treated patients did not deliver prematurely”.

Why Megadose Thiamine?

There is a lot more to this and I can only suggest that anybody wishing to be pregnant should obtain this book. It is, of course, mandatory for you to undertake this with the permission and care of your OB/GYN physician. However, do not expect that the physician will automatically accept the idea. You may have to show him/her the book. As I have said many times in posts on this website, the emerging truth concerning the application of vitamins in the treatment of disease and the preservation of health has not yet reached the collective psyche of the medical profession. It has been hard won by the few pioneers that have begun to practice what is now called Alternative Integrative Medicine.

It is quite obvious that you might ask the question, why, if this is so important in the lives and well-being of millions, it is not an acceptable practice in modern medicine by the majority of physicians? We all have known for many years that thiamine is acquired from the diet.  The recommended daily allowance (RDA) is only 1 to 1.5 mg. This minute dose acts as what is called a cofactor to many enzymes essential to energy production. Without sufficient cofactor, the enzymes do not function properly and their action gradually deteriorates. Thus, vitamin deficiency has long been regarded as a situation that only requires simple replacement of the RDA dose.

Unfortunately, what has not sufficiently been realized is that a megadose of the cofactor is required to resuscitate the enzymes that have been damaged by prolonged use of an overload of empty calories (high calorie malnutrition). Pregnancy requires energy for the development of the fetus as well as the health of the mother so the demand is greatly increased. Cells will use what is needed of the megadose for the resuscitation to take place and will discard the excess in urine. The beauty of this new way of thinking about treatment of disease is that it is non-toxic and harmless. We even know now that some of the diseases, previously thought to be entirely genetic in origin, respond to megadoses of vitamins. This has opened up a brand-new science called epigenetics that studies the effect of lifestyle and nutrition on genes. Genes are no longer considered to be solely in charge of our health destiny. We each have a responsibility towards the preservation of the blueprint (inheritance) by what we eat and our lifestyles.

Heart Problems and Insufficient Maternal Thiamine

In our book entitled “Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition” Dr. Marrs and I demonstrated that thiamine deficiency is widespread in America, causing diverse symptomology responsible for a host of puzzling diseases. We provided evidence that different forms of physical and mental stress result in an increased energy demand in the part of the brain that deals with environmental adaptation. It is suggested here that the stress of pregnancy, superimposed on marginal high calorie malnutrition, is responsible for the increase in heart failure. It is well known that the heart and brain have the highest metabolic rate, making these organs more susceptible to the effects of limited energy synthesis.

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 by Manuel Alejandro Leon from Pixabay.

This article was published originally on August 21, 2018

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Energy Deficiency and ASD

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I was a pediatrician at Cleveland Clinic from 1962 to 1982 and the clinical research, much of which I have published, was done during those years. I can distinctly remember that a patient with autism was considered to be unusually rare at that time. It was a habit of the pediatric staff to meet regularly with the residents in order to discuss clinical cases, particularly those that were uncommon or rare. I remember a case of autism coming up for one of those conferences because of its rarity. No longer rare, there are many ways in which a child can present symptoms, so the disease is now referred to as autistic spectrum disorder (ASD). This may imply that a lot of different disorders are conceived as being within a spectrum, each with a different cause, or it may simply refer to the wide variation of symptoms.

I looked up the statistics on the Internet and found that ASD today affects one in 68 children (1% of the childhood population). Parents who have a child in the spectrum have a 2% to 18% chance of having a second child affected, implying a genetic risk. I took early retirement from Cleveland Clinic and joined a private practice specializing in nutrient therapy. I became active in the group of physicians who are members of the American College for Advancement in Medicine (ACAM, acam@acam.org). A very big fraction of my patient population during those years was many children with ASD. My clinical experience between 1962 and 1982 had strongly suggested that thiamin(e) deficiency was common in the United States, in spite of the general medical opinion that it never occurred. During those years I had worked with an associate, a doctor who worked in the laboratory. Because of my clinical need, he had researched the literature for ways and means of accurately measuring thiamine deficiency. He had initiated a blood test known as transketolase activity and I need to explain this briefly.

Understanding How Thiamine Works and How to Test for Deficiency

Transketolase is the name of an enzyme whose activity is completely dependent on the presence of thiamine and magnesium, both known as cofactors to the enzyme. There are a series of biochemical reactions in which this enzyme plays an integral part. Known as the hexose monophosphate shunt, this series of reactions occurs in red blood cells. By taking some blood from a patient, the activity of this enzyme can be measured in the laboratory and is reported as transketolase activity (TKA). What we discovered was that the TKA could be quite normal when the symptoms of the patient strongly suggested thiamine deficiency. In order to prove that the patient was deficient, there was a second part to the test. Thiamine pyrophosphate (TPP), the biologically active form of thiamine in the body, had to be added to the reaction container and the transketolase activity measured again. If the TKA accelerated, it showed that the enzyme was lacking the necessary cofactor, in spite of it being in the normal range of activity with the first analysis. It was reported out as a percentage increase of activity as compared with the baseline (thiamine pyrophosphate effect or TPPE).

My friend in the laboratory had done a series of control tests on people that were purportedly healthy. His results compared favorably with reports of the test in the literature and these healthy people could have a TPPE of up to 18%. Anything over 18% for the TPPE guaranteed deficiency of thiamine or magnesium, so both of them would have to be supplemented for the benefit of the patient. Unfortunately, laboratories in prestigious institutions presently only do the TKA and assume that the patient does not have thiamine deficiency if the TKA is in the normal range. From my experience, I am aware that they are missing the majority of patients who have this deficiency. The TKA is not a valid indicator of deficiency by itself. Having given considerable thought to this, I concluded that if the enzyme is equipped with an adequate supply of thiamine there should be no acceleration in its activity after the addition of TPP. The only strictly normal TPPE would be zero (i.e. no TKA acceleration). The percentage acceleration of TKA would reveal a gradual deficiency compatible with no clinical significance until a certain increase in TPPE was recorded as being symptomatic of deficiency. Therefore a TPPE of, say, 15%  might be more clinically significant in one individual, whereas 20% might be less significant in another individual. The use of the test requires the clinical experience and adequacy of knowledge of the observer.

Clinical and Laboratory Experience

Without thiamine and magnesium as cofactors, the several enzymes dependent on them begin to become less and less efficient. One of these enzymes is essential to energy synthesis and so thiamine deficiency, because it powers pretty well every cell in the body, can literally cause any disease, since energy is integral to all functions of the body. Depending on the cellular distribution of the deficiency, the clinical expression will vary and there is no typical repetitive clinical expression (phenotype) for thiamine deficiency. However, the brain and heart being the most metabolically active organs are therefore much more susceptible to this deficiency. Thus, brain and heart symptoms are the commonest forms of clinical expression. Thus, it can be assumed that any gross deviation of behavior is evidence of electro-chemically driven changes in brain metabolism related to energy availability.

Case Evidence

Many of the children that I saw with ASD had an increase in their TPPE. Most of them with an accelerated TPPE had a TKA that was in the low normal range. When they were treated with thiamine, many of them responded clinically and their TPPE decreased into the acceptable range, so the evidence was published . The case histories of a mother and her two children were reported . The mother was a recovered alcoholic and alcohol is frequently responsible for causing thiamine deficiency. Some alcoholics react to sugar, particularly if there is a family history of alcoholism that suggests genetic risk. She and both of her children had symptoms that were typical of autistic spectrum disorder, but also they all were recognized to experience the clinical effects of dysautonomia. A description of beriberi clearly indicates that thiamine deficiency disrupts the normal functions of the autonomic nervous system (dysautonomia). All of them had intermittently abnormal transketolase studies indicating abnormal thiamine pyrophosphate homeostasis. Both children had unusual concentrations of arsenic in the urine. All of them had symptomatic improvement with diet restriction and supplementary vitamin therapy, but they quickly relapsed after ingestion of sugar, milk, or wheat. All three individuals became aware that their symptoms were related to their dietary indiscretion, but were quite unable to resist their ingestion of the “foods” that they all knew to be responsible for their relapse. The presence of arsenic in the urine was in keeping with our experience in finding the presence of heavy metals in ASD. My colleagues and I were so impressed with thiamine deficiency as a major cause of ASD that we conducted a pilot study, using a derivative of thiamin known as thiamin tetrahydrofurfuryl disulfide (TTFD). Eight of 10 children showed clinical and biochemical improvement .

The negative relationship of the brain with sugar is mindful of a case that I reported in 2016 and whose story appears on this website. A 14-year-old boy was strongly addicted to sugar and throughout the first eight years of his life his repetitive symptoms had been classified elsewhere as psychosomatic in nature. At the age of eight years it had been discovered that he had the relatively recently described disease known as eosinophilic esophagitis. He also had the classical clinical picture of dysautonomia. It was hypothesized that some form of genetic risk, coupled with thiamine deficiency from out-of-control sugar ingestion, was the responsible combination. The vagus nerve, whose course runs from the brain to the spleen, (and beyond) presides over the control of inflammation. The medical literature has reported food allergy as the cause of eosinophilic esophagitis. The vagus nerve requires acetylcholine as its neurotransmitter, a chemical that is derived from the citric acid cycle (CAC), the cellular “machine” that synthesizes energy. In turn, the nerve is dependent on thiamine that is essential for the entry of glucose into the CAC. Lacking the suppressive function of the vagus on inflammation resulted in a failure to suppress it in the esophagus. Thus, it was conjectured that thiamine deficiency was the primary underlying cause of the esophagitis.

Insufficient Energy and ASD: The Three Circles of Health

Mitochondria are very sensitive to environmental stressors such as toxicants, medication, immune activation, and metabolic disturbances suggesting that mitochondria are involved as a cause of ASD.

Figure 1. Three Circles of Health

 

From what has been written above, it must become clear to the reader that I am proposing a very different approach to the cause of ASD and disease in general. It is based on the use of Boolean algebra as represented in Figure 1. This is a statistical method of measuring the influence of variables by representing them as overlapping circles. The individual effect of one circle is represented by its area and its relationship with the other two circles by the area within the overlap. All three circles also overlap, representing the concept that disease might be 100% from one circle alone, by the combination of two defective circles, or by the variable combination of all three.

Genetics

The construction of the human body is based on a code in the form of DNA and represents a “blueprint”. Known as the genome, perfection in the code would create a perfect human body. However, we know that DNA has imperfections, but in most cases a human individual can get along quite well in spite of the imperfections.  Although an abnormal gene may be the single cause of disease, the late onset of most genetically determined conditions indicates that an additional factor is required to cause disease expression. This emphasizes the importance of the quality of nutrition in preserving health. For example, type 1 diabetes has a genetic risk, but is not usually expressed for many years, so another factor is necessary. That is why the disease is stress related, making its clinical appearance following something as simple as an infection, a divorce or an injury. Type 2 diabetes often has a genetic risk where either diet or stress, or both, may be initiators.

Epigenetics: Environment and Nutrition

Epigenetics is a relatively new science that seeks to explore how malnutrition and poor lifestyle can have a negative effect on our genes. There are several genetically determined diseases known as inborn errors of metabolism that make their appearance at birth. If any one of them is not recognized in the newborn infant, the result is often a mentally retarded individual. Some of them, perhaps the commonest being phenylketonuria (PKU) require a special diet initiated at birth in order to prevent the mental retardation. That is why in every state in the United States, a special laboratory has been set up to screen a blood test from every newborn infant, in spite of the rarity of the diseases. Sometimes, an infant is born with a gene that creates a risk for generating the disease, but it does not appear unless a secondary factor such as an infection or an injury (stressor) is experienced. There is a disease known as maple syrup urine disease (because the urine smells exactly like maple syrup) that can appear immediately at birth spontaneously or will only appear when the child is hit by some infection or trauma. There are some cases of this disease that respond to megadoses of the vitamin (thiamine/magnesium) that is normally necessary for the mechanism whose failure produces the disease. This has significant importance because a head injury or an infection might be blamed as the sole cause of a clinical problem, whereas the truth could be that the stress factor has initiated a metabolically determined disease previously unsuspected. If such a similar disease responds to the necessary associated vitamin, it can be said that the patient was successfully treated epigenetically.

Stress

In my view, this word is used too carelessly. It is most frequently used to describe the result of stress by saying that someone is “all stressed out”. So let us be clear that stress is some kind of force that a person has to meet and to which an adaptive response is required. It may be a mental force such as a divorce, a business deadline, or a physical assault such as an infection, or an injury. The three circles of health uses the philosophy proposed by Selye. This famous researcher used many forms of physical and mental injury (stress) on rats and studied the biological effects by examining their blood and tissues. He came to the conclusion that each animal went through a process of resistance that he called the General Adaptation Syndrome (GAS). The laboratory results that occurred if the GAS failed to restore health were strikingly similar to those registered in sick people and he proposed the idea that human diseases were the diseases of failure to resist or adapt to stress. What was completely revolutionary was that the GAS required some form of energy to power the machinery that enabled the animal to adapt.

In Selye’s time the biochemical mechanisms of energy synthesis were not well known. Today, these mechanisms are understood and our lives are spent in meeting the daily stresses to which we have to adapt. Our failure to meet the GAS may well be of course that the form of stress is overwhelming, such as a car collision or a virulent infection. However, what we meet on a daily basis is a mental or physical form of stress to which we have to adapt or from which we have to heal. The central factor is the mobilization of sufficient energy to meet the demands of defense. Therefore, the three circles of health predict that the cause of human disease agrees with the concept of the “diseases of adaptation” proposed by Selye.

Energy and the Ability to Adapt

Assuming that the adaptive machinery in the body is genetically adequate, all that is required is sufficient energy to drive it. The symptoms generated during the process of adaptation simply represent the locality of the energy deficiency and constitute a warning by their perception in the brain. They have to be interpreted for their underlying meaning rather than accepting them as the effects of a named disease such as Alzheimer’s or Parkinson’s. Since the brain is an electrochemical “machine”, the nature of the patient’s diet, as well as family history, are essential to beginning to unravel the problem. In the case of ASD, the mother’s diet during pregnancy is of vital importance. Occasionally, a seemingly irrelevant observation by a physician can be valid. I was riding in a car with a gentleman who had a group of infant’s shoes dangling behind the windscreen. I asked: ‘what was the significance?’ He responded by telling me that his first child died in infancy from a rare genetically determined disease. Subsequent children had survived and this was his method of keeping them in memory.

Nutrition as Medicine

When Homo sapiens arrived on the face of the earth, or even when his ancestors were present, the food was available and the general concept is that we were hunter gatherers. To find out what kind of food an animal should be taking, you have to look at the teeth. We have cutting teeth, canine teeth and grinding teeth, indicating that we are omnivores and can consume meat, vegetables and fruit. The necessary non-caloric nutrients (vitamins and essential minerals) were in the natural food. In the modern world, our food is far from natural and the high calorie content, particularly in the form of sweets, is overwhelming the cellular machinery that synthesizes energy. For this reason, many of the illnesses that haunt a physician’s office are merely a reflection of a mild to moderate energy deficiency in brain cells. If recognized for what they represent and treated with appropriate nutrition, the symptoms quickly disappear. If not, we can hypothesize that there may be permanent damage that is diagnosed as one of the neurodegenerative diseases.

The trouble with understanding this concept is that the distribution of the energy reducing mechanism, together with genetic risk, will vary from individual to individual. A child with a genetic risk, or, more commonly, a victim of poor maternal diet, is born a candidate for energy deficiency. That is why ASD can be the result of thiamine deficiency or any other mechanism that interrupts the flow of energy. However, the same deficiency can give rise to many other conditions presenting with an unpredictable array of symptoms. There is a great deal of evidence that food is burned (oxidized) in the cells of the body to create a form of chemical energy (ATP) that is transduced to electromagnetic energy. It is this energy that is used to drive physical and mental action. There is also evidence that a biological form of thiamine (thiamine triphosphate) is important in the electomagnetic transduction process, thus making thiamine uniquely indispensable. It is for this reason that I have spent many years emphasizing the life-giving properties of this extraordinary vitamin. I am not therefore surprised when I read that a constellation of symptoms called Parkinson’s disease has been reported to respond to treatment with thiamine.

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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