thiamine 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.

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. 

This article was published originally on May 11, 2020.

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Thiamine, Pregnancy, and the Energy Connection

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There is an old saying “for any workman who has only a hammer for a tool, everything is a nail”. Thus, I am in danger of writing article after article about one vitamin, B1, or thiamin/thiamine, but write I must. Thiamine is critical for energy production and the energetic demands of pregnancy are substantial. Insufficient thiamine during pregnancy can and does have negative impacts on both maternal and fetal health. Both Dr. Marrs and I have written about this previously, but it bears exploring further. Before we begin, however, let us review a few concepts.

Energy to Respond

In order to understand its therapeutic use in the treatment of many different conditions, you have to understand its function and how it differs from “taking medicine”. Let me first remind you that we live in a hostile environment to which we have to adapt in order to survive. Infection, trauma, weather, work assignments and a variety of changes in life’s journey (stress) have to be met as they occur. Assuming that our genetically determined “blueprint” is intact, all we require is energy. To meet the pressure of stress, an automatically increased supply of energy is necessary. Food provides us with fuel that must be burned (oxidized) in supplying that energy and thiamine is essential in igniting the fuel.

When we are attacked by a microorganism, the brain organizes a comprehensive defensive mechanism that we refer to as an illness or a disease. With trauma, healing requires increased energy so that the healing process can proceed. Let it be clearly understood once again that our food provides both the fuel and the vitamins that enable oxidation to supply the required energy. I have come to the conclusion that illness is either a genetically determined error in the DNA code, a failure to synthesize the energy requirement to meet stress, or a combination of the three. If we are attacked by a microorganism, a healthy organism defeats the foe. This is by no means a new idea. It just has not been put into practice, so we are still stuck with the antiquated concept that each disease is represented by a collection of symptoms and physical signs with a unique cause in each case that must be researched to find the magic cure. In order to understand why a thiamine supplement is so protective in pregnancy, I must try to show that any form of stress requires a genetically determined resistance and energy. It is illustrated by a case in my own clinical experience.

When Genetics, Trauma and Diet Collide: Cataracts and Galactosemia

Some years ago, a 6-year old boy was referred to me by an ophthalmologist, because he had been found to have cataracts in both eyes. The ophthalmologist knew that this could be a manifestation of a rare genetically determined disease known as galactosemia and had asked me to research it. There is a sugar in milk called lactose. When milk is consumed, the lactose is converted to galactose that is then broken down by a recessive gene inherited from each of the parents. In order to bear a child that has the potential to have the disease, the child must have obtained a gene from each parent. With two genes, the galactose accumulates in the blood and affects the eye, causing the density known as cataract.

The level of galactose can be determined in the laboratory and in the case of this child, it was in the normal range, at the time of the study. In the meantime, however, the laboratory had been asked to check the presence of the abnormal gene. It was reported that he had only one copy of the gene. With only one copy, the child was classified as a carrier and on general principles, he could not have the disease. So I sat down with the child’s mother to ask her about the diet that she had been giving and I found that she had a tremendous faith in the health manifestations of milk. Therefore she had insisted on multiple glasses of milk for the child. In addition the child had experienced a head injury with a fractured skull. When he returned to school, the school nurse had insisted that he have eye testing every two weeks because, she said “people go blind after an injury like this”. Whether this was an accurate statement or not, the child’s vision was perfectly normal immediately after his discharge from hospital. Three months later there was a dramatic change, causing her to refer the child to the ophthalmologist who had discovered the cataracts. I had to conclude that the combination of trauma, genetic risk and unknown dietary indiscretion combined to cause the disease. The “stress” of the head injury, or the genetic carrier state, or the excessive intake of milk, would not be damaging on their own. It was their coincidental relationship that precipitated the cataracts.

The Energetic Demands of Pregnancy

In 2013, I received a letter from Dr. John Irwin an OB/GYN specialist in Connecticut and his remarkable book: The Natural Way to a Trouble-Free Pregnancy: The Toxemia-Thiamine Connection. The letter said:

Dear Dr. Lonsdale,

I am writing to you, because I have found another mortal being who is particularly interested in the biological activities of thiamine. I had previously thought that I was nearly the loan believer in the benevolent effects of thiamine, particularly for the treatment and prophylaxis of the toxemias of pregnancy and its many associated problems. I had even written to the chief of the Cleveland Clinic OB-GYN about the “miracles” I was performing and offered to work with him in further development of the concepts, but my information seems to have experienced obstacles.

After Dr. Irwin had retired, he spent 25 years in the Commonwealth of the Northern Mariana Islands where he had been concentrating on the use of what he called “megathiamin, 100 mg daily” in the prevention of toxemia and many other complications of pregnancy. His first patient was introduced to him by an introductory meeting with a group of island doctors who were all American board-certified in their specialties. The patient had severe preeclampsia, had been sick for six weeks and was essentially moribund at 36 weeks of gestation. She also had severe heart disease and he recognized the compound symptoms of thiamine deficiency disease. In the face of the open skepticism of the other physicians, he started her on a 100 mg pill of thiamine daily. He reported that she was cured in six days. She had some fetal distress on the seventh day and was delivered of a 3 lbs. 12 oz. baby by cesarean section. The infant’s Apgar was 10-10, an extraordinary result in a situation where death of both mother and infant would be the expected outcome.

He then started all his patients on “prophylactic megathiamin” at the third trimester and he reported that it prevented the development of every type of toxemia completely, including eclampsia, preeclampsia, intrauterine growth retardation of the fetus, premature delivery, fetal death, premature rupture of membranes and in fact virtually any pregnancy complication. To anyone that contemplates pregnancy and can overcome her expected skepticism, this book is an absolute essential.

Thiamine, Energy, and Pregnancy

I believe that we can offer a rational explanation of what superficially appears to be “miraculous”. In many posts on this website I have commented on the energy relationship between stress and maintenance of well-being. There must always be a complete balance between energy synthesis and its utilization. In good health, the rate of synthesis automatically accelerates to meet any increased demand, although there must be a normal limit to that capacity. The stress in pregnancy is enormous. The mother is feeding her fast-growing baby as well as herself, giving rise to a marked increase in energy demand. Thiamine is the key to energy synthesis from the oxidation (burning) of glucose. Her physiology must meet this ever increasing demand to full-term. The failure of this equation obviously imperils both mother and fetus and it also explains many of the complications observed in the neonate’s immediate and future development. The dysregulation of body organs by the energy deficient brain explains the multiplicity of the complications because all of them have a common cause.

Unfortunately, many people have concluded that taking sugar will increase energy production by “throwing fuel on the fire”, a fact that has led to a great deal of energy deficiency illness. There has to be a normal glucose/thiamine ratio for healthy oxidation. Just as an excess of gasoline introduced into the cylinders of a car produces inefficient engine performance, an excess of glucose induces illness. If we insist on ingesting empty calories, we must optimize the glucose/thiamine ratio by supplementing thiamine, thus explaining Dr. Irwin’s success in eliminating many of the common complications associated with pregnancy.

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.

This article was published originally on February 11, 2019. 

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What Is Scoliosis?

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scoliosis and impaired oxidative metabolism

As everyone knows, the spinal column is made up of a series of bones known as vertebrae. Like bricks in a column, they collectively support the entire body in an upright position. Their anatomy is very complex because, collectively, they have to allow for the spinal column to bend in every direction without parting company with each other. Sometimes a child develops a permanent bend in the spinal column known as scoliosis. It usually develops relatively slowly and is usually watched by anxious parents as it becomes more severe. Anyone reading this who has had experience of it will know that the treatment is very advanced surgery in which the spinal column is straightened and supported with steel rods. This post is to try to explain why scoliosis happens and how it may possibly be prevented.

Brain Symmetry

Most people know that the left half of the body is controlled by the right side of the brain and vice versa. The reason for this asymmetry is unknown. However, asymmetry appears to be pretty important with many aspects of brain function. For example, I collected 17 patients, in each of whom their respective blood pressure was totally different in the two arms. The difference was so great that I imagined such an individual, when visiting a physician, would leave the office with a blood pressure pill if the pressure had been measured in the arm on the higher side, and without it if it had been taken in the arm on the low side. As most people know, the blood pressure is taken almost invariably in only one arm. The blood pressures in my 17 patients were compared with healthy controls. Although the pressures of controls varied only slightly in the two arms, the difference was extremely obvious when compared with the patients.

The asymmetry in the patients was greatly exaggerated, whereas in the controls it was minimal. This asymmetry is capable of increasing in direct relationship to loss of efficient metabolism in the control mechanisms in the brain. The loss of efficiency may be due to genetic effect or long-term malnutrition. These 17 patients had many symptoms, indicating that their autonomic nervous system was compromised because of poor oxidative metabolism. The symptoms responded to treatment with nutritional elements.

Dysautonomia

We have two nervous systems, known respectively as the voluntary and autonomic. The voluntary system enables us to use free will, whereas the autonomic is automatic and organizes brain/body functions that we cannot control voluntarily. The prefix dys means abnormal, so dysautonomia refers to abnormal function of that system. This can be due to genetic influence or from metabolic changes related to poor diet. One of the abnormalities that can occur is that the normal mild asymmetry in autonomic control can become exaggerated, giving more power to one side of the body than the other. Under normal healthy conditions, this asymmetry is much less marked. In fact, it is well known that all of us have some degree of asymmetry. One foot may be slightly bigger than the other or one eye may be a little bit more closed than the other. The autonomic nervous system is deployed to every part of the body and is the messenger system by which the brain controls all the organs that together, create body functions.

What Has This to Do with Scoliosis?

The spinal column is lined by very strong ligaments and muscles. It is these muscles that enable us to bend in every direction. However, those muscles are kept in what is called constant tone. Notice the hardness of the muscles in the low back. They feel to the touch like steel almost. This is because they are kept in tone as a permanent support. This tone is maintained through the autonomic nervous system by constant signals from the brainstem to the muscles surrounding the spinal column. The voluntary system can overcome the autonomic signals to enable us to bend as we wish. Asymmetric signaling to the muscles on either side of the spinal column occurs in health but may be only slight. If however, control mechanisms in the lower part of the brain are metabolically inefficient, asymmetric signaling evidently increases.   If the tonic signals have exaggerated asymmetry, the tone of the muscles on one side of the spinal column will have stronger signals than on the other side. This explains why the scoliosis occurs gradually, but we have to realize that the real cause of the disease is because of the exaggerated asymmetry in the autonomic nervous system. In other words, scoliosis can be a disease of the autonomic nervous system as well as from genetic changes in the vertebral column.

An experimental treatment for scoliosis was reported some years ago in which electrodes were attached to the weaker muscles on the convex side of the scoliosis and tonic electrical signals attempted to straighten the spinal column. I do not know what happened to that experiment, but it seems to me that scoliosis should be treated by preventive treatment of the dysautonomia. The patients with the asymmetric blood pressures all had evidence of dysfunctional oxidative metabolism in the lower part of the brain, an effect that can be produced by thiamine deficiency. All of them were treated by nutritional therapeutic measures with variable degrees of success. Quite a few of them, but not all, had thiamine deficiency as the underlying cause. It was concluded therefore that it was oxidative dysfunction, for any cause, in the brain that was the underlying cause of the exaggerated asymmetry, whether this was genetic or nutritional in origin. They responded to a number of intravenous infusions of water-soluble vitamins, all of which contained thiamine. The control mechanisms of the autonomic nervous system in the lower part of the brain are particularly prone to develop thiamine deficiency. Therefore this is an important cause of inefficient oxidative brain metabolism.

Prevention

As far as I know, prevention of scoliosis has never been attempted and what follows is therefore a hypothesis based on some evidence. It may well be that nutrition of the mother in pregnancy can induce faulty metabolism in the fetus that may deploy its effect in many different ways. We now know that thiamine deficiency is common in pregnancy and most of its complications can be prevented by taking a modest dose of thiamine, starting even before pregnancy. Since the major effect of thiamine deficiency is dysautonomia, perhaps the exaggeration of asymmetry can be prevented. The new science of epigenetics enables some modification of genetic defects. A mouse model has shown that the combination of a genetic risk factor with short-term gestational hypoxia (oxygen deficit) significantly increases the gene penetrance and severity of vertebral defects. There is no harm in a supplement of thiamine during pregnancy. Whether it would be capable of preventing scoliosis would depend on its disappearance from the medical literature and would be a long-term goal.

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. 

https://www.scientificanimations.com, CC BY-SA 4.0, via Wikimedia Commons

This article was published originally on August 28, 2017. 

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Heart Problems, Pregnancy, and Nutrient Deficiency

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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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How to Have a Healthy Pregnancy: Avoiding Preeclampsia and Toxemia

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A few months ago, I received a book from a doctor who had retired from his specialty in obstetrics and gynecology. It was accompanied by a letter that began as follows, “I am writing to you, because I have found another mortal being who is particularly interested in the biological activities of thiamine. I had previously thought that I was nearly the lone believer in the benevolent effects of thiamine, particularly for the treatment and prophylaxis of the toxemias of pregnancy and its many associated problems”. In this letter, he went on to tell me that he had hired himself out, in his retirement, to the government of the Commonwealth of the Northern Mariana Islands “to improve upon their system of obstetrical care”.

Severe Preeclampsia

On his first day he attended an introductory meeting with a group of island doctors who were all American Board Certified in their specialties. Their purpose was to introduce him to a patient who was 36 weeks pregnant. He described her as “essentially moribund” with severe preeclampsia, gestational cardiomyopathy, and some separation of the placenta (preeclampsia is the term used for severe pregnancy toxemia and cardiomyopathy is the term used for a sick heart. Separation of the placenta would mean that there would be bleeding into the uterus). She  was so sick that she had orthopnea (breathlessness while lying flat on her back. She could only breathe when sitting up in bed, a characteristic of heart failure). Spontaneous labor and delivery, he said, most likely would cause maternal and fetal death and that she would fail to come through a cesarean section. All in all, this was considered by all of the island doctors concerned to be a hopeless case. He suggested that she had beriberi, the vitamin B1 deficiency disease. The letter went on to say “in a private huddle the doctors decided that if the patient died while they were holding me up, they would be found solely guilty, so with anger, sneers and audible comments they told me to go ahead!” He gave the woman 100 mg of thiamine daily in a pill and she was physiologically cured in six days, sleeping flat and hiking the long halls for exercise to shake off her prolonged immobilization. On the seventh day, because of fetal distress, she was subjected to cesarean section, with the delivery of a 3 lbs. 12 oz. baby 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. Also, they might think that the doctor was deluded into thinking that all forms of toxemia were really beriberi and that he had treated this disease rather than toxemia. So the doctor started the clinic patients on prophylactic mega-thiamine for the second and third trimesters, preventing 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, among other possible complications. Again, the reader might well say that these were all patients on a tropical island. Consider however that this doctor had spent his professional lifetime in his attempt to bring healthy babies into the world. He was conversant with all the complications of pregnancy. Did the island doctors fail to recognize beriberi or is toxemia of pregnancy merely a manifestation of thiamine deficiency? Our preconceived idea that each disease is a separate entity with a separate cause and an individualized treatment may very well be completely wrong. If energy metabolism is compromised, the dysfunctional effects will be related to the cells most affected. The symptoms and physical or mental deterioration will be as variable as the distribution of the energy deficit.

There is a lot more to this and I can only suggest that anybody wishing to be pregnant should obtain this book by John B Irwin M.D. “The Natural Way to a Trouble-Free Pregnancy” with the subtitle “The Toxemia-Thiamine Connection”.

It is, of course, mandatory for you to undertake this with the permission and care of your OB/GYN physician if you are pregnant. 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 Complementary Medicine. They use few drugs and the results that they get are real.

Of RDAs and Mega-doses

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? The answer is because of the teaching of biochemistry in medical schools. We all have known for many years that thiamine is acquired from the diet.  The recommended daily allowance (RDA) is 1 to 1.5 mg. This minute dose acts as what is called a cofactor to many enzymes. Without sufficient cofactor, the enzymes do not function properly. Thus, vitamin deficiency has long been regarded as a situation that requires simple replacement of the cofactor. Therefore, the only dose required is that recommended as the RDA and mega-doses are regarded as being completely useless.

Unfortunately, what has not sufficiently been considered is that an overload of simple carbohydrate empty calories overwhelms the ability of thiamine to process  glucose derived from the food. Glucose is used by body cells as fuel and the energy supply that results from it must meet physical and mental demands for maintaining healthy life. The modern diet is grotesquely unnatural and, because of the overload of empty calories the enzymes that are starved of their cofactors, begin to deteriorate. In order to resuscitate them, the cofactors must be used in a pharmacological way to stimulate the respective enzymes back into a healthy state.

Pregnancy Energy Demands are Significant

Pregnancy requires energy for the development of the baby as well as the health of the mother so the demand is greater. Cells will use what is needed of the mega-dose 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 mega-doses 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.

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