thiamine sugar Archives - Hormones Matter

Sugar Intake and Thiamine

Published on May 23, 2022

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Between 1962 and 1982, I was a pediatrician at Cleveland Clinic, a multispecialty medical institution. Because I was a consultant pediatrician. doctors in a private practice referred some of their more difficult patients. I was confronted with a number of children who were experiencing emotional diseases such as Attention Deficit Disorder (ADD), Learning Disability, and Hyperactivity. The usual explanation for this kind of emotional disease is poor parenting. Therefore, I would sit down with the parents and discuss their approach. In most cases, it was healthy, but when I looked into the diet of the affected children, I found that in each and every case, it was full of empty calories, particularly from consumption of sugar and fat, consumed for their sense of taste. Indeed, this consumption was actively encouraged, since it provided the child with obvious pleasure.

Sugar Induced Cellular Energy Deficiency

I turned to the library and read the details concerning the processing of sugar and fat in the body. Without going into the details, vitamin B1 (thiamine) stands at the head of the complex machinery that enables our cells to turn food into energy. I concluded that cellular energy deficiency in the brain was causing distortion of normal brain function in these children, I looked into what research was available and I found a 1935 publication by Sir Rudolph Peters, a famous researcher who worked at Cambridge University. He was trying to discover the role of vitamin B1 (thiamine) in the body. It had only recently been discovered that dietary thiamine deficiency was the cause of beriberi.

It had also been found that thiamine deficiency-induced in pigeons produced the histopathology that had been observed in humans with beriberi. He was therefore able to study the action of thiamine by creating what is known as a brei, a preparation of brain cells taken while the pigeon was alive. He then placed it under a microscope. The cellular activity, known as respiration, could be studied. He made a similar preparation from the brain of a thiamine replete pigeon and placed the two together under a microscope. There was no difference in respiration between the thiamine deficient cells compared with those that were thiamine sufficient until glucose was added to the preparation. The thiamine sufficient cells immediately began to respire, whereas the thiamine deficient cells remained inactive. This showed that glucose was the main fuel for brain cells and that thiamine was necessary for its consumption. He called this the catatorulin effect. Not only this, but Peters found that the deficiency was more severe in the cells from the lower part of the thiamine deficient pigeon brain, providing an important clue. We now know that the lower part of the human brain is peculiarly sensitive to thiamine deficiency. This research was extremely important because it formed a foundation that led to understanding oxidative metabolism.

The high sugar diet was affecting the brains of these children and I found that supplementing them with thiamine made their emotional symptoms disappear. I was in fact imitating the catatorulin effect. I found this very intriguing and began library research on the biological role of thiamine that has continued to the present day.

Thiamine Is the Spark

Without going into details, it stands at the entry of glucose into the complex cellular machinery that produces the energy required for all the functions of the body. Much of our food is turned into glucose in the body and acts as cellular fuel, particularly in the brain. Oxidative metabolism, to put it simply, is the combustion of glucose. Combustion in the body is known as oxidation and although the analogy is too simple. Thiamine provides the spark like a spark plug in a car that ignites the gasoline.

If glucose provides fuel for the brain, the children with emotional disease were getting plenty of fuel, so how could I explain this excess as the cause? We have to turn to analogy. Some older people will remember that the early cars all possessed a choke mechanism that introduced a rich gasoline mixture to start a cold engine. But if the choke was not removed when the engine was warm, black smoke came out of the exhaust pipe and the engine ran poorly, indicating poor combustion and energy production. A similar thing happens in the body, particularly in the brain. An excess of fuel overwhelms the ability of cells to combine it with oxygen like a persistent choke. The result is that the brain cells work inefficiently, giving rise to changes in behavior. It made the administration of thiamine quite rational.

Using a vitamin for treatment was not even suggested at that time. I took early retirement and joined a private practice that specialized in nutrient treatment. This was an early example of what has come to be known as Orthomolecular Medicine, which involves the ingestion of molecules that are well recognized by the body.

Behavior is a function of the brain and whether it be purely mental, or gives rise to bodily activity, requires energy. Psychosomatic disease is not due to the patient’s imagination. It is the result of a declining ability to produce sufficient ATP. This leads to the obvious suggestion that disease is a variable manifestation of energy deficiency dependent on the severity of the deficiency and its cellular distribution.

Thiamine Deficiency and Dysautonomia

One of the important results of thiamine deficiency is dysautonomia, dysfunction of the autonomic nervous system. This is the nervous system by which body organs are controlled by the lower brain. The deficiency is rarely seen as a cause of disease in America so the symptoms are attributed to other “more acceptable” conditions. Usually neglected, sometimes for years, thiamine has to be given to the patient in mega-doses to restore normal function. Damage to the affected cells may cause poor or no response. The research on beriberi, exclusively performed in China and Japan, discovered that recovery was most likely when the blood sugar was normal. If it were high, recovery was slower and if it were low, recovery may not occur at all. The dose of thiamine had to be huge to cure a patient of long-standing beriberi after its deficiency had been found as the cause of a widespread disease that had occurred for thousands of years.

Prevalent in rice-consuming countries, if and when the peasants made more money, they would take the rice to a mill where the cusps were removed. They would then serve the white rice in a silver bowl and invite their friends to demonstrate their newly acquired affluence. Of course, they did not know that the vitamins were in the cusp around the grain.

Thiamine Dosing Varies

I had found, ironically enough, that my insomnia was caused by thiamine deficiency and my diet has been supplemented with it for years. Being an entirely new treatment, it requires some detailed research, but self-research is time-honored. So I am going to describe a recent experience that illustrates how thiamine affected my autonomic nervous system. I had noted that when I ate virtually any food at all, my nose would run. One day I was eating some canned pears and I experienced a rather severe choking fit and my nose ran like a faucet. I was taking 300 mg of Lipothiamine (thiamine tetrahydrofurfuryl disulfide) and 200 mg of a magnesium salt. I concluded that the dose of TTFD was too great and lacking in balance with magnesium, which I increased to 400 mg. I reduced the dose of TTFD to 250 mg. Even within days, there was an improvement. The pharynx, esophagus, and nostrils are controlled by the ANS and the dose change was born out of my unique clinical and biochemical experience. Although orthomolecular medicine is in its infancy, it is hoped that it will become the orthodox medicine of the future. Not only is it non-toxic, but it is also extremely efficient and I have helped thousands over my 61 years of practice.

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The Warburg Effect in Cancer

by Derrick Lonsdale MD, FACN, CNS

Published on September 19, 2017

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In the 1930s Otto Warburg won a Nobel Prize for an observation that has since become known as “the Warburg effect” in oncology. He had reported that most cancer cells predominantly produce energy by a high rate of glycolysis (sugar metabolism) rather than the low rate in most normal cells. The energy in cancer cells, that typically have a glycolytic (sugar metabolism in action) rate up to 200 times higher than normal cells, is produced by fermentation. This form of energy production does not require oxygen and is known as anaerobic metabolism (without oxygen). Normal cells derive their energy from a chemical process that does require oxygen, hence the term oxidative, or aerobic (requiring oxygen), metabolism. The process of fermentation in cancer cells is much less efficient in producing energy than that in normal cells that derive energy from oxidative metabolism. Curiously, this anaerobic metabolism happens in cancer cells even when oxygen is plentiful. Although this has been much studied, its importance, either in cause or effect, remains unclear. Warburg had postulated that this change in metabolism is the fundamental cause of cancer, a claim now known as the Warburg hypothesis or Warburg effect. Today, mutations in oncogenes (genes associated with cancer) are thought to be responsible for malignant transformation and the Warburg effect is considered to be a result of these mutations rather than the cause. In other words, does the Warburg effect originate the cancer or is it an effect of the cancer? It is a typical “chicken and egg” question.

The Role of Thiamine in Cancer

The relationship between supplemental vitamins and various types of cancer has been the focus of recent investigation. Supplemental vitamins have been reported to modulate cancer rates and a significant association has been demonstrated between cancer and low levels of thiamine in the blood (1). This also gives rise to a “chicken and egg” question. Is the low level of thiamine a result of treatment using chemotherapy and radiation or does it have a causative relationship? Thiamine deficiency is increasingly recognized in medically ill patients. Its prevalence among cancer patients is unknown. However, thiamine deficiency was found in 119 (55.3%) of 217 patients with various types of cancer. Risk factors included effects of chemotherapy or undergoing active treatment (2). It is possible to induce a certain type of tumor in mice. Thiamine supplementation between 12.5 and 250 times the recommended dietary allowance (RDA for mice) stimulated the tumors. Doses 2500 times the RDA resulted in 10% inhibition of tumor growth (3). This inhibitory effect of exceedingly high doses of thiamine is unexplained and certainly merits further study.

Thiamine as a Drug

The definition of a drug is “a medicine or other substance which has a physiological effect when ingested or otherwise introduced into the body”. Therefore, if thiamine is taken as a supplement, it must be considered to be a drug. Conventional wisdom sees thiamine as a food-borne particle whose function, in a minute concentration, is to assist the enzymes to which it is attached. The daily dose is governed by the RDA and is stated as 1 to 1.5 mg/day. For this reason, if its deficiency as a cause of symptoms is recognized in a given patient, the treatment would be considered to be simply replacement value. Any increase in that dose would inevitably be considered completely unnecessary. This is in spite of the hard-won history that treating beriberi demanded as much as 100 mg of thiamine a day for months. Of course, as I have mentioned in these pages many times, conventional wisdom also denies that beriberi, or any other form of vitamin deficiency, exists in America or any other developed culture. There are now many reports in the medical literature of thiamine being used in megadoses to treat virtually any disease associated with or caused by a breakdown in energy metabolism. It is therefore worth considering the potential mechanism in the already established place of thiamine, or its derivatives, in cancer.

We used to think that our genes dominated our body functions in a fixed way throughout life. The relatively new science of epigenetics tells us that nutrition and lifestyle have a powerful influence on our genetically determined mechanisms. Research in cancer has been almost completely dominated by study of the influence of specialized genes, known as oncogenes. The question that should arise is what, if ever, is the influence of malnutrition on these genes. Could thiamine deficiency “turn on” or otherwise influence oncogenes through epigenetic mechanisms? Our book (Lonsdale D, Marrs C. Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition) emphasizes that widespread thiamine deficiency exists in America because of an inordinate ingestion of sugar in all its different forms. The book supplies evidence that an overload of glucose ingestion provides “empty calories” that overwhelms the capacity of thiamine metabolism in processing the glucose. In other words, the intake of thiamine in the diet might be sufficient for a normal calorie load but insufficient for the load of empty calories. This is referred to as “high calorie malnutrition”. Calibration of diet depends on a study of three meals a day. We suggest that it is the inordinate consumption of sugar associated with almost all social activities that may make the difference. We question whether there is a potential relationship with the increasing incidence of cancer. Is sugar our ultimate enemy? Is our hedonistic consumption of it a threat to our civilization? Although this sounds like a fictional idea for a novel, understanding the complex role of thiamine in glucose metabolism should make us pause to wonder whether the pleasure derived from taste is a potential cause of our undoing.

Hypoxia, Thiamine and Cancer

Hypoxia is one of the hallmarks of the tumor microenvironment (referring to the local concentration of oxygen that exists around cells that become cancerous). It is the result of insufficient blood supply to support growing tumor cells (4). This would result in lack of oxygen, but also would restrict the supply of vitamins, including thiamine. It is interesting that thiamine deficiency results in a metabolic disturbance that induces a state similar to deficiency of oxygen and is known as pseudo-hypoxia (pseudo-, meaning false)(5).

The term vitamin was derived from the finding that each one of these chemical substances found in naturally occurring food is “vital” to life. Thiamine’s role is to turn chemical food substances into energy. Therefore, it must be recognized as having the same life-giving effect in the body as oxygen. Granted that it is not the only vitamin required for this, however, it appears to have a degree of importance that makes it the dominant factor. Early studies of the relationship of thiamine deficiency as the cause of beriberi showed that, as the disease progressed, there were different metabolic patterns marking the degree of deficiency. For example, patients with a normal blood sugar responded to thiamine easily. Those with a high blood sugar were slower to respond and those with a low blood sugar often didn’t respond at all. The far-reaching consequences of the increasing effect of thiamine deficiency as the disease progressed need to be understood better.

It is known that the part of the brain that enables us to adapt to and thrive in our hostile environment, is particularly susceptible to thiamine deficiency. Therefore, its deficiency provides effects that are exactly similar to partial deprivation of oxygen. Is it possible that thiamine deficiency, resulting as it does in loss of efficient oxidative metabolism, is the underlying factor that initiates the cancer by an epigenetic mechanism? The low dose/high dose administration of thiamine in producing the opposite effects may be a mystery of thiamine metabolism requiring further research. Perhaps thiamine deficiency activates the genetic mechanisms that are known to be involved in the transition of the normal cell into a cancerous one. It may be that some cancers (and a lot of other diseases) could be prevented by a rational approach to a diet that spares us from metabolic stress induced by this highly artificial “high calorie malnutrition”.

Although this article is written for general readership, references are included to show that the statements made within the article are supported by publication in the medical literature.

References

Lu’o’ng KV, Nguyen LT. The role of thiamine in cancer: possible genetic and cellular signaling mechanisms. Cancer Genomics Proteomics, 2013, 10 (4): 169-85.
Isenberg-Grzeda, E., Shen, M. J., Alici, Y., Wills, J., Nelson, C., & Breitbart, W. High rate of thiamine deficiency among inpatients with cancer referred for psychiatric consultation: results of a single site prevalence study. Psychooncology 2016. May 26. doi. 10. 1002/pon. 4155. [Epub ahead of print]
Comin-Anduix B, Boren J, Martinez S, et al. The effect of thiamine supplementation on tumor proliferation. A metabolic control analysis study Eur J Biochem, 2001, 268 (15): 4177-82.
Kumar V, Gabrilovich DI. Hypoxia-inducible factors in regulation of immune responses in tumor microenvironment. Immunology, 2014, 143 (4): 512-9.
Sweet RL, Zastre JA. HIF1-α-mediated gene expression induced by vitamin B1 deficiency. Int J Vitam Nutr Res 2013, 823 (3): 188-97.

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