ALDHYDE POISONING
Fermented Foods
Many health authorities today suggest that we eat fermented foods. These are foods to which one has added a yeast, fungus, mold or ferment, which is allowed to grow on the food.
This changes the chemistry of the food. Examples include yogurt, Kefir, sauerkraut, miso, all cheese, tempeh, natto, tofu, wine, beer, and some others.
Among the reasons some recommend these foods are to provide better flora for the intestines, and perhaps to produce certain vitamins and other chemical substances that are beneficial for the body. Some yeasts, for example, can produce many B-complex vitamins in the intestines.
Fermenting a food is a way of preserving it, in some cases, and cultures have used this method for millennia. Fermenting may also allow one to eat the food essentially raw, and yet have some of the benefits of cooking because the ferment or yeast may help break down the tough fibers in the vegetable, for example, as occurs in sauerkraut. Fermenting may have other benefits, as well, according to some scientists.
This changes the chemistry of the food. Examples include yogurt, Kefir, sauerkraut, miso, all cheese, tempeh, natto, tofu, wine, beer, and some others.
Among the reasons some recommend these foods are to provide better flora for the intestines, and perhaps to produce certain vitamins and other chemical substances that are beneficial for the body. Some yeasts, for example, can produce many B-complex vitamins in the intestines.
Fermenting a food is a way of preserving it, in some cases, and cultures have used this method for millennia. Fermenting may also allow one to eat the food essentially raw, and yet have some of the benefits of cooking because the ferment or yeast may help break down the tough fibers in the vegetable, for example, as occurs in sauerkraut. Fermenting may have other benefits, as well, according to some scientists.
PROBLEMS WITH FERMENTED FOODS
However, we find that eating fermented foods almost always causes something called aldehyde toxicity. Aldehydes are chemicals produced mainly by the action of yeasts, molds and fungi. Aldehydes are not lethal toxins but they definitely affect the body and damage one’s health.
According to a 2005 article in Crit Rev Toxicol. 2005 Aug;35(7):609-62. Aldehyde sources, metabolism, molecular toxicity mechanisms, and possible effects on human health by O'Brien PJ, Siraki AG, Shangari N., Department of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada. peter.obrien@utoronto.ca, the toxic effects of aldehydes are many.
They can include acting as haptens in allergenic hypersensitivity diseases, respiratory allergies, and idiosyncratic drug toxicity; the potential carcinogenic risks of the carbonyl body burden; and the toxic effects of aldehydes in liver disease, embryo toxicity/teratogenicity, diabetes/hypertension, sclerosing peritonitis, cerebral ischemia/neurodegenerative diseases, and other aging-associated diseases.
However, we find that eating fermented foods almost always causes something called aldehyde toxicity. Aldehydes are chemicals produced mainly by the action of yeasts, molds and fungi. Aldehydes are not lethal toxins but they definitely affect the body and damage one’s health.
According to a 2005 article in Crit Rev Toxicol. 2005 Aug;35(7):609-62. Aldehyde sources, metabolism, molecular toxicity mechanisms, and possible effects on human health by O'Brien PJ, Siraki AG, Shangari N., Department of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada. peter.obrien@utoronto.ca, the toxic effects of aldehydes are many.
They can include acting as haptens in allergenic hypersensitivity diseases, respiratory allergies, and idiosyncratic drug toxicity; the potential carcinogenic risks of the carbonyl body burden; and the toxic effects of aldehydes in liver disease, embryo toxicity/teratogenicity, diabetes/hypertension, sclerosing peritonitis, cerebral ischemia/neurodegenerative diseases, and other aging-associated diseases.
ACETALDEHYDE, A VERY COMMON AND POTENT NEUROTOXIN
Acetaldehyde is produced in many fermented products. It alters red blood cell structure. It has been known since 1941 that AH easily combines with red blood cell membrane proteins to convert the red blood cells into a "time-release capsule" for AH, releasing the AH in the body far from the site where it attached to the red blood cell (3).
As this happens, however, the membrane covering the red blood cell becomes stiffer. Yet in order to travel through the capillaries, which are the smallest blood vessels and which feed the trillions of individual cells, the red blood cell must be able to fold or deform.
The average red blood cell diameter is 7 microns; yet a typical capillary is only 2 microns in diameter. Red blood cells stiffened through chronic AH exposure will have difficulty deforming sufficiently to pass through capillaries. Consequently, red blood cell-carried oxygen to many cells is reduced. (3) (Our brains require 20% of all the oxygen we breathe!)
In addition, the work of K.K. Tsuboi and colleagues has shown that AH forms stable combinations with hemoglobin in red blood cells. This reduces the ability of red blood cells to accept, hold, and transport oxygen through the bloodstream, which is their primary function. (5)
Acetaldehyde decreases the ability of the protein tubulin to assemble into microtubules. (6) Microtubules are long, thin, tube-like structures that serve several functions in the brain cell. They help provide structural support to the nerve cell, somewhat like girders in a bridge or a building, keeping the nerve cell and the dendrites semi-rigid.
Dendrites are the feathery-looking extensions from the main body of the nerve cell which connect nerve cells to each other, with some neurons connecting through dendrites to as many as 100,000 other neurons. Microtubules also serve to transport nutrients and biochemical raw materials manufactured in the cell body to the dendrites. When this raw material transport is compromised, the dendrites will gradually atrophy and die off.
Two classic examples of brain pathology involving degeneration of the dendrites in humans are chronic alcoholic brain damage and Alzheimer's disease.
Acetaldehyde induces a deficiency of vitamin B1. Thiamin, or Vitamin B1, is so critical to brain and nerve function it is often called the "nerve vitamin." AH has a very strong tendency to combine with B1, as the work of Herbert Sprince, M.D. (discussed below) has shown. (7)
Unfortunately, in detoxifying AH through combination with it, B1 is destroyed. Moderately severe B1 deficiency in humans leads to a group of symptoms called Wernicke-Korsakoff syndrome. This syndrome is characterized by mental confusion, poor memory, poor neuromuscular coordination, and visual disturbances. Its primary accepted cause is chronic alcoholism. B1 is also necessary for the production of ATP bioenergy in all body cells including the brain, and the brain must produce and use 20% of the body's energy total, even while asleep.
Vitamin B1 is also essential for production of acetylcholine. Acetylcholine is one of the brain's major neurotransmitters, facilitating optimal memory, mental focus and concentration, and learning. Alzheimer's disease represents a rather extreme case of memory loss and impaired concentration due to destruction of acetylcholine-using brain cells.
In a classic experiment reported in 1942, R.R. Williams and colleagues found that even mild B1 deficiency in humans continued over a long period of time (the experiment ran six months) produces symptoms including apathy, confusion, emotional instability, irritability, depression, feelings of impending doom, fatigue, insomnia, and headaches, all symptoms of less-than-optimal brain function.
While I understand the benefits of fermented foods, the aldehyde problem more than offsets any benefits these foods produce. For this reason, I do not recommend fermented foods except for some sauerkraut, cheese, yogurt, kefir and a little miso. These appear to be safe, when eaten in moderation. For much more on this subject, read Fermented Foods on this website.
References
1. Cleary, J.P. The NAD Deficiency Diseases. J Orthomolecular Med, 1986, 1:164-74.
2. Galland, L.D. Nutrition and Candida Albicans, 1986 A Year in Nutritional Medicine, ed J. Bland. New Canaan :Keats Pub., 1986, 203-238.
3. Truss, C.O. Metabolic Abnormalities in Patients with Chronic Candidiasis: The Acetaldehyde Hypothesis. J Orthomolecular Psychiatry, 1984, 13:66-93.
4. Levine, S. and Kidd, P. Antioxidant Adaptation, pp. 70-71. San Francisco : Biocurrents Pub., 1986.
5. Tsuboi, K.K. et al. Acetaldehyde-Dependent Changes in Hemoglobin and Oxygen Affinity of Human Erythrocytes. Hemoglobin, 1981, 5:241-50.
6. Tuma, D.J. et al. The Interaction of Acetaldehyde with Tubulin, in: Ann NY Acad Sci, ed. E. Rubin , Vol. 492, 1987.
7. Sprince, H., et al. Protective Action of Ascorbic Acid and Sulfur Compounds against Acetaldehyde Toxicity: Implications in Alcoholism and Smoking. Agents and Actions, 1975, 5:164-73.
8. Williams, R.R., et al. Induced Thiamin (Vitamin B1) Deficiency in Man. Arch Int Med, 1942, 69:721-38.
1. Cleary, J.P. The NAD Deficiency Diseases. J Orthomolecular Med, 1986, 1:164-74.
2. Galland, L.D. Nutrition and Candida Albicans, 1986 A Year in Nutritional Medicine, ed J. Bland. New Canaan :Keats Pub., 1986, 203-238.
3. Truss, C.O. Metabolic Abnormalities in Patients with Chronic Candidiasis: The Acetaldehyde Hypothesis. J Orthomolecular Psychiatry, 1984, 13:66-93.
4. Levine, S. and Kidd, P. Antioxidant Adaptation, pp. 70-71. San Francisco : Biocurrents Pub., 1986.
5. Tsuboi, K.K. et al. Acetaldehyde-Dependent Changes in Hemoglobin and Oxygen Affinity of Human Erythrocytes. Hemoglobin, 1981, 5:241-50.
6. Tuma, D.J. et al. The Interaction of Acetaldehyde with Tubulin, in: Ann NY Acad Sci, ed. E. Rubin , Vol. 492, 1987.
7. Sprince, H., et al. Protective Action of Ascorbic Acid and Sulfur Compounds against Acetaldehyde Toxicity: Implications in Alcoholism and Smoking. Agents and Actions, 1975, 5:164-73.
8. Williams, R.R., et al. Induced Thiamin (Vitamin B1) Deficiency in Man. Arch Int Med, 1942, 69:721-38.
Source: Dr. Larry Wilson