Vitamins Blog
Vitamin E
Vitamins
Vitamin E occurs naturally as eight separate compounds (four tocopherols and four tocotrienols) with antioxidant activity. Most clinical research has focused on one of these compounds—alpha-tocopherol. The naturally occurring form of alpha-tocopherol is called D-alpha-tocopherol (or RRR-alpha tocopherol), and the synthetic form is called DL-alpha-tocopherol (or all-rac-alpha tocopherol). Although many studies have shown benefits from the synthetic form, the synthetic form contains isomers not normally found in the human body. Therefore, the naturally-occurring form—D-alpha-tocopherol—might be the preferred form.9
In addition, there is some evidence that supplements containing a mixture of all four vitamin E tocopherols (alpha, beta, gamma, and delta) may be safer and more effective than D-alpha-tocopherol by itself. One researcher has recommended that these mixed tocopherol supplements contain 50 to 100 mg of gamma-tocopherol per 400 IU of D-alpha-tocopherol. Also, water-miscible preparations of vitamin E may be better absorbed than fat-soluble preparations.10
The recommended dietary allowance for vitamin E is low, just 15 mg or approximately 22 International Units (IU) per day. The most commonly recommended amount of supplemental vitamin E for adults is 400 to 800 IU per day. However, some leading researchers suggest taking only 100 to 200 IU per day, since trials that have explored the long-term effects of different supplemental levels suggest no further benefit beyond that amount. In addition, research reporting positive effects with 400 to 800 IU per day has not investigated the effects of lower intakes.1 For tardive dyskinesia, the best results have been achieved from 1,600 IU per day,2 a large amount that should be supervised by a healthcare practitioner.
Sources
Wheat germ oil, nuts and seeds, whole grains, egg yolks, and leafy green vegetables all contain vitamin E. Certain vegetable oils should contain significant amounts of vitamin E. However, many of the vegetable oils sold in supermarkets have had the vitamin E removed in processing. The high amounts found in supplements, often 100 to 800 IU per day, are not obtainable from eating food.
Possible Deficiencies
Severe vitamin E deficiencies are rare. People with a genetic defect in a vitamin E transfer protein have severe vitamin E deficiency, characterized by low blood and tissue levels of vitamin E and progressive nerve abnormalities.3, 4
Low vitamin E status has been associated with an increased risk of rheumatoid arthritis5 and major depression.6 Women with preeclampsia have been found to have lower blood levels of vitamin E than women without the condition.7
Very old people with type 2 diabetes have shown a significant age-related decline in blood levels of vitamin E, irrespective of their dietary intake.8
References
2. Hashim S, Sajjad A. Vitamin E in the treatment of tardive dyskinesia: a preliminary study over 7 months at different doses. Int Clin Psychopharmacol 1988;13:147-55.
3. Traber MG. Vitamin E. In: Shils ME, Olsen JA, Shike M, Ross AC (eds). Modern Nutrition in Health and Disease. Baltimore: Williams & Wilkins, 1999, 347-62.
4. Cavalier L, Ouahchi K, Kayden HJ, et al. Ataxia with isolated vitamin E deficiency: heterogeneity of mutations and phenotypic variability in a large number of families. Am J Hum Genet 1998;62:301-10.
5. Knekt P, Heliovaara M, Aho K, et al. Serum selenium, serum alpha-tocopherol, and the risk of rheumatoid arthritis. Epidemiology 2000;11:402-5.
6. Maes M, De Vos N, Pioli R, et al. Lower serum vitamin E concentrations in major depression. Another marker of lowered antioxidant defenses in that illness. J Affect Disord 2000;58:241-6.
7. Kharb S. Total free radical trapping antioxidant potential in pre-eclampsia. Int J Gynaecol Obstet 2000;69:23-6.
8. Polidori MC, Mecocci P, Stahl W, et al. Plasma levels of lipophilic antioxidants in very old patients with type 2 diabetes. Diabetes Metab Res Rev 2000;16:15-9.
9. Gaby, AR. Nutritional Medicine. Concord, NH: Fritz Perlberg Publishing, 2011.
10. Gaby, AR. Nutritional Medicine. Concord, NH: Fritz Perlberg Publishing, 2011.
11. Roob JM, Khoschsorur G, Tiran A, et al. Vitamin E attenuates oxidative stress induced by intravenous iron in patients on hemodialysis. J Am Soc Nephrol 2000;11:539-49.
12. Panel on Dietary Antioxidants and Related Compounds, Food and Nutrition Board, Institute of Medicine, National Academy of Sciences. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academy Press, Washington, D.C., 2000.
13. Graat JM, Schouten EG, Kok FJ. Effect of daily vitamin E and multivitamin-mineral supplementation on acute respiratory tract infections in elderly persons: a randomized controlled trial. JAMA 2002;288:715-21.
14. Skrha J, Sindelka G, Kvasnicka J, Hilgertova J. Insulin action and fibrinolysis influenced by vitamin E in obese type 2 diabetes mellitus. Diabetes Res Clin Pract 1999;44:27-33.
15. Zoler ML. Supplemental vitamin E linked to heart failure. Fam Pract News 2003 (October 1):28 [News report].
16. Miller ER III, Pastor-Barriuso R, Dalal D, et al. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med 2005;142:37-46.
REFERENCES
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Vitamin D
Food & Supplements Program
Vitamin D Products Comparison Table
unit conversions: Vits A, D, E, B3
Vitamin D is a hormone, not a vitamin. Hormones act as signaling molecules, which affect how cells work. Vitamin D not only influences bone formation, but immune function, other hormones (including sex and thyroid hormones) and coagulation. The RDA remains at the 1970 value of 400 IU, while most people need between 4,000 and 10,000 IU. Recently the units of vitamin D have been changed from IU’s to mcg. The pdf below shows the conversion. Recent data suggests that the best time to take vitamin D is before bedtime, as some of the activities of sleep can be enhanced by the presence of higher levels of vitamin D.
Vitamin D levels should be checked at a minimum of once a year. Primary Care Practitioners should include Vit D levels in annual preventive testing. Levels can be influenced by several factors including: gut function (fat absorption), presence of vitamins A, E and K, presence of toxins including lead (Pb), and other hormone levels.
Best Vitamin D article from Alternative Medicine Review 2005
Related Posts
Vitamin D as an Anti–Thrombotic Agent
Vitamin D and Cancer
Vitamin D and Autoimmune Diseases
References
Vitamin C, Ascorbic Acid
Food & Supplements Program
Vitamins
Vitamin C and Collagen
Vitamin C and the Bowels
Vitamin C and Detoxification
This page is under development. Working links will provide starting information. Please let us know about your interest in this page by emailing us here, and check back soon.
Vitamin E, Tocopherols, Tocotrienols
Vitamins
Vitamin E Products Comparison Table
unit conversions: Vits A, D, E, B3
Chemistry and biology of vitamin E.2005
This article that includes Bruce Ames as the senior researcher discusses sesame oil’s unique characteristic
γ-Tocopherol, the major form of vitamin E in the US diet, deserves more attention.2001Â
Related Links
Pellagra
Link to Niacin
Link to Tryptophan
Tryptophan and niacin deficiency causes pellagra. The main symptoms of pellagra are dermatitis, dementia, and diarrhea. This is because niacin deficiency is most noticeable in body parts with high rates of cell turnover, such as your skin or gastrointestinal tract.
In the late 1800’s eastern civilization (North America, Canada and Europe) was eating more corn (maize) as a staple food. Corn contains niacytin, a form of niacin that humans can’t digest and absorb unless prepared properly. South American culture had figured out that corn needed to prepared by “nixtamalization,” in which the whole kernel is treated with a solution of alkali such as limewater (calcium hydroxide, NOT the lime fruit). (This process also removes up to 97–100% of aflatoxins from mycotoxin-contaminated corn). In 1901, the Beall degerminator was patented and used to separate the grit from the germ in corn processing. However this process of degermination without nixtamalization reduces the niacin content of the cornmeal by 90%. Today, this process is employed in the production of tortillas and tortilla chips (but not corn chips), tamales, hominy, and many other items. There is no precise date when the technology was developed, but the earliest evidence of nixtamalization is found in Guatemala’s southern coast, with equipment dating from 1200–1500 BCE.
In 1915, Joseph Goldberger, a well-regarded researcher, was assigned to study pellagra by the Surgeon General of the United States. He showed pellagra was linked to diet by observing the outbreaks of pellagra in orphanages and mental hospitals. Goldberger noted that children between the ages of 6 and 12 (but not older or younger children at the orphanages) and patients at the mental hospitals (but not doctors or nurses) were the ones who seemed most susceptible to pellagra. Goldberger theorized that a lack of meat, milk, eggs, and legumes made those particular populations susceptible to pellagra. By modifying the diet served in these institutions with “a marked increase in the fresh animal and the leguminous protein foods,” Goldberger was able to show that pellagra could be prevented. By 1926, Goldberger established that a diet that included these foods, or a small amount of brewer’s yeast prevented pellagra.
Most of the niacin in mature cereal grains is present as niacytin, which is niacin bound up in a complex with hemicellulose which is nutritionally unavailable. In mature corn this may be up to 90% of the total niacin content. The preparation method of nixtamalization using the whole dried corn kernel made this niacin nutritionally available and reduced the chance of developing pellagra. Niacytin is concentrated in the aleurone and germ layers which are removed by milling. The milling and degerming of corn in the preparation of cornmeal became feasible with the development of the Beall degerminator which was originally patented in 1901 and was used to separate the grit from the germ in corn processing.[49] However this process of degermination reduces the niacin content of the cornmeal.
The US did not implement Goldberger’s recommendations until ____ by requiring all flour/corn (? clarify) to be fortified with niacinamide, which continues to this day. Canada waited another year or so, but would fortify the corn sent to Europe due to European demand.
https://en.wikipedia.org/wiki/Pellagra
https://en.wikipedia.org/wiki/Nixtamalization
THIS SECTION IS BEING EDITED
Dermatitis related to pellagra usually causes a rash on the face, lips, feet, or hands. In some people, dermatitis forms around the neck, a symptom known as Casal necklace.
Primary pellagra is caused by diets low in niacin or tryptophan. Tryptophan can be converted to niacin in the body, so not getting enough can cause niacin deficiency.
Primary pellagra is most common in developing countries that depend on corn as a staple food. Corn contains niacytin, a form of niacin that humans can’t digest and absorb unless prepared properly.
Secondary pellagra occurs when your body can’t absorb niacin. Things that can prevent your body from absorbing niacin include:alcoholism
eating disorders
certain medications, including anti-convulsants and immunosuppressive drugs
gastrointestinal diseases, such as Crohn’s disease and ulcerative colitis
cirrhosis of the liver
carcinoid tumors
Hartnup disease
niacin synthesis, since B6 (pyridoxine) is a required cofactor in the tryptophan-to-niacin reaction.
Several therapeutic drugs can provoke pellagra. These include the antibiotics isoniazid, which decreases available B6 by binding to it and making it inactive, so it cannot be used in niacin synthesis,[11] and chloramphenicol; the anti-cancer agent fluorouracil; and the immunosuppressant mercaptopurine.[10]
If maize is not nixtamalized, it is a poor source of tryptophan, as well as niacin. Nixtamalization corrects the niacin deficiency, and is a common practice in Native American cultures that grow corn. Following the corn cycle, the symptoms usually appear during spring, increase in the summer due to greater sun exposure, and return the following spring. Indeed, pellagra was once endemic in the poorer states of the U.S. South, such as Mississippi and Alabama, where its cyclical appearance in the spring after meat-heavy winter diets led to it being known as “spring sickness” (particularly when it appeared among more vulnerable children), as well as among the residents of jails and orphanages as studied by Dr. Joseph Goldberger.[12]
Third, it may be caused by excess leucine, as it inhibits quinolinate phosphoribosyl transferase (QPRT) and inhibits the formation of niacin or nicotinic acid to nicotinamide mononucleotide (NMN) causing pellegra like symptoms to occur.
The native New World cultivators who first domesticated corn (maize) prepared it by nixtamalization, in which the grain is treated with a solution of alkali such as lime. Nixtamalization makes the niacin nutritionally available and prevents pellagra. When maize was cultivated worldwide, and eaten as a staple without nixtamalization, pellagra became common.
In 1937, Conrad Elvehjem, a biochemistry professor at the University of Wisconsin-Madison, showed that the vitamin niacin cured pellagra (manifested as black tongue) in dogs. Later studies by Dr. Tom Spies, Marion Blankenhorn, and Clark Cooper established that niacin also cured pellagra in humans, for which Time Magazine dubbed them its 1938 Men of the Year in comprehensive science.
Research conducted between 1900 and 1950 found the number of cases of women with pellagra was consistently double the number of cases of afflicted men.[41] This is thought to be due to the inhibitory effect of estrogen on the conversion of the amino acid tryptophan to niacin.[42] Some researchers of the time gave a few explanations regarding the difference.
unknown toxin in corn.[31] The Spartanburg Pellagra Hospital in Spartanburg, South Carolina, was the nation’s first facility dedicated to discovering the cause of pellagra. It was established in 1914 with a special congressional appropriation to the U.S. Public Health Service (PHS) and set up primarily for research. In 1915, Joseph Goldberger, assigned to study pellagra by the Surgeon General of the United States, showed it was linked to diet by observing the outbreaks of pellagra in orphanages and mental hospitals. Goldberger noted that children between the ages of 6 and 12 (but not older or younger children at the orphanages) and patients at the mental hospitals (but not doctors or nurses) were the ones who seemed most susceptible to pellagra.[32] Goldberger theorized that a lack of meat, milk, eggs, and legumes made those particular populations susceptible to pellagra. By modifying the diet served in these institutions with “a marked increase in the fresh animal and the leguminous protein foods,” Goldberger was able to show that pellagra could be prevented. By 1926, Goldberger established that a diet that included these foods, or a small amount of brewer’s yeast, prevented pellagra.
Casimir Funk, who helped elucidate the role of thiamin in the etiology of beriberi, was an early investigator of the problem of pellagra. Funk suggested that a change in the method of milling corn was responsible for the outbreak of pellagra,[50] but no attention was paid to his article on this subject.
Pellagra developed especially among the vulnerable populations in institutions such as orphanages and prisons, because of the monotonous and restricted diet. Soon pellagra began to occur in epidemic proportions in states south of the Potomac and Ohio rivers. The pellagra epidemic lasted for nearly four decades beginning in 1906. It was estimated that there were 3 million cases and 100,000 deaths due to pellagra during the epidemic.
Casimir Funk, who helped elucidate the role of thiamin in the etiology of beriberi, was an early investigator of the problem of pellagra. Funk suggested that a change in the method of milling corn was responsible for the outbreak of pellagra, but no attention was paid to his article on this subject.
Pellagra developed especially among the vulnerable populations in institutions such as orphanages and prisons, because of the monotonous and restricted diet. Soon pellagra began to occur in epidemic proportions in states south of the Potomac and Ohio rivers. The pellagra epidemic lasted for nearly four decades beginning in 1906.[51] It was estimated that there were 3 million cases and 100,000 deaths due to pellagra during the epidemic.