Plentiful intakes of antioxidants have been associated with reduced risk of some chronic diseases, in the same way that generous intakes of fruits, vegetables and grains have been associated with similar health benefits.
Some examples of scientific evidence are the following:
Cancer
People with high beta-carotene intakes have about one-third the cancer risk as people with low beta-carotene intakes.
Source: Peto R. Cancer Surveys 1983;2:327-340.
People with higher intakes of vitamin C have about half the risk for many types of cancer, compared to people with low vitamin C intakes.
Source: Block G. Am J Clin Nutr 1991;53:270S-282S.
People with low intakes of several antioxidants have more DNA damage than people with generous intakes.
Source: Ames BN. Metat Res 2001;475:7-20.
People with the highest intakes of vitamin C, E, and beta-carotene have a significantly lower risk of lung cancer.
Source: Yong LC et al. Am J Epidemiol 1997;146:231-43.
Men who took vitamin E supplements for 10 years or more had a 30% lower risk of bladder cancer.
Source: Michaud DS et al. Am J Epidemiol 2000;152:1145-53.
There are over 66 studies showing cancer-prevention activity of green tea, black tea, and their constituents. These include cancer reduction in the skin, lung, oral cavity, esophagus, stomach, liver, pancreas, bladder, small intestine, colon and prostate.
Source: Lambert JD et al. Am J Clin Nutr 05;81:284S- 291S.
Heart Disease
Elderly people who took dietary supplements of both vitamin C and vitamin E had a decreased risk of death from heart disease as well as overall mortality.
Source: Losonczy KG, Harris TB, Havlik RJ. Am J Clin Nutr 1996;64:190- 196.
Men who took vitamin supplements had a 70% lower risk of dying from heart disease and a 50% lower risk of a heart attack. Source: Meyer F, Bairati I, Dagenasis GR. Can J Cardiol 1996;12:930-934.
In the Nurses' Health Study involving over 87,000 women, there was a 41% reduction in risk of heart disease for those who took vitamin E for more than two years.
Source: Stampfer MJ, Hennekens CH, Manson JE, et al. New Engl J Med 1993;328:1444-1449.
In the Nurses' Health Study vitamin C supplements were also related to a lower risk of heart disease.
Source: Osganian SK et al. J Am Coll Cardiol 2003;42:246-52.
In the Health Professionals Follow-Up Study involving almost 40,000 men, there was a 37% reduction in risk of heart disease in men who took vitamin E for more than two years. The average intake in the lowest risk group was 400 IU per day.
Source: Rimm EB, Stampfer MJ. Ascherio A, et al. New Engl J Med 1993;328:1450-1456.
To date, 17 human group studies have been published on flavonoid intake and the risk of coronary artery disease and stroke. Positive studies have shown reduction in mortality risk of up to 65%.
Source: Arts ICW and Hollman PCH. Am J Clin Nutr 2005;81:317S-325S.
The largest and longest study to date, done as part of the Harvard- based Nurses' Health Study and Health Professionals Follow-up Study, included almost 110,000 men and women whose health and dietary habits were followed for 14 years. The higher the average daily intake of fruits and vegetables, the lower the chances of developing cardiovascular disease. Compared with those in the lowest category of fruit and vegetable intake (less than 1.5 servings a day), those who averaged 8 or more servings a day were 30% less likely to have had a heart attack or stroke.
Source: Joshipura KJ, et al. Ann Intern Med 2001 Jun 19;134(12):1106-14.
Other Chronic diseases
Several long-term studies have shown a reduced risk of cataracts in those who have taken vitamin C and/or Vitamin E for more than 10 years.
Source: Jacques PF et al. Arch Ophthalmol 2001;119:1009-19.
The Age-Related Eye Disease Study (AREDS) at NIH found that daily supplementation with antioxidants, zinc, and copper delayed progression of age- related macular degeneration.
Source: AREDS report no. 8. Arch Ophthalmol 2001;119:1417-36.
Research has shown a significant relationship between flavonoid intakes and the occurrence of asthma.
Source: Knekt P et al. Am J Clin Nutr 2002;76:560-8.
Other research suggests antioxidants may help support lung function and protect the lungs from oxidative damage.
Source: Schunemann HJ et al. Am J Respir Crit Care Med 2001;163:1246-55.
In a study on Alzheimer's disease, high levels of vitamin E delayed progression of the disease.
Source: Sano M et al. N Engl J Med 1997;336:1216- 22.
Source: USANA Health Sciences
This blog is intended for any readers interested in the latest research on nutritional health as published by the company who the author works for. The company researches from sources of high scientific reputation as well as through their relationship with the Linus Pauling Institute.
Thursday, November 30, 2006
Friday, November 24, 2006
Part II of IV: Antioxidants - Sources and Dietary Intakes Antioxidants
Sources and Dietary Intakes Antioxidants can be vitamins, minerals, enzymes or plant derived nutrients called phytonutrients. The major vitamin antioxidants are vitamin C, vitamin E, beta-carotene, while selenium is the major mineral antioxidant. Many researchers and nutritionists discuss and report on "antioxidants" as if these were the only sources of importance. A thorough examination of antioxidants and their importance to human health must include a much larger list of compounds that are present in healthy, varied diet. The following list is an example of the wide variety of phytonutrient antioxidants present in a healthy diet:
Phytochemical : Food Source
Allyl Sulfides : Onions, garlic, leeks, chives
Carotenoids (e.g. lycopene, lutein, zeaxanthin) : Tomatoes, carrots, watermelon, kale, spinach
Curcumin : Turmeric
Flavonoids (e.g. anthocyanadins, resveratrol, quercitin, catechins) : Grapes, blueberries, strawberries, cherries, apples, grapefruit, cranberries, raspberries, blackberries
Glutathione : Green leafy vegetables
Indoles : Broccoli, cauliflower, cabbage, brussels sprouts, bok choy
Isoflavones : Legumes (peas, soybeans)
Isothiocyanates (e.g. sulforaphane) : Broccoli, cauliflower, cabbage, brussels sprouts, bok choy
Lignans : Seeds (flax seeds, sunflower seeds)
Monoterpenes : Citrus fruit peels, cherries, nuts
Phytic Acid : Whole grains, legumes
Phenols, polyphenols, phenolic compounds (e.g. ellagic acid, ferrulic acid, tannins) : Grapes, blueberries, strawberries, cherries, grapefruit, cranberries, raspberries, blackberries, tea
Saponins : Beans, legumes
Allyl Sulfides : Onions, garlic, leeks, chives
Carotenoids (e.g. lycopene, lutein, zeaxanthin) : Tomatoes, carrots, watermelon, kale, spinach
Curcumin : Turmeric
Flavonoids (e.g. anthocyanadins, resveratrol, quercitin, catechins) : Grapes, blueberries, strawberries, cherries, apples, grapefruit, cranberries, raspberries, blackberries
Glutathione : Green leafy vegetables
Indoles : Broccoli, cauliflower, cabbage, brussels sprouts, bok choy
Isoflavones : Legumes (peas, soybeans)
Isothiocyanates (e.g. sulforaphane) : Broccoli, cauliflower, cabbage, brussels sprouts, bok choy
Lignans : Seeds (flax seeds, sunflower seeds)
Monoterpenes : Citrus fruit peels, cherries, nuts
Phytic Acid : Whole grains, legumes
Phenols, polyphenols, phenolic compounds (e.g. ellagic acid, ferrulic acid, tannins) : Grapes, blueberries, strawberries, cherries, grapefruit, cranberries, raspberries, blackberries, tea
Saponins : Beans, legumes
Recommendations by the National Cancer Institute, the U.S.D.A., other government agencies and nutrition experts are to eat a minimum of 5-13 servings of fruits and vegetables per day, depending on calorie needs. Based on these recommendations, a typical varied diet would provide approximately 200-600 mg of vitamin C and 10-20 mg (16,000-32,000 IU) of carotenoids.
Overall, polyphenols are the most abundant antioxidants in the diet. Their total dietary intake could be as high as 1 gram/day in a mixed, varied diet of fruits, vegetables, grains, and beverages.
Possible intakes of other phytonutrient antioxidants would be:
- anthocyandins " 2 oz black grapes 1,500 mg;
- proanthocyanidins " 100-300 mg/d red wine;
- catechins " 50 mg day " tea (one cup brewed green tea " 240-320 mg catechins), chocolate, apples, pears, grapes, red wine;
- isoflavones " 50 mg/day from soy foods;
- chlorogenic acid " as high as 800 mg/day coffee drinkers.
Although it may seem reasonable that a consistently healthy and varied diet could provide high doses of antioxidants, the average American gets a total of just three servings of fruits and vegetables a day. The latest dietary guidelines call for five to thirteen servings of fruits and vegetables a day, depending on one's caloric intake. For a person who needs 2,000 calories a day to maintain weight and health, this translates into nine servings, or 4½ cups per day.
The 2001-2002 NHANES survey of dietary intakes shows that 93% of Americans fail to get even the Estimated Average Requirement (EAR) for vitamin E, let alone the RDA. More than half of adults fail to get even the average requirement for vitamin A. About one-third of non-smokers and two-thirds of smokers fall short on minimum vitamin C requirements.
If the governmental dietary recommendations are meant to be taken seriously, then it follows that it would be better for people to achieve recommended amounts of nutrients than to fall short. Obviously, since the average intake of 3 servings or less of fruits and vegetables fails to provide minimum levels of even basic vitamins, intakes of the numerous other antioxidants are sure to be well under optimal and beneficial levels.
It has been established that a good multivitamin can fill in gaps in missing vitamins, but availability of broad spectrum antioxidant supplements has lagged behind. Although there is much to be learned about the characteristics of the literally hundreds of dietary antioxidants, it seems reasonable that providing supplements of various antioxidant classes may fill in nutritional gaps and provide many of the benefits missing from the typical American diet.
Source: USANA Health Sciences
Saturday, November 18, 2006
Part I of IV: Antioxidants - What are they?
Oxidation is a natural process that happens to all cells in nature, including the cells in your body. Antioxidants provide an important defense against the daily assault of free radicals on healthy cells. This Essentials of Health four-part series will review the function, benefits, sources, and safety of dietary antioxidants.
Free radicals are atoms or groups of atoms with an odd (unpaired) number of electrons and can be formed when oxygen interacts with certain molecules. Once formed these highly reactive radicals can start a chain reaction, like dominoes. Their chief danger comes from the damage they can do when they react with important cellular components such as DNA, or the cell membrane.
Cells may function poorly or die if this occurs. To prevent free radical damage the body has a defense system of antioxidants. Antioxidants are molecules that can safely interact with free radicals and terminate the chain reaction before vital tissues and cells are damaged. Although there are several enzyme systems within the body that scavenge free radicals, the principle micronutrient (vitamin/mineral) antioxidants are vitamin E, beta-carotene, vitamin C and selenium.
The body cannot manufacture these micronutrients so they must be supplied in the diet. In addition, there are literally hundreds of plant derived nutrients (phytonutrients) that act as important antioxidants in the diet. It is impossible to avoid damage by free radicals.
Free radicals arise from sources both inside (endogenous) and outside (exogenous) our bodies. Oxidants that develop from processes within our bodies form as a result of normal breathing, metabolism, and inflammation. Exogenous free radicals form from environmental factors such as pollution, sunlight, strenuous exercise, X-rays, smoking and alcohol. Our antioxidant systems are not perfect, so as we age, cell parts damaged by oxidation accumulate.
Source: USANA Health Sciences
Wednesday, November 15, 2006
Nutritional health: allergies
Description
Allergic disorders are characterized by potentially harmful reactions to extrinsic materials or allergens. They include allergic rhinitis (hay fever), atopic dermatitis, anaphylaxis, hives, and blood transfusion reactions.(1)
The immune response is the bodys defense mechanism which identifies and destroys harmful foreign organisms. Allergic reactions are an overreaction of the bodys defense mechanism. This overreaction can lead to swelling, itching and many other symptoms all with varying degrees of severity.
It is important to remember that the immune response is vital for protecting the body from foreign invaders and when working correctly its importance cannot be understated. Asthma and allergies are among the most common health problems, with as many as 50 million Americans afflicted with asthma, hay fever or other allergy-related conditions.
The preponderance of food allergies are caused by eggs, milk, wheat, fish, shellfish, nuts, peanuts, soybeans and rice.
One of the most severe allergic reactions is anaphylaxis, which is "marked by the sudden onset of rapidly progressive urticaria (a vascular reaction of the skin) and respiratory distress." (2)
Causes
The reasons that the body overreacts to a particular antigen are not well understood. It is known that it takes time and repeated exposure to an antigen for an allergic response to take place. There is also evidence that susceptibility to allergies have a hereditary component.
At Risk
There is a genetic predisposition for atopic allergies, but not for any particular allergy itself. (3)
Prevention and Management
General: Avoid the materials or organisms that initiate the allergic reaction. This may mean avoiding certain foods or environments.
Nutritional Influences:
Avoid foods that contain ingredients which cause allergic reactions. Vitamin A deficiencies may increase inflammatory responses.(4) Nicotinamide has been shown to enhance the effectiveness of glucocorticoids in the treatment of allergic reactions. (5) Pantothenic Acid: In one clinical trial the majority of more than 100 patients with allergic rhinitis who took pantothenic acid had almost instant relief. (6) Vitamin C: May have a protective effect on airway hyperactivity in some patients with exercise induced asthma.(7) Vitamin E: In elderly patients vitamin E supplementation reduced hypersensitivity reactions to various antigens and vaccines.(8) Selenium: Selenium supplementation may be beneficial to patients with intrinsic asthma. (9) Zinc, Selenium and Copper: Levels may be low in children with allergic colitis. (10) Iron: High body iron stores may increase free radical production and may also elevate asthma risk.(11) Proanthocyanidins: May reduce adverse allergic and inflammatory responses.(12)
Meydani SN, Meydani M, Blumberg JB, Leka LS, Siber G, Loszewski R, Thompson C, Pedrosa MC, Diamond RD, Stollar BD. Vitamin E supplementation and in vivo immune response in healthy elderly subjects. A randomized controlled trial. JAMA 1997 May 7;277(17):1380-6.OBJECTIVE: To determine whether long-term supplementation with vitamin E enhances in vivo, clinically relevant measures of cell-mediated immunity in healthy elderly subjects. DESIGN: Randomized, double-blind, placebo-controlled intervention study. SETTING AND PARTICIPANTS: A total of 88 free-living, healthy subjects at least 65 years of age. INTERVENTION: Subjects were randomly assigned to a placebo group or to groups consuming 60, 200, or 800 mg/d of vitamin E for 235 days. MAIN OUTCOME MEASURES: Delayed-type hypersensitivity skin response (DTH); antibody response to hepatitis B, tetanus and diphtheria, and pneumococcal vaccines; and autoantibodies to DNA and thyroglobulin were assessed before and after supplementation. RESULTS: Supplementation with vitamin E for 4 months improved certain clinically relevant indexes of cell-mediated immunity in healthy elderly. Subjects consuming 200 mg/d of vitamin E had a 65% increase in DTH and a 6-fold increase in antibody titer to hepatitis compared with placebo (17% and 3-fold, respectively), 60-mg/d (41% and 3-fold, respectively), and 800-mg/d (49% and 2.5-fold, respectively) groups. The 200-mg/d group also had a significant increase in antibody titer to tetanus vaccine. Subjects in the upper tertile of serum alpha-tocopherol (vitamin E) concentration (>48.4 micromol/L [2.08 mg/dL]) after supplementation had higher antibody response to hepatitis B and DTH. Vitamin E supplementation had no effect on antibody titer to diphtheria and did not affect immunoglobulin levels or levels of T and B cells. No significant effect of vitamin E supplementation on autoantibody levels was observed. CONCLUSIONS: Our results indicate that a level of vitamin E greater than currently recommended enhances certain clinically relevant in vivo indexes of T-cell-mediated function in healthy elderly persons. No adverse effects were observed with vitamin E supplementation.
References
1 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52-66.
2 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52.
3 Tabers Cyclopedic Medical Dictionary. 16th ed. Philadelphia:FA Davis Company; 1985. p 120.
4 Wiedermann U, Chen XJ, Enerblack L, Hanson LA, Kahu H, Dahlgren UI. Vitamin A deficiency increases inflammatory responses. Scand J Immunolo 1996 Dec;44(6):58-84.
5 Kosogorova LS, Kovalenko NN, Liubenko VA, Novosad FI. Recovery of immunological responsiveness in patients with bronchial asthma during nicotinamide treatment. Probl Tuberk 1996;(5):41-4.
6 Martin W. On treating allergic disorders. Letter. Townsend Letter for Doctors 1991 Aug/Sep:671-1.
7 Cohen HA, Neuman I, Nahum H. Blocking effect of vitamin C in exercise-induced asthma. Arch Pediatr Adolese Med 1997 Apr;151(4):367-70.
8 Meydani SN, Meydani M, Blumberg JB, Leka LS, Siber G, Loszewski R, Thompson C, Pedrosa MC, Diamind RD, Stollar BD. Vitamin E supplementation and in vivo immune response in healthy elderly subjects. A randomized controlled trial. JAMA 1997 May 7;277(17):1380-6.
9 Kadrabova J, Madaric A, Kovacikova Z, Podivinsky F, Ginter E, Gazdik F. Selenium status is decreased in patients with intrinsic asthma. Biol Trace Elem Res 1996 Jun;52(3):241-8.
10 Ojuawo A, Lindley KJ, Milla PJ. Serum zinc, selenium and copper concentration in children with allergic colitis. East Afr Med J 1996 Apr;73(4):236-8.
11 Greene LS. Asthma and oxidant stress: nutritional, environmental, and genetic risk factors. J Am Coll Nutr 1995 Aug;14(4):317-24.
12 Read MA. Flavonoids: naturally occurring anti-inflammatory agents [comment]. Am J Pathol 1995;147(2):235-7.
Source: USANA Health Sciences
Allergic disorders are characterized by potentially harmful reactions to extrinsic materials or allergens. They include allergic rhinitis (hay fever), atopic dermatitis, anaphylaxis, hives, and blood transfusion reactions.(1)
The immune response is the bodys defense mechanism which identifies and destroys harmful foreign organisms. Allergic reactions are an overreaction of the bodys defense mechanism. This overreaction can lead to swelling, itching and many other symptoms all with varying degrees of severity.
It is important to remember that the immune response is vital for protecting the body from foreign invaders and when working correctly its importance cannot be understated. Asthma and allergies are among the most common health problems, with as many as 50 million Americans afflicted with asthma, hay fever or other allergy-related conditions.
The preponderance of food allergies are caused by eggs, milk, wheat, fish, shellfish, nuts, peanuts, soybeans and rice.
One of the most severe allergic reactions is anaphylaxis, which is "marked by the sudden onset of rapidly progressive urticaria (a vascular reaction of the skin) and respiratory distress." (2)
Causes
The reasons that the body overreacts to a particular antigen are not well understood. It is known that it takes time and repeated exposure to an antigen for an allergic response to take place. There is also evidence that susceptibility to allergies have a hereditary component.
At Risk
There is a genetic predisposition for atopic allergies, but not for any particular allergy itself. (3)
Prevention and Management
General: Avoid the materials or organisms that initiate the allergic reaction. This may mean avoiding certain foods or environments.
Nutritional Influences:
Additional Information Disclaimer: These websites, addresses and/or phone numbers are provided for information purposes only. USANA, Inc. makes no claim, actual or implied, regarding the content or validity of the information obtained from these outside sources.
AbstractsMeydani SN, Meydani M, Blumberg JB, Leka LS, Siber G, Loszewski R, Thompson C, Pedrosa MC, Diamond RD, Stollar BD. Vitamin E supplementation and in vivo immune response in healthy elderly subjects. A randomized controlled trial. JAMA 1997 May 7;277(17):1380-6.OBJECTIVE: To determine whether long-term supplementation with vitamin E enhances in vivo, clinically relevant measures of cell-mediated immunity in healthy elderly subjects. DESIGN: Randomized, double-blind, placebo-controlled intervention study. SETTING AND PARTICIPANTS: A total of 88 free-living, healthy subjects at least 65 years of age. INTERVENTION: Subjects were randomly assigned to a placebo group or to groups consuming 60, 200, or 800 mg/d of vitamin E for 235 days. MAIN OUTCOME MEASURES: Delayed-type hypersensitivity skin response (DTH); antibody response to hepatitis B, tetanus and diphtheria, and pneumococcal vaccines; and autoantibodies to DNA and thyroglobulin were assessed before and after supplementation. RESULTS: Supplementation with vitamin E for 4 months improved certain clinically relevant indexes of cell-mediated immunity in healthy elderly. Subjects consuming 200 mg/d of vitamin E had a 65% increase in DTH and a 6-fold increase in antibody titer to hepatitis compared with placebo (17% and 3-fold, respectively), 60-mg/d (41% and 3-fold, respectively), and 800-mg/d (49% and 2.5-fold, respectively) groups. The 200-mg/d group also had a significant increase in antibody titer to tetanus vaccine. Subjects in the upper tertile of serum alpha-tocopherol (vitamin E) concentration (>48.4 micromol/L [2.08 mg/dL]) after supplementation had higher antibody response to hepatitis B and DTH. Vitamin E supplementation had no effect on antibody titer to diphtheria and did not affect immunoglobulin levels or levels of T and B cells. No significant effect of vitamin E supplementation on autoantibody levels was observed. CONCLUSIONS: Our results indicate that a level of vitamin E greater than currently recommended enhances certain clinically relevant in vivo indexes of T-cell-mediated function in healthy elderly persons. No adverse effects were observed with vitamin E supplementation.
References
1 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52-66.
2 Diseases. Springhouse (PA): Springhouse Corporation;1993. p 52.
3 Tabers Cyclopedic Medical Dictionary. 16th ed. Philadelphia:FA Davis Company; 1985. p 120.
4 Wiedermann U, Chen XJ, Enerblack L, Hanson LA, Kahu H, Dahlgren UI. Vitamin A deficiency increases inflammatory responses. Scand J Immunolo 1996 Dec;44(6):58-84.
5 Kosogorova LS, Kovalenko NN, Liubenko VA, Novosad FI. Recovery of immunological responsiveness in patients with bronchial asthma during nicotinamide treatment. Probl Tuberk 1996;(5):41-4.
6 Martin W. On treating allergic disorders. Letter. Townsend Letter for Doctors 1991 Aug/Sep:671-1.
7 Cohen HA, Neuman I, Nahum H. Blocking effect of vitamin C in exercise-induced asthma. Arch Pediatr Adolese Med 1997 Apr;151(4):367-70.
8 Meydani SN, Meydani M, Blumberg JB, Leka LS, Siber G, Loszewski R, Thompson C, Pedrosa MC, Diamind RD, Stollar BD. Vitamin E supplementation and in vivo immune response in healthy elderly subjects. A randomized controlled trial. JAMA 1997 May 7;277(17):1380-6.
9 Kadrabova J, Madaric A, Kovacikova Z, Podivinsky F, Ginter E, Gazdik F. Selenium status is decreased in patients with intrinsic asthma. Biol Trace Elem Res 1996 Jun;52(3):241-8.
10 Ojuawo A, Lindley KJ, Milla PJ. Serum zinc, selenium and copper concentration in children with allergic colitis. East Afr Med J 1996 Apr;73(4):236-8.
11 Greene LS. Asthma and oxidant stress: nutritional, environmental, and genetic risk factors. J Am Coll Nutr 1995 Aug;14(4):317-24.
12 Read MA. Flavonoids: naturally occurring anti-inflammatory agents [comment]. Am J Pathol 1995;147(2):235-7.
Source: USANA Health Sciences
Saturday, November 11, 2006
Antioxidants block prostate cancer
In experimental mice that naturally develop prostate cancer, supplementing with antioxidants vitamin E, lycopene and selenium effectively blocks the development or progression of prostate cancer.
According to a study published in the Journal of Cancer Research, dietary antioxidants (vitamin E, selenium, and lycopene) inhibited prostate cancer development in a group of mice that naturally develop prostate cancer. The prostate cancer disease process in these mice is similar to the human process in many respects, providing a good research model for the natural history of human prostate cancer. Treatment of animals with the antioxidants resulted in a 4-fold reduction in the incidence of prostate cancer compared with the untreated animals. Prostate cancer developed in 73.68% (14 of 19) and 100% (19 of 19) of the animals from the standard and high fat diet, respectively. In contrast, tumors developed in only 10.53% (2 of 19) and 15.79% (3 of 19) of the animals in the standard and high fat diets supplemented with antioxidants. These observations support results from a growing body of research indicating a significant protective benefit of antioxidants on the development of prostate cancer.
Source: Antioxidants block prostate cancer in lady transgenic mice, Venkateswaran V, Fleshner NE, Sugar LM, Klotz LH, Cancer Res. 2004 Aug 15;64(16):5891-6.
According to a study published in the Journal of Cancer Research, dietary antioxidants (vitamin E, selenium, and lycopene) inhibited prostate cancer development in a group of mice that naturally develop prostate cancer. The prostate cancer disease process in these mice is similar to the human process in many respects, providing a good research model for the natural history of human prostate cancer. Treatment of animals with the antioxidants resulted in a 4-fold reduction in the incidence of prostate cancer compared with the untreated animals. Prostate cancer developed in 73.68% (14 of 19) and 100% (19 of 19) of the animals from the standard and high fat diet, respectively. In contrast, tumors developed in only 10.53% (2 of 19) and 15.79% (3 of 19) of the animals in the standard and high fat diets supplemented with antioxidants. These observations support results from a growing body of research indicating a significant protective benefit of antioxidants on the development of prostate cancer.
Source: Antioxidants block prostate cancer in lady transgenic mice, Venkateswaran V, Fleshner NE, Sugar LM, Klotz LH, Cancer Res. 2004 Aug 15;64(16):5891-6.
Wednesday, November 08, 2006
Nutritional health: acne
Description
Acne vulgaris, the most common form of acne, is an inflammatory disease of the sebaceous (oil secreting) glands and hair follicles of the skin. It is characterized by comedones (blackheads) , papules (pimples), and pustules (blisters). (1)
(c) One new theory is that a deficiency of pantothenic acid may play a role in some cases.(5)
At Risk
This disease is most common in adolescence. Acne activity is primarily dependent on the genetic sensitivity of the hair follicle and oil gland to androgenic (male) hormones circulating in the blood stream.
Prevention and Management
General:
Most teenage acne will clear as the follicles mature and become less sensitive to the hormone induced changes, however in some, it will persist well into adulthood, especially those with strong genetic tendencies toward acne. The most important method of prevention is to keep the skin clean and free from dirt and oil.(6)
Nutritional Influences:
A low-fat, high-fiber, nutrient-dense diet adequate in vitamins and minerals and low in sugar, refined and convenience foods should be consumed. In one experimental study, patients experienced a rapid clearing of acne following supplementation with one ounce of bran cereal daily.(7) More studies are needed to determine if a high fiber diet is useful in treating acne.
Blood zinc levels are often lower in people who suffer from acne.(8)
Studies have shown that selenium is beneficial for treating acne pustules, possibly because one of the functions of selenium is to help fight infections. Patients with low RBC glutathione peroxidase levels and pustular acne responded best to selenium supplementation.(9)
Vitamin E works closely with selenium. Syndromes caused by selenium deficiency overlap those caused by a vitamin E deficiency; because of the close relationship, vitamin E and selenium are often combined to make treatment more effective.(10)
Vitamin A and its synthetic derivatives appear to be beneficial; high doses are needed, however. Because of the potential for toxicity, vitamin A and vitamin A derivatives should be used only under medical supervision.
Vitamin E affects the biologic utilization of vitamin A. The absorption of vitamin A is markedly impaired in vitamin E deficient animals.(11,12)
Excess supplementation of iodine may cause or exacerbate acneiform eruptions.(13) Kelp as a dietary supplement (14) or fast foods (15) may contain sufficient iodine for this adverse effect.
A deficiency of omega-6 essential fatty acids in the pilosebaceous epithelium might account for follicular hyperkeratosis in acne.(16)
Abstracts
Kremer JM, Bigaouette J. Nutrient intake of patients with rheumatoid arthritis is deficient in pyridoxine, zinc, copper, and magnesium. J Rheumatol 1996 Jun;23(6):990-4. OBJECTIVE: To determine nutrient intake of patients with active rheumatoid arthritis and compare it with the typical American diet (TAD) and the recommended dietary allowance (RDA). METHODS: 41 patients with active RA recorded a detailed dietary history. Information collected was analyzed for nutrient intake of energy, fats, protein, carbohydrate, vitamins and minerals, which were then statistically compared with the TAD and the RDA. RESULTS: Both men and women ingested significantly less energy from carbohydrates [women 47.4% (6.4) vs 55% RDA. p = 0.0001: men = 48.9% (7.4). p = 0.025] and more energy from fat [women = 36.8% (4.5) vs 30% RDA. p = 0.001 and men = 35.2% (5.9) p = 0.02]. Women ingested significantly more saturated and mono-unsaturated fat than the RDA (p = 0.02 and p = 0.04 respectively) while men ingested significantly less polyunsaturated fat (PUFA) (p = 0.0001). Both groups took in less fiber (p = 0.0001). Deficient dietary intake of pyridoxine was observed vs the RDA for both sexes (men and women p = 0.0001). Deficient folate intake was seen vs the TAD for men (p = 0.02) with a deficient trend in women (p = 0.06). Zinc and magnesium intake was deficient vs the RDA in both sexes (p values < or =" 0.001)" p =" 0.004" p =" 0.02">Leung LH. Pantothenic acid deficiency as the pathogenesis of acne vulgaris. Med Hypotheses 1995 Jun;44(6):490-2. For years, the pathogenesis of acne vulgaris has been known to be strongly influenced by hormonal factors. However, the exact role of and the interrelationship among the various hormones in question have not been well elucidated. Here, I wish to suggest a radically different theory for its pathogenesis and relate its basic pathology to a deficiency in pantothenic acid, a vitamin hitherto not known to cause any deficiency syndrome in humans. Hence, the effect of hormonal factors in this disease entity becomes secondary to that of the availability of pantothenic acid. A complete cure of this condition is effected by a very liberal replacement therapy with the vitamin.
References
(1) Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation. 1997. p 1173.
(2) Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation. 1997. p 1173.
(3) Rosenberg EW, Kirk BS. Acne diet reconsidered. Arch Dermatol 1981;117:193-95.
(4) Klurfeld DM. The Diet and Acne. Archives of Dermatology 1983;119(4):276.
(5) Leung LH. Pantothenic acid deficiency as the pathogenesis of acne vulgaris. Med Hypotheses 1995 Jun;44(6):490-2
(6) Somer E. The Essential Guide to Vitamins and Minerals. New York:HarperPerennial. 1992.
(7) Putzier E. Dermatomycoses and an antifungal diet. Wiener Medizinische Wochenschrift 1989 Aug 31;139(15-16): 379-80.
(8) Pohit J et al. Zinc status of acne vulgaris patients. J Appl Nutr 1985;37(1):18-25.
(9) Michaelsson G, Edqvist L. Erythrocyte glutathione peroxidase activity in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol (Stockh) 1984;64(1):9-14.
(10) Michaelsson G, Edqvist L. Erythrocyte glutathione peroxidase activity. in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol (Stockh) 1984;64(1):9-14.
(11) Ames SR. Factors affecting absorption, transport and storage of vitamin A. Am J Clin Nutr 1969;22:934.
(12) Ayers S Jr, Mihan R. Acne vulgaris and lipid peroxidation: New concepts in pathogenesis and treatment. Int J Dermatol 1978;17:305.
(13) Hitch JM. Acneiform eruptions induced by drugs and chemicals. JAMA 1967;200:879-80.
(14) Fischer AA. Contact Dermatitis. 3rd ed. Philadelphia:Lea and Febiger;1986. p 593.
(15) How nutritious are fast-foods? Consum Rep 1975;40:278-81.
(16) Downing DT et al. Essential fatty acids and acne vulgaris. J Am Acad Dermatol 1986;14:221-25.
Source
Disclaimer: The information provided is strictly educational and not intended as medical advice. For diagnosis and treatment, consult your health care professional. This information may be copied and freely distributed only if all text remains intact and unchanged.
Acne vulgaris, the most common form of acne, is an inflammatory disease of the sebaceous (oil secreting) glands and hair follicles of the skin. It is characterized by comedones (blackheads) , papules (pimples), and pustules (blisters). (1)
Causes
(a) Many factors can cause acne. Research has centered on hormonal dysfunction and oversecretion of sebum as possible primary causes.(2) A diet high in fat can contribute to acne vulgaris. Acne is associated with oily skin due to an excess of sebum, the fatty secretion of the sebaceous glands. Eating fat increases sebum production.(3,4)
(c) One new theory is that a deficiency of pantothenic acid may play a role in some cases.(5)
At Risk
This disease is most common in adolescence. Acne activity is primarily dependent on the genetic sensitivity of the hair follicle and oil gland to androgenic (male) hormones circulating in the blood stream.
Prevention and Management
General:
Most teenage acne will clear as the follicles mature and become less sensitive to the hormone induced changes, however in some, it will persist well into adulthood, especially those with strong genetic tendencies toward acne. The most important method of prevention is to keep the skin clean and free from dirt and oil.(6)
Nutritional Influences:
A low-fat, high-fiber, nutrient-dense diet adequate in vitamins and minerals and low in sugar, refined and convenience foods should be consumed. In one experimental study, patients experienced a rapid clearing of acne following supplementation with one ounce of bran cereal daily.(7) More studies are needed to determine if a high fiber diet is useful in treating acne.
Blood zinc levels are often lower in people who suffer from acne.(8)
Studies have shown that selenium is beneficial for treating acne pustules, possibly because one of the functions of selenium is to help fight infections. Patients with low RBC glutathione peroxidase levels and pustular acne responded best to selenium supplementation.(9)
Vitamin E works closely with selenium. Syndromes caused by selenium deficiency overlap those caused by a vitamin E deficiency; because of the close relationship, vitamin E and selenium are often combined to make treatment more effective.(10)
Vitamin A and its synthetic derivatives appear to be beneficial; high doses are needed, however. Because of the potential for toxicity, vitamin A and vitamin A derivatives should be used only under medical supervision.
Vitamin E affects the biologic utilization of vitamin A. The absorption of vitamin A is markedly impaired in vitamin E deficient animals.(11,12)
Excess supplementation of iodine may cause or exacerbate acneiform eruptions.(13) Kelp as a dietary supplement (14) or fast foods (15) may contain sufficient iodine for this adverse effect.
A deficiency of omega-6 essential fatty acids in the pilosebaceous epithelium might account for follicular hyperkeratosis in acne.(16)
Abstracts
Kremer JM, Bigaouette J. Nutrient intake of patients with rheumatoid arthritis is deficient in pyridoxine, zinc, copper, and magnesium. J Rheumatol 1996 Jun;23(6):990-4. OBJECTIVE: To determine nutrient intake of patients with active rheumatoid arthritis and compare it with the typical American diet (TAD) and the recommended dietary allowance (RDA). METHODS: 41 patients with active RA recorded a detailed dietary history. Information collected was analyzed for nutrient intake of energy, fats, protein, carbohydrate, vitamins and minerals, which were then statistically compared with the TAD and the RDA. RESULTS: Both men and women ingested significantly less energy from carbohydrates [women 47.4% (6.4) vs 55% RDA. p = 0.0001: men = 48.9% (7.4). p = 0.025] and more energy from fat [women = 36.8% (4.5) vs 30% RDA. p = 0.001 and men = 35.2% (5.9) p = 0.02]. Women ingested significantly more saturated and mono-unsaturated fat than the RDA (p = 0.02 and p = 0.04 respectively) while men ingested significantly less polyunsaturated fat (PUFA) (p = 0.0001). Both groups took in less fiber (p = 0.0001). Deficient dietary intake of pyridoxine was observed vs the RDA for both sexes (men and women p = 0.0001). Deficient folate intake was seen vs the TAD for men (p = 0.02) with a deficient trend in women (p = 0.06). Zinc and magnesium intake was deficient vs the RDA in both sexes (p values < or =" 0.001)" p =" 0.004" p =" 0.02">Leung LH. Pantothenic acid deficiency as the pathogenesis of acne vulgaris. Med Hypotheses 1995 Jun;44(6):490-2. For years, the pathogenesis of acne vulgaris has been known to be strongly influenced by hormonal factors. However, the exact role of and the interrelationship among the various hormones in question have not been well elucidated. Here, I wish to suggest a radically different theory for its pathogenesis and relate its basic pathology to a deficiency in pantothenic acid, a vitamin hitherto not known to cause any deficiency syndrome in humans. Hence, the effect of hormonal factors in this disease entity becomes secondary to that of the availability of pantothenic acid. A complete cure of this condition is effected by a very liberal replacement therapy with the vitamin.
References
(1) Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation. 1997. p 1173.
(2) Diseases. 2nd ed. Springhouse (PA):Springhouse Corporation. 1997. p 1173.
(3) Rosenberg EW, Kirk BS. Acne diet reconsidered. Arch Dermatol 1981;117:193-95.
(4) Klurfeld DM. The Diet and Acne. Archives of Dermatology 1983;119(4):276.
(5) Leung LH. Pantothenic acid deficiency as the pathogenesis of acne vulgaris. Med Hypotheses 1995 Jun;44(6):490-2
(6) Somer E. The Essential Guide to Vitamins and Minerals. New York:HarperPerennial. 1992.
(7) Putzier E. Dermatomycoses and an antifungal diet. Wiener Medizinische Wochenschrift 1989 Aug 31;139(15-16): 379-80.
(8) Pohit J et al. Zinc status of acne vulgaris patients. J Appl Nutr 1985;37(1):18-25.
(9) Michaelsson G, Edqvist L. Erythrocyte glutathione peroxidase activity in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol (Stockh) 1984;64(1):9-14.
(10) Michaelsson G, Edqvist L. Erythrocyte glutathione peroxidase activity. in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol (Stockh) 1984;64(1):9-14.
(11) Ames SR. Factors affecting absorption, transport and storage of vitamin A. Am J Clin Nutr 1969;22:934.
(12) Ayers S Jr, Mihan R. Acne vulgaris and lipid peroxidation: New concepts in pathogenesis and treatment. Int J Dermatol 1978;17:305.
(13) Hitch JM. Acneiform eruptions induced by drugs and chemicals. JAMA 1967;200:879-80.
(14) Fischer AA. Contact Dermatitis. 3rd ed. Philadelphia:Lea and Febiger;1986. p 593.
(15) How nutritious are fast-foods? Consum Rep 1975;40:278-81.
(16) Downing DT et al. Essential fatty acids and acne vulgaris. J Am Acad Dermatol 1986;14:221-25.
Source
Disclaimer: The information provided is strictly educational and not intended as medical advice. For diagnosis and treatment, consult your health care professional. This information may be copied and freely distributed only if all text remains intact and unchanged.
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