jueves, enero 26, 2006

Dietary Supplement Fact Sheet: Vitamin A and Carotenoids

Dietary Supplement Fact Sheet: Vitamin A and Carotenoids

Office of Dietary Supplements NIH Clinical Center National Institutes of Health
Table of Contents

Vitamin A: What is it?

Vitamin A is a family of fat-soluble compounds that play an important role in vision, bone growth, reproduction, cell division, and cell differentiation (in which a cell becomes part of the brain, muscle, lungs, etc.) [1-5]. Vitamin A helps regulate the immune system, which helps prevent or fight off infections by making white blood cells that destroy harmful bacteria and viruses [1,6-10]. Vitamin A also may help lymphocytes, a type of white blood cell, fight infections more effectively.

Vitamin A promotes healthy surface linings of the eyes and the respiratory, urinary, and intestinal tracts [8]. When those linings break down, it becomes easier for bacteria to enter the body and cause infection. Vitamin A also helps maintain the integrity of skin and mucous membranes, which also function as a barrier to bacteria and viruses [9-11].

Retinol is one of the most active, or usable, forms of vitamin A, and is found in animal foods such as liver and whole milk and in some fortified food products. Retinol is also called preformed vitamin A. It can be converted to retinal and retinoic acid, other active forms of the vitamin A family [1].

Provitamin A carotenoids are darkly colored pigments found in plant foods that can be converted to vitamin A. In the United States, approximately 26% and 34% of vitamin A consumed by men and women, respectively, is provided by provitamin A carotenoids [1]. Common carotenoids found in foods are beta-carotene, alpha-carotene, lutein, zeaxanthin, lycopene, and cryptoxanthin [11]. Of the 563 identified carotenoids, fewer than 10% are precursors for vitamin A [12]. Among these, beta-carotene is most efficiently converted to retinol [1,13-15]. Alpha-carotene and beta-cryptoxanthin are also converted to vitamin A, but only half as efficiently as beta-carotene [1]. Lycopene, lutein, and zeaxanthin are carotenoids that do not have vitamin A activity but have other health promoting properties [1]. The Institute of Medicine (IOM) encourages consumption of carotenoid-rich fruits and vegetables for their health-promoting benefits.

Some carotenoids, in addition to serving as sources of vitamin A, have been shown to function as antioxidants in laboratory tests. However, this role has not been consistently demonstrated in humans [1]. Antioxidants protect cells from free radicals, which are potentially damaging by-products of oxygen metabolism that may contribute to the development of some chronic diseases [3,14-15].

What foods provide vitamin A?

Retinol is found in animal foods such as whole eggs, milk, and liver. Most fat-free milk and dried nonfat milk solids sold in the United States are fortified with vitamin A to replace the amount lost when the fat is removed [16]. Fortified foods such as fortified breakfast cereals also provide vitamin A. Provitamin A carotenoids are abundant in darkly colored fruits and vegetables. The 2000 National Health and Nutrition Examination Survey (NHANES) indicated that major dietary contributors of retinol are milk, margarine, eggs, beef liver and fortified ready-to-eat cereals, whereas major contributors of provitamin A carotenoids are carrots, cantaloupes, sweet potatoes, and spinach [17].

Animal sources of vitamin A are well absorbed and used efficiently by the body. Plant sources of vitamin A are not as well absorbed as animal sources. Tables 1 and 2 suggest many sources of vitamin A and provitamin A carotenoids [18].

Table 1: Selected animal sources of vitamin A [18]
FoodVitamin A (IU)*%DV**
Liver, beef, cooked, 3 ounces27,185545
Liver, chicken, cooked, 3 ounces12,325245
Milk, fortified skim, 1 cup50010
Cheese, cheddar, 1 ounce2846
Milk, whole (3.25% fat), 1 cup2495
Egg substitute, ¼ cup2265

Table 2: Selected plant sources of vitamin A (from beta-carotene) [18]
FoodVitamin A (IU)*%DV**
Carrot juice, canned, ½ cup22,567450
Carrots, boiled, ½ cup slices13,418270
Spinach, frozen, boiled, ½ cup11,458230
Kale, frozen, boiled, ½ cup9,558190
Carrots, 1 raw (7½ inches)8,666175
Vegetable soup, canned, chunky, ready-to-serve, 1 cup5,820115
Cantaloupe, 1 cup cubes5,411110
Spinach, raw, 1 cup2,81355
Apricots with skin, juice pack, ½ cup2,06340
Apricot nectar, canned, ½ cup1,65135
Papaya, 1 cup cubes1,53230
Mango, 1 cup sliced1,26225
Oatmeal, instant, fortified, plain, prepared with water, 1 cup1,25225
Peas, frozen, boiled, ½ cup1,05020
Tomato juice, canned, 6 ounces81915
Peaches, canned, juice pack, ½ cup halves or slices47310
Peach, 1 medium3196
Pepper, sweet, red, raw, 1 ring (3 inches diameter by ¼ inch thick)3136

* IU = International Units.
** DV = Daily Value. DVs are reference numbers based on the Recommended Dietary Allowances (RDAs). They were developed to help consumers determine if a food contains a lot or a little of a nutrient. The DV for vitamin A is 5,000 IU. Most food labels do not list vitamin A content. The percent DV (%DV) column in the table above indicates the percentage of the DV provided in one serving. A food providing 5% or less of the DV is a low source while a food that provides 10-19% of the DV is a good source. A food that provides 20% or more of the DV is high in that nutrient. It is important to remember that foods that provide lower percentages of the DV also contribute to a healthful diet. For foods not listed in this table, refer to the U.S. Department of Agriculture's Nutrient Database Web site:

What are recommended intakes of vitamin A?

Recommendations for vitamin A are provided in the Dietary Reference Intakes (DRIs) developed by the Institute of Medicine (IOM) [1]. DRI is the general term for a set of reference values used for planning and assessing nutrient intake in healthy people. Three important types of reference values included in the DRIs are Recommended Dietary Allowances (RDA), Adequate Intakes (AI), and Tolerable Upper Intake Levels (UL). The RDA recommends the average daily dietary intake level that is sufficient to meet the nutrient requirements of nearly all (97-98%) healthy individuals in each age and gender group [1]. An AI is set when there are insufficient scientific data to establish a RDA. AIs meet or exceed the amount needed to maintain nutritional adequacy in nearly all people. The UL, on the other hand, is the maximum daily intake unlikely to result in adverse health effects [1].

In Table 3, RDAs for vitamin A are listed as micrograms (mcg) of Retinol Activity Equivalents (RAE) to account for the different biological activities of retinol and provitamin A carotenoids [1]. Table 3 also lists RDAs for vitamin A in International Units (IU), which are used on food and supplement labels (1 RAE = 3.3 IU).

Table 3: Recommended Dietary Allowances (RDAs) for vitamin A
(mcg RAE)
(mcg RAE)
(mcg RAE)
(mcg RAE)
(mcg RAE)
(1,000 IU)
(1,320 IU)
(2,000 IU)
(3,000 IU)
(2,310 IU)
(2,500 IU)
(4,000 IU)
(3,000 IU)
(2,310 IU)
(2,565 IU)
(4,300 IU)

There is insufficient information to establish a RDA for vitamin A for infants. AIs have been established based on the amount of vitamin A consumed by healthy infants fed breast milk (Table 4) [1].

Table 4: Adequate Intakes (AIs) for vitamin A for infants
Age (months)Males and females (mcg RAE)
0-6400 (1,320 IU)
7-12500 (1,650 IU)

The NHANES III survey (1988-1994) found that most Americans consume recommended amounts of vitamin A [19]. More recent NHANES data (1999-2000) show average adult intakes to be about 3,300 IU per day, which also suggests that most Americans get enough vitamin A [20].

There is no RDA for beta-carotene or other provitamin A carotenoids. The IOM states that consuming 3 to 6 mg of beta-carotene daily (equivalent to 833-1,667 IU vitamin A) will maintain blood levels of beta-carotene in the range associated with a lower risk of chronic diseases [1]. A diet that provides five or more servings of fruits and vegetables per day and includes some dark green and leafy vegetables and deep yellow or orange fruits should provide sufficient beta-carotene and other carotenoids.

When can vitamin A deficiency occur?

Vitamin A deficiency is common in developing countries but rarely seen in the United States. Approximately 250,000 to 500,000 malnourished children in the developing world go blind each year from a deficiency of vitamin A [1]. In the United States, vitamin A deficiency is most often associated with strict dietary restrictions and excess alcohol intake [21]. Severe zinc deficiency, which is also associated with strict dietary limitations, often accompanies vitamin A deficiency. Zinc is required to synthesize retinol binding protein (RBP) which transports vitamin A. Therefore, a deficiency in zinc limits the body's ability to mobilize vitamin A stores from the liver and transport vitamin A to body tissues [1].

Night blindness is one of the first signs of vitamin A deficiency. In ancient Egypt, it was known that night blindness could be cured by eating liver, which was later found to be a rich source the vitamin [2]. Vitamin A deficiency contributes to blindness by making the cornea very dry and damaging the retina and cornea [22].

Vitamin A deficiency diminishes the ability to fight infections. In countries where such deficiency is common and immunization programs are limited, millions of children die each year from complications of infectious diseases such as measles [23]. In vitamin A-deficient individuals, cells lining the lungs lose their ability to remove disease-causing microorganisms. This may contribute to the pneumonia associated with vitamin A deficiency [2,6-7].

There is increased interest in subclinical forms of vitamin A deficiency, described as low storage levels of vitamin A that do not cause overt deficiency symptoms. This mild degree of vitamin A deficiency may increase children's risk of developing respiratory and diarrheal infections, decrease growth rate, slow bone development, and decrease likelihood of survival from serious illness [24-25]. Children in the United States who are considered to be at increased risk for subclinical vitamin A deficiency include:
  • toddlers and preschool age children;
  • children living at or below the poverty level;
  • children with inadequate health care or immunizations;
  • children living in areas with known nutritional deficiencies;
  • recent immigrants or refugees from developing countries with high incidence of vitamin A deficiency or measles;
  • children with diseases of the pancreas, liver, or intestines, or with inadequate fat digestion or absorption.
A deficiency can occur when vitamin A is lost through chronic diarrhea and through an overall inadequate intake, as is often seen with protein-calorie malnutrition. Low blood retinol concentrations indicate depleted levels of vitamin A. This occurs with vitamin A deficiency but also can result from an inadequate intake of protein, calories, and zinc, since these nutrients are needed to make RBP [1]. Iron deficiency can also affect vitamin A metabolism, and iron supplements provided to iron-deficient individuals may improve vitamin A nutriture as well as iron status [1].

Excess alcohol intake depletes vitamin A stores. Also, diets high in alcohol often do not provide recommended amounts of vitamin A [1]. It is very important for people who consume excessive amounts of alcohol to include good sources of vitamin A in their diets. However, supplemental vitamin A may not be recommended for individuals who abuse alcohol because their livers may be more susceptible to potential toxicity from high doses of vitamin A [26]. A medical doctor would need to evaluate this situation and determine the need for supplemental vitamin A.

Who may need extra vitamin A to prevent a deficiency?

Vitamin A deficiency rarely occurs in the United States, but the World Health Organization (WHO) and the United Nations International Children's Emergency Fund (UNICEF) recommend vitamin A administration for all children diagnosed with measles in communities where vitamin A deficiency is a serious problem and where death from measles is greater than 1%. In 1994, the American Academy of Pediatrics recommended vitamin A supplementation for two subgroups of children likely to be at high risk for subclinical vitamin A deficiency: children 6 to 24 months of age hospitalized with measles and hospitalized children older than 6 months [27].

Fat malabsorption can result in diarrhea and prevent normal absorption of vitamin A. Over time this may result in vitamin A deficiency. Those conditions include:
  • Celiac disease:
    Often referred to as sprue, celiac disease is a genetic disorder. People with celiac disease are intolerant to a protein called gluten found in wheat and some other grains. In celiac disease, gluten can trigger damage to the small intestine, where most nutrient absorption occurs. Approximately 30% to 60% of people with celiac disease have gastrointestinal-motility disorders such as diarrhea [28].They need to follow a gluten-free diet to avoid malabsorption and other symptoms.
  • Crohn's disease:
    This inflammatory bowel disease affects the small intestine. People with Crohn's disease often experience diarrhea, fat malabsorption, and malnutrition [29].
  • Pancreatic disorders:
    These often result in fat malabsorption [30-31], since the pancreas secretes enzymes important for fat absorption. Without these enzymes, it is difficult to absorb fat. Many people with pancreatic disease take pancreatic enzymes in pill form to prevent fat malabsorption and diarrhea.
Healthy adults usually have a reserve of vitamin A stored in their livers and should not be at risk of deficiency during periods of temporary or short-term fat malabsorption. Long-term problems absorbing fat, however, may result in deficiency. In these instances physicians may recommend supplemental vitamin A [9].

Vegetarians who do not consume eggs and dairy foods need provitamin A carotenoids to meet their need for vitamin A [1]. They should include a minimum of five servings of fruits and vegetables in their daily diet and regularly choose dark green leafy vegetables and orange and yellow fruits to consume recommended amounts of vitamin A.

What are some current issues and controversies about vitamin A?

Vitamin A, beta carotene and cancer
Surveys suggest an association between diets rich in beta-carotene and vitamin A and a lower risk of many types of cancer [32]. A higher intake of green and yellow vegetables or other food sources of beta carotene and/or vitamin A may decrease the risk of lung cancer [2,33-34]. However, a number of studies that tested the role of beta-carotene supplements in cancer prevention did not find them to be protective. In the Alpha-Tocopherol Beta-Carotene (ATBC) Cancer Prevention Study, over 29,000 men who regularly smoked cigarettes were randomized to receive 20 mg beta-carotene alone, 50 mg alpha-tocopherol alone, supplements of both, or a placebo for 5 to 8 years. Incidence of lung cancer was 18% higher among men who took the beta-carotene supplement. Mortality was 8% greater in these men, as compared to those receiving other treatments or placebo [35]. Similar results were seen in the Carotene and Retinol Efficacy Trial (CARET), a lung cancer chemoprevention study that provided subjects with supplements of 30 mg beta-carotene and 25,000 IU retinyl palmitate (a form of vitamin A) or a placebo. This study was stopped after researchers discovered that subjects receiving beta-carotene had a 46% higher risk of dying from lung cancer [36-37].

The IOM states that "beta-carotene supplements are not advisable for the general population," although they also state that this advice "does not pertain to the possible use of supplemental beta-carotene as a provitamin A source for the prevention of vitamin A deficiency in populations with inadequate vitamin A nutriture" [1].

Vitamin A and osteoporosis
Osteoporosis, a disorder characterized by porous and weak bones, is a serious public health problem for more than 10 million Americans, 80% of whom are women. Another 18 million Americans have decreased bone density which precedes the development of osteoporosis. Many factors increase the risk for developing osteoporosis, including being female, thin, inactive, at advanced age, and having a family history of osteoporosis. An inadequate dietary intake of calcium, cigarette smoking, and excessive intake of alcohol also increase the risk [38-40].

Researchers are now examining a potential new risk factor for osteoporosis: an excess intake of vitamin A. Animal, human, and laboratory research suggests an association between greater vitamin A intake and weaker bones [40-41]. Worldwide, the highest incidence of osteoporosis occurs in northern Europe, a population with a high intake of vitamin A [42]. However, decreased biosynthesis of vitamin D associated with lower levels of sun exposure in this population may also contribute to this finding.

One small study of nine healthy individuals in Sweden found that the amount of vitamin A in one serving of liver may impair the ability of vitamin D to promote calcium absorption [43]. To further test the association between excess dietary intakes of vitamin A and increased risk for hip fractures, researchers in Sweden compared bone mineral density and retinol intake in approximately 250 women with a first hip fracture to 875 age-matched controls. They found that a dietary retinol intake greater than 1,500 mcg/day (more than twice the recommended intake for women) was associated with reduced bone mineral density and increased risk of hip fracture as compared to women who consumed less than 500 mcg/day [44].

This issue was also examined by researchers with the Nurses Health Study, who looked at the association between vitamin A intake and hip fractures in over 72,000 postmenopausal women. Women who consumed the most vitamin A in foods and supplements (greater than or equal to 3,000 mcg/day as retinol equivalents, which is over three times the recommended intake) had a significantly increased risk of experiencing a hip fracture as compared to those consuming the least amount (less than 1,250 mcg/day). The effect was lessened by use of estrogens. These observations raise questions about the effect of retinol because retinol intakes greater than 2,000 mcg/day were associated with an increased risk of hip fracture as compared to intakes less than 500 mcg [45].

A longitudinal study in more than 2,000 Swedish men compared blood levels of retinol to the incidence of fractures in men. The investigators found that the risk of fractures was greatest in men with the highest blood levels of retinol (greater than 75 mcg per deciliter [dL]). Men with blood retinol levels in the 99th percentile (greater than 103 mcg per dL) had an overall risk of fracture that exceeded the risk among men with lower levels of retinol by a factor of seven [46]. However, high vitamin A intake does not necessarily equate to high blood levels of retinol. Age, gender, hormones, and genetics also influence these levels. Researchers did not find any association between blood levels of beta-carotene and risk of hip fracture. Researchers' findings, which are consistent with the results of animal, in vitro (laboratory), and epidemiologic studies, suggest that intakes above the UL, or approximately two times that of the RDA for vitamin A, may pose subtle risks to bone health that require further investigation.

The Centers for Disease Control and Prevention (CDC) reviewed data from NHANES III (1988-94) to determine whether there was any association between bone mineral density and fasting blood levels of retinyl esters, a form of vitamin A [47]. No significant associations between blood levels of retinyl esters and bone mineral density in 5,800 subjects were found.

There is no evidence of an association between beta-carotene intake, especially from fruits and vegetables, and increased risk of osteoporosis. Current evidence points to a possible association with vitamin A as retinol only. If you have specific questions regarding your intake of vitamin A and risk of osteoporosis, discuss this information with your physician or other qualified healthcare practitioner to determine what's best for your personal health.

What are the health risks of too much vitamin A?

Hypervitaminosis A refers to high storage levels of vitamin A in the body that can lead to toxic symptoms. There are four major adverse effects of hypervitaminosis A: birth defects, liver abnormalities, reduced bone mineral density that may result in osteoporosis (see previous section), and central-nervous-system disorders [1,48-49].

Toxic symptoms can also arise after consuming very-large amounts of preformed vitamin A over a short period of time. Signs of acute toxicity include nausea and vomiting, headache, dizziness, blurred vision, and muscular uncoordination [1,48-49]. Although hypervitaminosis A can occur when large amounts of liver are regularly consumed, most cases result from taking excess amounts of the nutrient in supplements.

The IOM has established Tolerable Upper Intake Levels (ULs) for vitamin A that apply to healthy populations [1]. The UL was established to help prevent the risk of vitamin A toxicity. The risk of adverse health effects increases at intakes greater than the UL. The UL does not apply to malnourished individuals receiving vitamin A either periodically or through fortification programs as a means of preventing vitamin A deficiency. It also does not apply to individuals being treated with vitamin A by medical doctors for diseases such as retinitis pigmentosa.

Table 5: Tolerable Upper Intake Levels (ULs) for retinol
(2,000 IU)
(2,000 IU)
(3,000 IU)
9-131,700 (5610 IU)
14-182,800 (9,240 IU)2,800 (9,240 IU)2,800 (9,240 IU)2,800 (9,240 IU)
19+3,000 (10,000 IU)3,000 (10,000 IU)3,000 (10,000 IU)3,000 (10,000 IU)

Retinoids are compounds that are chemically similar to vitamin A. Over the past 15 years, synthetic retinoids have been prescribed for acne, psoriasis, and other skin disorders [50]. Isotretinoin (Roaccutane® or Accutane®) is considered an effective anti-acne therapy. At very high doses, however, it can be toxic, which is why this medication is usually saved for the most severe forms of acne [51-53]. The most serious consequence of this medication is birth defects. It is extremely important for sexually active females who may become pregnant and who take these medications to use an effective method of birth control. Women of childbearing age who take these medications are advised to undergo monthly pregnancy tests to make sure they are not pregnant.

What are the health risks of too many carotenoids?

Provitamin A carotenoids such as beta-carotene are generally considered safe because they are not associated with specific adverse health effects. Their conversion to vitamin A decreases when body stores are full. A high intake of provitamin A carotenoids can turn the skin yellow, but this is not considered dangerous to health.

Recent clinical trials that associated beta-carotene supplements with a greater incidence of lung cancer and death in current smokers raise concerns about the effects of beta-carotene supplements on long-term health. However, conflicting studies make it difficult to interpret the health risk. For example, the Physicians Health Study compared the effects of taking 50 mg beta-carotene every other day to a placebo in over 22,000 male physicians and found no adverse health effects [54]. Also, a trial that tested the ability of four different nutrient combinations to inhibit the development of esophageal and gastric cancers in 30,000 men and women in China suggested that after five years those participants who took a combination of beta-carotene, selenium, and vitamin E had a 13% reduction in cancer deaths [55]. One point to consider is that there may be a relationship between alcohol and beta-carotene because men who consumed more than 11 grams/day of alcohol (approximately one drink per day) were more likely to show an adverse response to beta-carotene supplementation in one lung cancer trial [1].

The IOM did not set ULs for carotene or other carotenoids. Instead, it concluded that beta-carotene supplements are not advisable for the general population. As stated earlier, however, they may be appropriate as a provitamin A source for the prevention of vitamin A deficiency in specific populations [1].

Vitamin A intakes and healthful diets

According to the 2005 Dietary Guidelines for Americans, "Nutrient needs should be met primarily through consuming foods. Foods provide an array of nutrients and other compounds that may have beneficial effects on health. In certain cases, fortified foods and dietary supplements may be useful sources of one or more nutrients that otherwise might be consumed in less than recommended amounts. However, dietary supplements, while recommended in some cases, cannot replace a healthful diet [56]." For more information about building a healthful diet, refer to the Dietary Guidelines for Americans ( and the U.S. Department of Agriculture's food guidance system (My Pyramid;
  1. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press, Washington, DC, 2001.
  2. Gerster H. Vitamin A-functions, dietary requirements and safety in humans. Int J Vitam Nutr Res 1997;67:71-90. [PubMed abstract]
  3. Futoryan T, Gilchrest BE. Retinoids and the skin. Nutr Rev 1994;52:299-310. [PubMed abstract]
  4. Hinds TS, West WL, Knight EM. Carotenoids and retinoids: A review of research, clinical, and public health applications. J Clin Pharmacol 1997;37:551-8. [PubMed abstract]
  5. Ross AC, Gardner EM. The function of vitamin A in cellular growth and differentiation, and its roles during pregnancy and lactation. Adv Exp Med Biol 1994;352:187-200. [PubMed abstract]
  6. Ross AC. Vitamin A and retinoids. In: Modern Nutrition in Health and Disease. 9th Edition (edited by Shils ME, Olson J, Shike M, Ross AC). Lippincott Williams and Wilkins, New York, 1999, pp. 305-27.
  7. Ross AC, Stephensen CB. Vitamin A and retinoids in antiviral responses. FASEB J 1996;10:979-85. [PubMed abstract]
  8. Semba RD. The role of vitamin A and related retinoids in immune function. Nutr Rev 1998;56:S38-48. [PubMed abstract]
  9. Ross DA. Vitamin A and public health: Challenges for the next decade. Proc Nutr Soc 1998;57:159-65. [PubMed abstract]
  10. Harbige LS. Nutrition and immunity with emphasis on infection and autoimmune disease. Nutr Health 1996;10:285-312. [PubMed abstract]
  11. de Pee S, West CE. Dietary carotenoids and their role in combating vitamin A deficiency: A review of the literature. Eur J Clin Nutr 1996;50 Suppl 3:S38-53. [PubMed abstract]
  12. Bendich A, Olson JA. Biological actions of carotenoids. FASEB J 1989:3;1927-32 [PubMed abstract]
  13. Olson JA, Kobayashi S. Antioxidants in health and disease: Overview. Proc Soc Exp Biol Med 1992;200:245-7. [PubMed abstract]
  14. Olson JA. Benefits and liabilities of vitamin A and carotenoids. J Nutr 1996;126:1208S-12S. [PubMed abstract]
  15. Pavia SA, Russell RM. Beta-carotene and other carotenoids as antioxidants. J Am Coll Nutr 1999;18:426-33. [PubMed abstract]
  16. Guthrie HA, Picciano MF. Human Nutrition. Mosby, St. Louis, MO, 1995.
  17. Harrison EH. Mechanisms of digestion and absorption of dietary vitamin A. Annu Rev Nutr 2005;25:5.1-5.18.
  18. U.S. Department of Agriculture, Agricultural Research Service. 2004. USDA National Nutrient Database for Standard Reference, Release 17. Nutrient Data Laboratory Home Page,
  19. Bialostosky K, Wright JD, Kennedy-Stephenson J, McDowell M, Johnson CL. Dietary Intake of Macronutrients, Micronutrients, and Other Dietary Constituents: United States 1988-94. Vital and Health Statistics 2002;11(245):6-99. US Department of Agriculture, Agricultural Research Service, 2004.
  20. U.S. Department of Health and Human Services. Advance Data from Vital and Health Statistics. Dietary Intake of Selected Vitamins for the United States Population: 1999-2000. Centers for Disease Control and Prevention. National Center for Health Statistics. Number 339, 2004.
  21. Rodrigues MI, Dohlman CH. Blindness in an American boy caused by unrecognized vitamin A deficiency. Arch Ophthalmol 2004;122:1228-9.
  22. Sommer A. Nutritional Blindness: Xeropthalmia and Keratomalacia. Oxford University Press, London and New York, 1982.
  23. Ross AC. Vitamin A status: Relationship to immunity and the antibody. Proc Soc Exp Biol Med 1992;200:303-20. [PubMed abstract]
  24. Stephens D, Jackson PL, Gutierrez Y. Subclinical vitamin A deficiency: A potentially unrecognized problem in the United States. Pediatr Nurs 1996;22:377-89. [PubMed abstract]
  25. Butler JC, Havens PL, Sowell AL, Huff DL, Peterson DE, Day SE, Chusid MJ, Benning RA, Circo R, Davis JP. Measles severity and serum retinol (vitamin A) concentration among children in the United States. Pediatrics 1993;91:1176-81. [PubMed abstract]
  26. Leo MA, Lieber CS. Alcohol, vitamin A, and beta-carotene: Adverse interactions, including hepatotoxicity and carcinogenicity. Am J Clin Nutr 1999;69:1071-85. [PubMed abstract]
  27. Committee on Infectious Diseases. Vitamin A treatment of measles. Pediatrics 1993;91:1014-5. [PubMed abstract]
  28. Tursi A. Gastrointestinal motility disturbances in celiac disease. J Clin Gastroenterol 2004;38:642-5.
  29. Krok KL, Lichtenstein GR. Nutrition in Crohns disease. Curr Opin Gastroenterol 2003;19:148-53.
  30. Kiehne K, Gunther R, Folsch U. Malnutrition, steatorrhoea and pancreatic head tumour. Eur J Gastroenterol Hepatol 2004;16:711-3.
  31. Bell CS, Shepherd RW. Editorial: Optimising nutrition in cystic fibrosis. J Cyst Fibros 2002;1:47-50.
  32. Fontham ETH. Protective dietary factors and lung cancer. Int J Epidemiol 1990;19:S32-S42. [PubMed abstract]
  33. Koo LC. Diet and lung cancer 20+ years later: more questions than answers? Int J Cancer 1997;Suppl10:22-9. [PubMed abstract]
  34. Rock CL, Jacob RA, Bowen PE. Update on the biological characteristics of the antioxidant micronutrients: Vitamin C, vitamin E, and the carotenoids. J Am Diet Assoc 1996;96:693-702. [PubMed abstract]
  35. Albanes D, Heinonen OP, Taylor PR, Virtamo J, Edwards BK, Rautalahti M, Hartman AM, Palmgren J, Freedman LS, Haapakoski J, Barrett MJ, Pietinen P, Malila N, Tala E, Lippo K, Salomaa ER, Tangrea JA, Teppo L, Askin FB, Taskinen E, Erozan Y, Greenwald P, Huttunen JK. Alpha-tocopherol and beta-carotene supplement and lung cancer incidence in the alpha-tocopherol, beta-carotene cancer prevention study: Effects of base-line characteristics and study compliance. J Natl Cancer Inst 1996;88:1560-70. [PubMed abstract]
  36. Redlich CA, Blaner WS, Van Bennekum AM, Chung JS, Clever SL, Holm CT, Cullen MR. Effect of supplementation with beta-carotene and vitamin A on lung nutrient levels. Cancer Epidemiol Biomarkers Prev 1998;7:211-14. [PubMed abstract]
  37. Pryor WA, Stahl W, Rock CL. Beta carotene: from biochemistry to clinical trials. Nutr Rev 2000;58:39-53.
  38. National Institutes of Health. Osteoporosis prevention, diagnosis, and therapy. NIH Consensus Statement Online, 2000 March 27-29, 2000:1-36.
  39. National Osteoporosis Foundation. NOF osteoporosis prevention-risk factors for osteoporosis. 2003.
  40. Binkley N, Krueger D. Hypervitaminosis A and bone. Nutr Rev 2000;58:138-44. [PubMed abstract]
  41. Forsyth KS, Watson RR, Gensler HL. Osteotoxicity after chronic dietary administration of 13-cis-retinoic acid, retinyl palmitate or selenium in mice exposed to tumor initiation and promotion. Life Sci 1989;45:2149-56. [PubMed abstract]
  42. Whiting SJ, Lemke B. Excess retinol intake may explain the high incidence of osteoporosis in northern Europe. Nutr Rev 1999;57:249-50. [PubMed abstract]
  43. Johansson S, Melhus H. Vitamin A antagonizes calcium response to vitamin D in man. J Bone Miner Res 2001;16:1899-1905. [PubMed abstract]
  44. Melhus H, Michaelsson K, Kindmark A, Bergstrom R, Holmberg L, Mallmin H, Wolk A, Ljunghall S. Excessive dietary intake of vitamin A is associated with reduced bone mineral density and increased risk of hip fracture. Ann Intern Med 1998;129:770-8. [PubMed abstract]
  45. Feskanich D, Singh F, Willett WC, Colditz GA. Vitamin A intake and hip fractures among postmenopausal women. J Am Med Assoc 2002;287:47-54. [PubMed abstract]
  46. Michaelsson K, Lithell H, Vessby B, Mehus H. Serum retinol levels and the risk of fracture. N Engl J Med 2003;348:287-94.
  47. Ballew C, Galuska D, Gillespie C. High serum retinyl esters are not associated with reduced bone mineral density in the third National Health and Nutrition Examination Survey, 1988-94. J Bone Miner Res 2001;16:2306-12. [PubMed abstract]
  48. Bendich A, Langseth L. Safety of vitamin A. Am J Clin Nutr 1989;49:358-71. [PubMed abstract]
  49. Udall JN, Greene HL. Vitamin update. Pediatr Rev 1992;13:185-94. [PubMed abstract]
  50. Soprano DR, Soprano KJ. Retinoids as teratogens. Annu Rev Nutr 1995;15:111-32. [PubMed abstract]
  51. Orafanos CE, Zouboulis CC, Almond-Roesler B, Geilen CC. Current use and future potential role of retinoids in dermatology. Drugs 1997;53:358-88. [PubMed abstract]
  52. Meigel WN. How safe is oral isotretinoin? Dermatology 1997;195:22-28, 38-40. [PubMed abstract]
  53. Hathcock JN. Vitamin and Mineral Safety. Council for Responsible Nutrition, Washington, DC, 1997, pp. 26-27.
  54. Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, Belanger C, LaMotte F, Gaziano JM, Ridker PM, Willett W, Peto R. Lack of effect of long-term supplementation with beta-carotene on the incidence of malignant neoplasm and cardiovascular disease. N Eng J Med 1996;334:1145-9. [PubMed abstract]
  55. Blot WJ, Li J-Y, Taylor PR, Guo W, Dawsey S, Wang G-Q, Yang CS, Zheng S-F, Gail M, Li G-Y, Yu Y, Liu B-Q, Tangrea J, Sun Y-H, Liu F, Fraumeni JF, Zhang Y-H, Li B. Nutrition intervention trials in Linxian, China: supplementation with specific vitamin/mineral combinations, cancer incidence, and disease-specific mortality in the general population. J Natl Cancer Inst 1993;85:1483-92. [PubMed abstract]
  56. U.S. Department of Health and Human Services, U.S. Department of Agriculture. Dietary Guidelines for Americans 2005. Washington, DC: U.S. Government Printing Office, 2005.
  57. U.S. Department of Agriculture. 2005.

Do You Yahoo!? La mejor conexión a Internet y 2GB extra a tu correo por $100 al mes.

Experta asegura que el tipo grasa ingerida determinante desarrollo obesidad

Experta dice tipo grasa ingerida determinante desarrollo obesidad

Un estudio realizado por la investigadora de la Universidad de Navarra Patricia Pérez Matute concluye que el tipo de grasa ingerida resulta determinante en el desarrollo o prevención de la obesidad.

El trabajo, fruto de una tesis doctoral, ha sido distinguido con el 'Premio del Centro de Información de Cerveza y Salud I' que otorga la Real Academia de Doctores de España, según informó hoy en un comunicado la Universidad de Navarra.

La tesis, que forma parte de la línea especial de investigación 'Nutrición, Salud y Obesidad' del departamento de Fisiología y Nutrición de la Facultad de Farmacia, señala que no todas las grasas de la dieta afectan de igual manera al organismo ni todas hacen engordar de la misma forma a quién las ingiere.

En este sentido, la investigación se ha basado en el conocimiento de que la ingesta de grasas saturadas (como las presentes en bollería o embutidos) parece inducir el desarrollo de obesidad, mientras que los ácidos grasos poliinsaturados de la familia de los Omega-3 (pescado azul como el salmón y atún) parecen prevenir y mejorar tanto la obesidad como la resistencia insulínica.

Para llevar a cabo el estudio, el primer objetivo fue determinar los efectos de varios ácidos grasos de la dieta sobre la producción de una hormona (leptina) producida por células de la grasa (adipocitos) que está implicada en el control del peso corporal, según dichas fuentes que precisaron que también se estudiaron las acciones de la administración oral en ratas de uno de los ácidos grasos Omega-3 de la dieta, el llamado 'EPA'.

A pesar de los resultados obtenidos, Pérez Matute advierte que antes de incluir determinados ingredientes en los alimentos por considerarlos beneficiosos para la salud, 'se deben realizar un gran número de estudios en humanos para descartar posibles efectos secundarios derivados de la ingesta de dichas sustancias'.

En 2004, la revista Clinical Science distinguió la investigación de una parte de su estudio, titulado 'Papel de la grasa de la dieta en la regulación de la leptina y otros genes implicados en el control del peso', durante un congreso internacional que tuvo lugar en Brighton (Inglaterra).

Terra Actualidad - EFE

Do You Yahoo!? La mejor conexión a Internet y 2GB extra a tu correo por $100 al mes.

miércoles, enero 25, 2006


La preocupación excesiva por la dieta sana puede convertirse en un indicador de ortorexia.

La preocupación excesiva por la dieta sana puede convertirse en un indicador de ortorexia.

Divulgación Científica

Ortorexia: preocupación patológica por la dieta sana

La presión social podría conducir, en algunos casos, a la presencia de ortorexia.
El siglo XXI ha dado paso a nuevos trastornos alimenticios dentro de los cuales se encuentra la ortorexia, una patología que se caracteriza por la obsesión de un individuo por la comida sana. Aunque por el momento no se ha determinado el abordaje óptimo de esta condición, psiquiatras y endocrinos siguen trabajando en esta cuestión.

· J. Manzarbeitia - 13/01/2006

Los trastornos nutricionales, como anorexia, bulimia u obesidad, se han convertido en un problema sanitario real del siglo XXI. Un nuevo concepto, la ortorexia ha pasado recientemente a formar parte de estos trastornos en el hábito nutricional y constituye uno de los procesos que han despertado el interés de los grupos de psiquiatras y endocrinos.

El concepto de ortorexia ha sido introducido por el Dr. Bratman y consiste en la preocupación excesiva por la dieta sana, de tal modo que llega a convertirse en obsesión.

Trastornos diferentes

A diferencia de la anorexia nerviosa, la persona que sufre ortorexia no está preocupada por el sobrepeso, ni tienen una percepción errónea de su aspecto físico, sino que su preocupación se centra en mantener una dieta equilibrada y sana.

En muchos casos, la ortorexia se convierte en un estilo de vida; la obsesión por la comida sana puede llegar a interferir con las actividades rutinarias de la vida diaria, las relaciones interpersonales e, incluso, puede poner en peligro la integridad física.

Según el Dr. Bratman si una persona nunca toma algo sin preguntarte si es sano, si la dieta le ha llevado a cierto aislamiento social o ha disminuido su peso debido al control dietético estricto se debe solicitar una valoración por el médico para confirmar el padecimiento de ortorexia.


Para algunos autores, se puede clasificar como un trastorno obsesivo - compulsivo y, aunque son necesarios trabajos de investigación para determinar las causas de esta enfermedad, ya se ha postulado el posible origen genético.

Para otros autores, la ortorexia está claramente influencia por presiones sociales, al igual que la anorexia y la bulimia, trastornos estos ocasionados por el culto al cuerpo perfecto. Pesikoff afirma que la ortorexia es un trastorno característico de las personas de clase alta, porque los productos dietéticos orgánicos son caros y no toda la población puede tener acceso a ellos.

El tratamiento de las personas que sufren ortorexia no está claro: debe ser una terapia dual, combinando el tratamiento psiquiátrico con el farmacológico; según los especialistas, es difícil que las personas obsesionadas por los productos naturales acepten tomar los preparados farmacéuticos.

Lic. Nut.Miguel Leopoldo Alvarado Saldaña

Fundación ProSalud A. C. Seattle Washington.

Correo Yahoo!
Espacio para todos tus mensajes, antivirus y antispam ¡gratis!
Regístrate ya -


Volver al INICIO

El huevo tiene una enorme riqueza nutricional, y su inclusión en la dieta presenta, por ello, un gran interés en cuanto a beneficios nutricionales y sanitarios1,2,3. Sin embargo, en la década de los setenta comenzó a extenderse en todo el mundo un exagerado temor al colesterol, por su implicación en el riesgo de padecer enfermedades cardiovasculares. El huevo, como alimento de elevado contenido en colesterol, comenzó a ser denostado y su consumo a decrecer considerablemente en los países occidentales2.

Posteriormente, los estudios realizados sobre el tema han puesto de relieve que sólo un 20% de la población responde con elevaciones de colesterol plasmático a ingestas relativamente elevadas de colesterol dietético. Causas genéticas, y otros factores como el transito intestinal rápido o lento, el sedentarismo y la obesidad pueden influir también en la modificación de la colesterolemia. Por otra parte, otros componentes de la dieta como la ingesta de fibra, los fitoesteroles y otros esteroles de la fauna marina pueden interferir en la absorción del colesterol.

Los resultados de los estudios en epidemiología nutricional realizados en los últimos años indican la débil elevación del colesterol plasmático con los cambios del colesterol dietético2,4.

Concretamente el mayor estudio epidemiológico realizado (con 118.000 varones y mujeres) para analizar la relación entre consumo de huevos y padecimiento de enfermedades cardiovasculares puso de relieve que el consumo de hasta un huevo por día no tenía un impacto significativo en la mortalidad por este tipo de procesos4. En tres grupos de jóvenes sanos se evaluó el efecto del consumo de 3, 7 y 14 huevos semanales. Después de 5 meses de dieta controlada, no hubo diferencias significativas en los lípidos plasmáticos5.

El mismo ensayo llevado a cabo en adultos sanos, con adicción de 2 huevos/día a su dieta habitual, puso de relieve que a las 6 semanas el colesterol HDL había aumentado un 10%, el colesterol total un 4% y la relación colesterol total / HDL-colesterol no se había modificado6. Por otra parte, el estudio de Kerver et al.7 puso de relieve que las personas que tomaban más de cuatro huevos por semana tenían cifras inferiores de colesterol sérico que los que consumían uno (o menos) huevos por semana.

Por tanto la preocupación acerca del colesterol del huevo es una cuestión que está ya superada a la luz de las recientes investigaciones. La evidencia de que el consumo de huevos no está relacionado con el incremento del riesgo cardiovascular es una de las conclusiones que se desprenden de los resultados del trabajo desarrollado por el equipo del profesor Sung I. Koo, del Departamento de Nutrición Humana de la Universidad de Kansas (Estados Unidos) sobre los efectos positivos de la lecitina o fosfatidilcolina presente en la yema del huevo, que además de ser una excelente fuente de colina y actúar en el desarrollo de la función cerebral y la memoria, limita la absorción del colesterol que contiene el huevo. Los resultados muestran la primera evidencia científica de que la fosfatidilcolina de la yema de huevo reduce de forma significativa la absorción intestinal de colesterol 8.

Recientes investigaciones ponen de relieve que los huevos son fuente de carotenoides (luteina, zeaxantina) facilmente disponibles, y que estos componentes antioxidantes pueden ayudar en la prevención de la degeneración macular y contribuir a retrasar la aparición de cataratas9.

Las restricciones en el consumo de huevos y la consideración de este alimento como peligroso por su contenido en colesterol, no están avaladas por los numerosos y exhaustivos estudios científicos realizados en las dos últimas décadas2. Para reducir el riesgo cardiovascular, es mucho más importante limitar la ingesta de grasas totales y saturadas, combatir la obesidad y modificar los estilos de vida característicos de sociedades occidentales, especialmente el sedentarismo10.

Ver citas bibliográficas

Apdo. Correos 3.383 - 28080 Madrid
Tel: 34-91- 534 32 65 Fax: 34-91- 534 32 65

Lic. Nut.Miguel Leopoldo Alvarado Saldaña

Fundación ProSalud A. C. Seattle Washington.



Es un Blog de Nutri-Tips, Gaceta Oficial de ProSalud A. C. / O. N. G.
(Organización Mundial de Salud y Nutriologia Ortomolecular.
Fundación sin fines de lucro para la promoción de la salud por metidos naturales.

Los Sitios Web, Foros de Internet Blogs de ProSalud A. C. y su contenido son propiedad de Editorial DHIA (Editorial Digital Hispano-Americana).Diseñador, Editor y Administrador del Web: Lic. Nut. Miguel Leopoldo Alvarado
Correo electrónico:
El Sitio Web: