Vitamin A-rich foods include milk, cheese, butter, eggs, liver, and some fish, including herring, sardines, and tuna. Shark, halibut, and polar bear liver oils are exceptionally high in vitamin A. Spinach, carrots, papaya, oranges, sweet potatoes, and cantaloupes are all excellent sources of pre-vitamin A. Vegetable oils, white lard, white corn, grains, meat, and legumes are not good sources of vitamin A or pre-vitamin A.
Milk 2% (8 fl oz) — 500 IU; Cream Cheese (1 oz) — 405 IU; Cheddar Cheese (3.5 oz) — 1059 IU; 1 medium boiled egg (280 IU); 1 medium scrambled egg (420 IU); 3.5 ounces of beef braised liver (35679 IU); 3.5 ounces of veal braised liver (26883 IU); 3.5 ounces of herring (
Vitamin A is fat-soluble, according to its biochemistry. Retinol, retinol, retinoic acid, and b-carotene are all forms of vitamin A. Retinyl esters are the predominant form of vitamin A in foods of animal origin, such as eggs, milk, butter, and liver. Retinol that has been esterified with a fatty acid like palmitic acid is called a retinyl ester. Retinol’s hydroxyl group has bonded with the fatty acid. While plants don’t have vitamin A, they have plenty of pre-vitamin A compounds. A group of chemicals known as carotenoids is a precursor to vitamin A. Although there are more than 500 different carotenoids, only roughly 50 can be converted into vitamin A. All-trans b-carotene is the most crucial. To emphasize that all double bonds are in the trans conformation rather than the cis conformation, the prefix all-trans is used for the compound name. Carotenoids are abundant in dark green, orange, and yellow vegetables. Cryptoxanthin and a-carotene are two more types of pre-vitamin A. Mammals cannot convert all carotenoids to vitamin A. Lutein, lycopene, and canthaxanthin are some examples.
Epithelial cell support (for healthy lungs and trachea), embryonic testicular development and vigor, and eye health are just a few of vitamin A’s many uses. Only the first function can be supported by retinoic acid in the diet. The liver is unable to accumulate retinoic acid. It is possible to convert between retinal, retinyl esters, and retinol. Retinoic acid is produced when the retina is oxidized. Dietary retinyl esters, retinol, or retinal can help with all three vitamin A roles. Retinoic acid can be synthesized from these precursors, but retinal cannot be synthesized from retinoic acid. Retinoic acid and topical tretinoin are helpful treatments for various dermatological conditions.
In the United States, people at risk for vitamin A deficiency include those with conditions like irritable bowel syndrome, cancer, malaria, pneumonia, and anorexia. Patients with appendectomy, burns, cirrhosis, or biliary blockage have an elevated need for this vitamin. Excretion rates may rise under stress. A lack of zinc and protein can impair transport. Those with prematurity, CF, or rheumatic fever are also at a higher risk.
Night blindness is the first indication of vitamin A insufficiency, which can progress to corneal ulceration, Bitot’s spots, and ultimately blindness if left untreated. Other symptoms include bone thickening, lung edema, epithelium keratinization, hearing loss, urinary calculi, and salivary gland keratinization. Males eventually stop producing sperm. Women reabsorb fetuses.
Ingesting large amounts of preformed vitamin A is associated with numerous health risks. Liver damage and potential birth abnormalities may result from chronic exposure to 7,500-15,000 mg performed retinol equivalents (RE) daily. Those between 18 and 54 can safely consume 7,500 RE (25,000 IU) daily for an extended period. It took six years of use before it became harmful to the liver. One case of toxicity at doses as low as 1,500–3,000 mgm (5,000–10,000IU) has been reported. Still, these findings cannot be replicated and run counter to the great majority of the medical literature. There is no evidence that individuals, including pregnant women and the elderly, should avoid supplements containing 3,000 mg RE (10,000 IU).
Even when beta-carotene is consumed in large quantities, there is no evidence that the conversion to vitamin A leads to vitamin A toxicity. Hypercarotenemia-related skin discoloration has been the only well-documented risk associated with high beta-carotene consumption. Lung cancer and beta-carotene will be examined further on. Two studies, the ATBC trial and the CARET, out of the many published on beta-carotene, suggest the supplement may have adverse side effects. Beta-carotene is safe, according to the available data.
The skin becomes dry and pruritic in the early stages of chronic hypervitaminosis, the liver gets enlarged and cirrhotic, and the nervous system, where an increase in intracranial tension resembles the symptoms of a brain tumor. Congenital abnormalities such as premature skeletal growth and temporary hydrocephalus have been linked to maternal hypervitaminosis. Other symptoms include anorexia, vomiting, hair loss, nystagmus, gingivitis, glossitis, lymph node enlargement, and a prolonged clotting time. Women of childbearing should not use isotretinoin unless they have disfiguring acne that no other treatment has helped. Long-term usage of isotretinoin causes hyperlipidemia. Neurotoxicity from vitamins is a possible side effect of hypervitaminosis. Headaches, pseudotumor cerebri, and embryotoxic
consequences have all been recorded in patients who were administered vitamin A analogs or retinoids, all closely related to hypervitaminosis’s neurological symptoms. The central nervous system (CNS) is more permeable to vitamin A and its analogs than any other vitamin, and retinoids have numerous impacts on enzyme activity and gene expression, making vitamin A neurotoxicity more likely than any other vitamin. An overdose of vitamins can induce harm that looks like illness. After 49 months of observation, retinol consumption was associated with increased alkaline phosphatase activity of 7%, triacylglycerol activity of 11%, total cholesterol activity of 3%, and high-density lipoprotein activity of 1%. Both retinol (in the amount of 7,576 RE, or 25,000 IU) and a placebo were given to the subjects regularly. Long-term intake of 7,576 RE vitamin A should be regarded with caution due to reports linking a 1% increase in cholesterol concentrations to a 2% increase in the risk of coronary artery disease.
Too much vitamin A in the diet has been linked to an increased risk of osteoporosis. Bone density decreased by 6%, and the risk of hip fracture increased by 100%, according to two studies, when participants consumed more than 1.5 mg of vitamin A daily. This vitamin weakens bones by increasing their resorption rate when there is excess in the body.
According to a single epidemiological investigation, reproduction, and development cannot occur without vitamin A. Malformations have been linked to supplement doses greater than 10,000 IU/d. There is no evidence of teratogenicity at doses up to 30,000 IU/d in nonhuman primates. Pregnant women in industrialized countries or those with otherwise nutritionally adequate diets may not need to ingest more than the Recommended Dietary Allowance of preformed vitamin A as supplements (2670 IU or 800 RE/d), even though no study has reported adverse effects of this dose. Multiple animal studies show only a very low danger if vitamin A doses up to 30,000 IU/d (9,000 g RE/d) occur inadvertently during pregnancy. Numerous species exposed to extremely high dosages of beta-carotene showed no signs of teratogenicity or vitamin A toxicity.
Vitamin A overdose is a potential concern for the elderly who take vitamin A supplements. Long-term vitamin A supplement use (>5y) was linked to higher fasting plasma retinyl esters and biochemical evidence of liver damage. Elderly people showed a 2.5-fold rise in plasma retinyl esters compared to non-users for vitamin supplement intakes between 5,001 and 10,000 IU/d, whereas young adults showed a 1.5-fold increase.
Both ethanol and retinol can be converted to their respective aldehydes in vitro using alcohol and other dehydrogenase isozymes. In hepatic microsomes, new retinol metabolism routes have been discovered; these pathways involve cytochrome P450s. Given the overlapping metabolic pathways involved, multiple interactions between retinol, ethanol, and other medications should be no surprise. Consumption of retinoids and carotenoids is reduced, and the breakdown of retinol is sped up due to the cross-induction of degradative enzymes when one consumes alcohol or drugs chronically. Deficiency leads to hepatic and extrahepatic disease, such as carcinogenesis and fetal defect. Vitamin A supplements are advised for treating vitamin A deficiency. Retinol’s inherent hepatotoxicity is exacerbated by alcohol use, adding another layer of complexity. The combination of beta-carotene with ethanol causes hepatotoxicity; until recently, beta-carotene was thought to be harmless. Beta-carotene supplements may also increase the risk of cardiovascular disease in heavy drinkers and smokers. Ethanol causes vitamin A deficiency and increases the toxicity of vitamin A and beta-carotene. Treatments intended to restore vitamin A levels in alcoholics must account for the diminished effectiveness of retinol and beta-carotene due to alcohol consumption.
Patients with vitamin A deficiency are treated with retinol or retinyl esters. Vitamin A has a recommended daily allowance of 1 milligram of retinol. Vitamin A’s biological activity is measured in international units (IU) to compare different vitamin A types.
James Goodwin discusses carotenoids and cancer. He argues that studies linking carotenoids to a reduced risk of lung cancer are the most robust of any study between antioxidants and cancer. According to research, consumption of dark green and yellow vegetables is inversely related to the chance of developing lung cancer. Higher overall vitamin A intake, especially from vegetable sources, was associated with a reduced risk of lung cancer (particularly squamous cell carcinoma) in one research. Carotenoids were found to have a protective effect in men at all cigarette smoking levels in the Western Electric Study. Those in the lowest carotene intake quartile at baseline had a sevenfold increased chance of developing lung cancer.
The preventive effect of beta-carotene on lung cancer has been controversially studied. The ATBC Cancer Prevention Study, which examined the impact of antioxidant supplementation, found that smokers taking beta-carotene supplements had a considerably higher risk of developing lung cancer. The CARET trial of asbestos workers reached the same conclusion. In the ATBC and CARET studies, participants were given 20 and 30 milligrams daily. However, CARET found some evidence that beta-carotene might help ex-smokers avoid developing lung cancer. The longer-term PHS experiment showed no higher risk in contrast to these other trials.
Some have hypothesized that the negative results seen in the CARET and ATBC trials can be attributed to the hepatotoxic effects of alcohol or excessive retinal consumption. For beta-carotene to have a beneficial impact, substantial contemporaneous smoking is a prerequisite. Beta-carotene treatment reduces, rather than increases, lung cancer rates in ex-smokers, whose tissues would have been exposed to specific mutagenic and carcinogenic effects of cigarette smoke.
Cancers of the breast, esophagus, cervix, pancreas, and colon have all shown promise for treatment by carotenoids, according to research. ACCORDING TO ANOTHER STUDY, vitamin A supplementation has been shown to reduce the incidence of breast cancer by around half in women with inadequate vitamin A intake. A nutrition study in Linxian, China, found that supplementation with retinol and zinc might protect against the development of gastric neoplasia in people younger than 65.[28] Carotenoid consumption also appeared to reduce the risk of bladder cancer in people younger than 65.
Smokers who took a Cis-retinoic acid supplement had a lower risk of developing squamous cell carcinoma of the head and neck, and those who took a beta-carotene supplement had their oral leukoplakia improve.[28,29] Beta-carotene was also inversely related to the growth of thyroid cancer.
There is no positive or negative effect on heart disease or cancer prevention in women who use beta-carotene supplements for two years. The authors state that those who consume many beta-carotene-rich fruits and vegetables have reduced cancer chances.
According to Dr. Dutta’s findings, beta-carotene supplementation increases a protective protein called heat shock protein (HSP-70) in individuals with Barrett’s esophagus. Dr. Dutta has previously shown that supplementing with beta-carotene alleviates these individuals’ burning feelings. In vitro, studies have also demonstrated that beta-carotene can kill cancer cells.
Long-term vitamin C supplementation and dietary carotenoids were found to reduce cataract risk.
Tomatoes and tomato derivatives are a good source of lycopene. Some forms of cancer may be protected by eating foods rich in lycopene. Lycopene’s protective benefits may result from several different pathways. Lycopene metabolism is poorly understood. Lycopene oxidation metabolites with potential biological activity have been detected in human plasma. Tomatoes contain beneficial antioxidants, some of which are released during cooking. Nutritional and health studies have found that monounsaturated oils like olive and canola oil improve lycopene absorption. According to a study, consuming 70–75 mg/d of lycopene can enhance plasma concentrations needed to improve human health.
It was concluded that eating tomato-based items would lessen lymphocyte DNA’s sensitivity to oxidative damage.
The chance of developing prostate cancer may decrease if you eat dishes made with tomatoes. Prostate cancer and aggressive prostate cancer were both correlated negatively with lycopene consumption. According to several observational studies, there may be no protective impact of lycopene on the risk of prostate cancer.
All tumors were similarly protected against in the studies. Raw tomatoes may have a favorable effect on this population because they are the single most distinctive aspect of the Mediterranean diet. Lycopene is effective against lung neoplasia and bladder cancer in animal experiments.
Complications of diabetes are made worse by elevated levels of free radical activity and lipid oxidation, which reduce glucose clearance in peripheral tissues. Beta-carotene’s ability to scavenge peroxyl radicals and display substantial antioxidant activity, thanks to its extensive system of conjugated double bonds, suggests a preventive impact against the development of type 2 DM. The risk of developing type 2 diabetes can be reduced by eating more vegetables high in carotenoids, according to several studies. Type 2 diabetes is less common, given a diet higher in vegetables. Substances other than beta-carotene are likely responsible for the risk decrease associated with carotenoid-rich veggies. Beta-carotene supplementation for an average of 12 years did not reduce the risk of type 2 diabetes. A lower plasma beta-carotene concentration was associated with a higher incidence of diabetes in a study of hemodialysis patients. The chance of developing type 2 diabetes was lowered by 55% in a study comparing blood beta-carotene and risk. However, this link was considerably diminished after correcting for cardiovascular risk variables. Glucose intolerance was inversely associated with plasma levels of other carotenoids, including lycopene and cryptoxanthin.
Younger insulin-dependent diabetic individuals have much lower plasma retinol levels, while diabetic patients with nephropathy have drastically changed alpha-tocopherol levels. Significant and independent reductions in plasma retinal, or its ratio to cholesterol, were seen in the younger sample of diabetes as compared to controls. Similar findings were seen in patients with type 2 DM, but two other trials found no evidence of vitamin A shortage in subjects with Type 2 DM.
Researchers found that people who ate more vitamin A had better insulin-mediated glucose elimination.
In a study, beta-carotene supplementation had no discernible effect on the development of melanomas. Among doctors given 50 mg of beta-carotene, there was a non-significant 17% decrease in the incidence of melanoma.
Preventing pregnancy-related anemia may be aided by increasing dietary intake of vitamin A. Pregnant women with anemia were evaluated for their response to vitamin A and iron therapy. Supplementing with vitamin A and iron resulted in the highest hemoglobin levels, with vitamin A accounting for roughly a third of the response and iron for the remaining two-thirds. Women who were anemic before supplementing had a 35% success rate after receiving vitamin A, a 68% success rate after receiving iron, a 97% success rate after receiving both, and a 16% success rate after receiving a placebo.
Vitamin A supplementation or a sufficient diet has been shown to reduce morbidity and mortality among children in low-income nations significantly. Premature infants and people with severe diseases like measles may benefit from vitamin A supplementation in industrialized countries, as many people with relative vitamin A deficiency.
Measles infection mortality and morbidity can be decreased by treatment with high vitamin A. Serum vitamin A concentrations are low in children with acute respiratory syncytial virus (RSV) infection. Treatment of previously healthy infants with respiratory syncytial virus infection at doses of 12,500-25,000IU is safe and well tolerated, according to one study. [65] However, a high-dose vitamin A therapy trial among children aged one month to 6 years found no evidence of vitamin A’s beneficial effect for treating RSV infection.
According to specific reports, patients with Crohn’s disease may benefit from vitamin A therapy. Patients in remission from Crohn’s condition did not benefit from vitamin A treatment in one long-term research.
Vitamin A is crucial for developing epithelial cells, which is why it is used to keep the lungs and trachea healthy, as well as for the reproductive system and vision. Dietary retinyl esters, retinal, and retinal, but not retinoic acid, can help with these three vitamin A functions. Bone, protein, and growth hormone can’t be made without vitamin A, not to mention that it boosts the immune system. Vitamin A’s precursor, beta-carotene, has antioxidant properties and may improve resistant system performance. Many antioxidant carotenoids, such as a-carotene, zeaxanthin, lutein, and lycopene, do not get converted into vitamin A in any appreciable proportion.
Night blindness; retinopathy; photosensitivity; conjunctivitis and blepharitis; macular degeneration; cataract; most infections; urethral infection; recurrent otitis media; immune function; minor injuries; measles; HIV support; Crohn’s disease; menorrhagia; premenstrual syndrome; abnormal pap smear; peptic ulcer; acne; alcohol withdrawal.
The first sign of a vitamin A deficiency is night blindness; if treated early on, xerophthalmia, corneal ulceration, and blindness can be avoided. Vitamin A and carotenoids have been shown to reduce the likelihood of developing cataracts. Loss of lung elasticity, epithelium keratinization, keratinization of the salivary glands, urinary calculi, and decreased hearing may all be avoided with adequate intake of vitamin A. Acne, psoriasis, Darier’s disease, and premature skin age may all respond well to treatment with retinoic acid or topical tretinoin. Preventing anemia in pregnant women may be aided by raising their vitamin A levels.
Increased vitamin A consumption has reduced the chance of developing lung cancer, particularly squamous cell carcinoma. The risk of developing lung cancer doubled in people with low serum carotenoids. Cancers of the breast, cervix, esophagus, pancreas, and colon may all benefit from carotenoids, according to research. Research suggests that vitamin A may reduce the chance of developing gastric neoplasia and head and neck squamous cell carcinoma. Consumption of carotenoids has been linked to a lower incidence of bladder cancer, and lycopene may make lymphocyte DNA more resistant to oxidative damage. Beta-carotene supplements have been found to have a protective effect against the development of thyroid cancer and reverse oral leukoplakia. It’s possible that beta-carotene can prevent the onset of type 2 diabetes. Beta-carotene supplementation was associated with a marginally lower risk of melanoma.
Patients with chronic intestinal diarrhea, cancer, malaria, pneumonia, and anorexia nervosa are at increased risk of vitamin B12 deficiency and should be supplemented accordingly. Patients undergoing appendectomy, burn treatment, cirrhosis, or biliary blockage may benefit from vitamin supplementation since stress can increase vitamin excretion. Vitamin A supplements are recommended for premature infants, those with cystic fibrosis, and people with rheumatic fever.
Vitamin A at 5000 IU per day with 100% beta-carotene is what we advise for adults. About 3/4 of a serving of cooked spinach, 2 1/2 servings of raw carrots, five servings of raw papaya, and 1/5 of a baked sweet potato will provide this amount. In the age range of 18-54, it is generally accepted that a dose of 25000 IU is safe. No indication converting beta-carotene to vitamin A adds to vitamin A toxicity. Thus, it is safe to take even at significant levels.
Excess vitamin A is harmful to the liver and the nervous system. Congenital abnormalities, such as early skeletal development and transitory hydrocephalus, can occur in a pregnant woman’s unborn child. Caution is warranted because chronic use is linked to elevated cholesterol levels and a higher likelihood of coronary heart disease. Consumption over recommended levels is also associated with an increased risk of hip fractures and osteoporosis.
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Medical Doctors’ Organic Food (http://www.doctorsnaturalchoice.net)
Doctor Scott E. Conard.
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The Optimal Preference of Doctors
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