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Dr. Bernard Presser D.C.
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Vitamin A complex is an essential nutrient complex, fundamentally required for health. Functions of vitamin A in cell differentiation, growth, and survival exemplify its essentiality. Vitamin A is important for visual development, building strong bones and teeth, reproduction, normal development of epithelial tissues, optimal immune system function, production of RNA, and many other things. Deficiency of vitamin A affects the conjunctiva, cornea, and retina of the eye with consequences such as dry eye (xerophthalmia), night blindness, and corneal destruction. Risks of macular degeneration and cataract are reduced as ingestion of vitamin A or carotenoids are increased. Epithelial defects of the skin and linings of the respiratory, gastrointestinal, and genitourinary tracts occur with vitamin A deficits. Persons suffering from severe eczema or psoriasis often have low blood levels of vitamin A. Many types of respiratory tract illnesses such as bronchiolitis, pneumonia, and chronic obstructive pulmonary disease are associated with reduced blood levels. Development of abnormal respiratory tissue cells is less likely with increased vitamin A levels. Deficiency leads to loss of ciliated cells in the lungs. Vitamin A promotes mucin secretion and microvilli formation by mucous membranes, including those of the gastrointestinal tract. It prompts secretion of gastric juices for proper digestion and protects mucous membranes of the mouth, nose, throat, and lungs.
Vitamin A complex deficiency affects bone growth (thickening), male reproduction (atrophy of testes, cessation of spermatogenesis), and female reproduction (defective uterus, placental necrosis, abnormal fetal development, genitourinary and ocular defects in developing embryos, fetal resorption). Vitamin A has anticarcinogenic actions and research continues to elucidate its protective roles against cancer. Mechanisms of vitamin A function in controlling cell differentiation and cancer development led to the study of vitamin A's control in gene expression. Gene activation establishes vitamin A (in the form of its metabolite, retinoic acid) as a hormone which is stored in the liver and secreted into the bloodstream when needed. Vitamin A "is central to normal immune function" and is important in lowering morbidity of infectious and inflammatory illnesses - from measles to malaria, from acne to arthritis. Vitamin A is known to boost production of antibodies and white blood cells such as macrophages and T cells. It helps regulate T lymphocytes and thymocytes, increase natural killer cell numbers and activity, and regulate growth and activity of B cells. Individuals with low vitamin A status are more likely to have impaired natural killer cells, and are more susceptible to inflammation, aggravation of pre-existing inflammatory states, infection, and cancer. Vitamin A has a role in tissue regeneration, and offsets tumor formation and development.
A correlation exists between consumption of vitamin A complex in the diet and insulin's ability to control glucose. People with "impaired glucose tolerance" (which can lead to diabetes) have lower concentrations of carotenoids in their blood than healthy people. The thyroid gland requires more vitamin A than other glands and cannot function without it. A lack of sufficient vitamin A may result in subtle cognitive difficulties. Mice fed diets lacking vitamin A have diminished chemical changes in the brain considered properties of learning and memory. Vitamin A helps not only reconnection of retinoid receptors critical for vision, but also helps sensory perception, language processing, and attention capacity in autistic children. Although deficiency can cause malformation in the developing embryo, recent studies suggest that there is a window of time in pregnancy during which increasing levels of vitamin A "can reverse the adverse effects of genetic deficiency." As vitamin A status improves, so do hemoglobin values. Chronic vitamin-A deficiency leads to degeneration of the structures of the ear. Decreased auditory function is associated with low vitamin A levels. Stroke victims with high levels of vitamin A are more likely to recover without damage. Efficient uptake of minerals and proper use of water-soluble vitamins require adequate vitamin A from the diet. Vitamin A inhibits the effects of mineral-blocking phytic acid and increases absorption of iron from whole wheat. Increased absorption of iron and folic acid occur with improved vitamin A levels. "Vitamin A deficiency is associated with a wide range of effects on various cell types" because cellular actions are mediated via this nutrient.
Vitamin A complex is identified as retinol or any of several related fat-soluble compounds that have similar biological activity. The body converts retinol into the hormone retinoic acid which travels through the bloodstream and into cells. Retinol esters are naturally present in the fat of animal foods such as liver, kidney, fish liver oils, eggs, and unpasteurized whole-milk products. Retinol intake is variable, not only due to availability of concentrated food sources, but also by seasonal variation of content in foods such as unpasteurized milk. Retinol in a synthetic manufactured form is sold as ‘vitamin A' supplements or placed in "fortified foods" such as breakfast cereals (including instant oatmeal), meal replacement beverages, nonfat and low-fat milk products, margarine, some cheeses, and other products. Retinol is referred to as preformed vitamin A, the form the body uses as vitamin A. But fragmented or artificially-made preformed A is missing precursors and synergists, thus not regarded by the body as a food complex.
Carotenoids are fat-soluble pigments from plants, algae, and some types of bacteria. More than 700 carotenoids have been identified, about 40 or so are known to be commonly consumed in the US diet, and 20 or more are found in "quantifiable amounts" in human serum and tissues. Most research studies have focused on only six carotenoids: beta-carotene, alpha-carotene, lutein, lycopene, zeaxanthin, and beta-cryptoxanthin. But "not all carotenoids are alike." There are wide differences in the activities of individual carotenoids. Science has only scratched the surface. Although often called "vitamin A", carotenoids are actually provitamin A, meaning they are the raw materials that must be converted by the body into retinol.
There is much controversy about the conversion of carotenoids. The latest equivalences thought to reflect differences in bioavailability and vitamin A activity of carotenoids compared with retinol are classified as Retinol Equivalents (RE) or Retinol Activity Equivalents (RAE). Currently, 1 RE or RAE is equivalent to 1 microgram (mcg) retinol, 12 mcg beta-carotene (12:1), 24 mcg other carotenoids (24:1). Actually, relative equivalents of beta-carotene to retinol range anywhere from 2:1 to 26:1 (mcgs). An average equivalency ratio of 6:1 (6 mcg beta-carotene = 1 mcg retinol) was proposed by the World Health Organization as merely an approximation that is not applicable to all people or all diets. "The real conversion factor for specific foods under specific circumstances depends on many factors." Also, the numbers often represent a "new science on the vitamin A activity of purified [isolated, often synthetic] B-carotene compared to retinol." The biological activity of carotenoids as part of whole foods is not always reflected in the numbers, though some research with whole foods is taking place. Interference in the conversion of carotenoids to retinol may occur with low fat intake, diabetes, low thyroid function, celiac disease, intestinal parasites, pancreatic disease, cystic fibrosis, cirrhosis of the liver, bile duct obstruction, excessive stress, excessive alcohol consumption, deficiencies of zinc or protein or other nutrients, high intake of sodium nitrites and nitrates (as in luncheon meats, hot dogs, sausage, bacon, ham), high intake of refined polyunsaturated oils, high intake of iron-fortified foods, and use of a variety of medications including cholesterol-lowering drugs.
Vitamin A complex is metabolized through the liver. Retinol is stored in the liver in the form of its esters with the help of certain enzymes that convert it to its storage form. Unlike retinol, carotenoids are not primarily stored in the liver. Rather, they are deposited widely throughout the body in fat cells, adrenal glands, and other fatty tissues. The hormone form of retinol, retinoic acid, is regulated for concentration in tissues and circulation primarily by the liver. Cellular retinol-binding protein, found throughout bodily tissues, has key functions in retinoid metabolism. Minerals such as zinc and iron improve vitamin A status and potentiate its effect. A deficit of zinc, for example, limits the bioavailability of vitamin A. Protein, vitamin E complex, and dietary fats enhance carotenoid absorption and use. Other synergists include B vitamins (especially B2, B3, and B12), vitamin C complex, calcium, thyroid hormone, testosterone, melanocyte-stimulating hormone, and growth hormone. Plasma levels of vitamin C drop with vitamin A depletion; the occurrence and action of vitamins A and C often coincide. Vitamin D occurs naturally with vitamin A in many foods. Vitamin E and A complexes work together in a balancing manner. Insulin and thyroid hormone stimulate intestinal conversion of carotenoids to retinol. Thyroid hormone increases vitamin A storage in the liver, balances decreased basal metabolism, and increases utilization of vitamin A. With vitamin A depletion, levels of progesterone, testosterone, aldosterone, and cortisol decrease. Production of many steroid hormones is stimulated by vitamin A. Obviously, vitamin A does not work by itself. Many factors influence its absorption, use, and effectiveness.
Serum or blood levels of vitamin A complex decline during the acute phase response to inflammation, infection, and trauma (due, at least in part, to decreased release from the liver), then typically rebound (come back up to prior level or higher) during resolution of the acute phase response (as it is again released from the liver). However, in severe or chronic inflammation or infection, loss of vitamin A from body stores occurs without a rebound. So blood tests alone do not necessarily indicate vitamin A status, bioavailability, potency, function, adjustments, compensations, or effects. i
VITAMIN A TOXICITY
The current "daily value" for vitamin A is 5,000 IU (1,500 micrograms [mcg]). The "tolerable upper intake level" is 10,000 IU (3,000 mcg) per day for adults and less for children. Although vitamin A has been given in doses from 10,000 IU to 500,000 IU daily, not everyone can safely take high doses. Reports show that liver toxicity can appear in people who take from 25,000 to 50,000 IU a day. "Dangerous levels" can build up if large doses are taken over time. Side effects (unwanted effects) including nausea, fatigue, loss of appetite, headaches, dry itchy skin, irritability, nerve lesions, insomnia, bone/joint pain, and hair loss may occur starting at about 30,000 IU a day taken long-term. One study found that women taking more than 10,000 IU a day from supplements (not from food) had nearly five times the risk of having babies with birth defects. This stirred the government to set the new 10,000 IU upper limit for vitamin A. "The lack of relationship of high intake of vitamin A from food is curious..." said one researcher, as food was not associated with birth defects. Also notable is that "serum retinol levels have been shown to be increased more by ingestion of a supplement than by ingestion of liver with comparable vitamin A content." A 3.5-ounce piece of liver contains over 37,000 IU of retinol. Yet liver and other foods containing substantial amounts of vitamin A do not cause toxic reactions. Associations between use of high-dose supplemental vitamin A by pregnant women and malformations, developmental abnormalities, other birth defects, and spontaneous abortion have been documented. Doses ranged from 25,000 to 150,000 IU per day. Nevertheless, most infants born after "high" vitamin A exposure are normal without any major malformations.
Although vitamin A complex is essential to a healthy respiratory tract, high doses of supplemental vitamin A will not expedite recovery from acute lower respiratory ‘infection' such as pneumonia. Several large trials showed that vitamin A supplements had no effect on mortality from respiratory diseases. In fact, high concentrations of vitamin A may be more harmful than beneficial, causing adverse effects such as enhancing the severity of pneumonia, increasing symptoms of respiratory illness, and producing toxic effects. However, higher-than-average intake of vitamin A from FOOD is protective and decreases the risk of respiratory problems such as abnormal bronchial tissue. Transmission of HIV to babies has been correlated with levels of vitamin A in mothers. Mothers with the highest bodily levels of vitamin A complex have a very low transmission rate of just 7.2%. But there is increased risk of transmission when vitamin A and beta-carotene supplements are used. Food sources of vitamin A enhance iron absorption by counteracting the inhibitory effect of phytic acid in grains, but supplements of vitamin A in the form of retinyl palmitate have no effect on iron absorption. Retinyl palmitate may increase risk of recurrence of head and neck cancers, but vitamin A from food is known to help prevent such cancers. Toxicity has been reported following vitamin A supplement use in the treatment of other malignant diseases.
High doses of vitamin A supplements produce adverse skeletal effects in laboratory animals and in case studies of humans. Increased alkaline phosphatase activity (indicating bone disease), high blood calcium, low parathyroid hormone, and increased bone resorption have been found in people taking doses of 200,000 to 500,000 IU daily. A study of 70,000 postmenopausal nurses showed that those consuming at least 6,600 IU of vitamin A over an 18-year period had nearly double the risk of fractures compared with those consuming the least. Long-term intake of high amounts of vitamin A "may promote the development of osteoporotic hip fractures in women." Daily intakes of even 5,000 to 10,000 IU retinol have been associated with a reduction in bone mineral density and an increased risk of hip fractures. Men with an average ingestion of 5,000 IU of vitamin A per day are more prone to fractures than those getting less. "The amounts of retinol in fortified foods and vitamin supplements may need to be reassessed." An editorial concluded that the "optimal source is from foods in our diets, not the dietary supplements often taken..." Some scientists feel "it's pretty conclusive now that there's a bad effect of supplementation."
In virtually every study on vitamin A toxicity, it is isolated, synthetic supplements that are associated with adverse effects, not foods. Experimental animals and human subjects receive or are taking retinyl acetate, retinyl palmitate, or a synthetic retinoic acid derivative. Even small amounts of synthetic forms of vitamin A may be toxic, the actual amount differing with individuals and factors such as liver health. It is the toxicity of synthetic forms of vitamin A that produce the publicity about alleged dangers of vitamin A. Natural food sources of vitamin A are well tolerated at even high doses.
Actually, high amounts from the diet are needed to prevent birth defects, respiratory diseases, cancers, fractures, and other problems. Traditional diets of peoples around the globe were rich in vitamin A, often containing ten times the current recommended daily value. There has never been an indication of anything but healthful benefits from natural food forms of vitamin A, even for pregnant women. Warnings against vitamin A in foods usually include mention of Arctic explorers who, years ago, died from vitamin A overdose because they ate polar bear livers (several million IUs). But in 1988 it was discovered that polar bear and seal livers tend to accumulate cadmium, a toxic metal. The symptoms of cadmium poisoning were the same as those suffered by the Arctic explorers.
A supposed toxic dose of 100,000 IU vitamin A per day is found in 3 tablespoons of high vitamin cod liver oil, 6 to 9 tablespoons of regular cod liver oil, two-and-one-half 100-gram-servings of duck liver, about three 100-gram servings of beef liver, seven pounds of butter, or 309 egg yolks. Yet people have eaten such amounts with no toxic effects. There is a huge difference between isolated, manufactured retinol found in most supplements or added to fabricated foods and the natural vitamin A COMPLEX with its numerous synergistic co-factors (some of which aid proper handling and processing of vitamin A in the body) in REAL foods. Not only is the synthetic version less acceptable to the body, less biologically active, less effective (or potent), and less useable, it is also more likely to cause a REVERSE effect, contributing to imbalance, distress, and disturbance. Real vitamin A complex contains complex molecules, double bonds, a multiplicity of forms, various isomers, aldehydes, esters, acids, alcohols, and unknown factors.
The manufactured or synthetic version is usually in the form of retinyl ("vitamin A") acetate or retinyl ("vitamin A") palmitate. Vitamin A palmitate, for example, may begin as citral (lemon grass oil); is placed through many stages of refining, alteration, and processing to become vitamin A acetate; then it is combined with ethyl palmitate, (a refined fatty acid from palm oil) to complete it. This final product has absolutely nothing to do with whole food. The FDA lists vitamin A acetate and palmitate as having "well-recognized toxicity" when consumed at levels of 25,000 IU per day or higher, though some studies suggest toxicity occurs in some people at lower levels. Adverse effects include severe liver injury (such as cirrhosis), bone and cartilage pathologies, elevated intracranial pressure, and birth defects in infants whose mothers consumed supplements during pregnancy. Some studies indicate that the use of water-miscible, emulsified, and solid preparations cause more chronic problems of toxicity (and may be 10 times as toxic) than oil-based preparations! Thus, solid tablets or powders containing synthetic vitamin A are more toxic than perles containing oil. Vitamin D appears to help protect against toxicity from isolates. ii
Carotenoids have many important biochemical functions which make them key nutritional substances. Some of these functions make them vital both as vitamin A (when they are converted) and in their own right. Thus, "the biological activity of carotenoids extends beyond provitamin A."
Carotenoids support the health of the skin, even help protect it from cancer. Carotenoids are essential to the health and protection of the eyes. Depletion of carotenoids such as zeaxanthin and lutein is associated with cataracts and macular degeneration. Carotenoid status relates to lung function and respiratory health. Food sources may protect against exercise-induced asthma. Foods rich in carotenoids seem to reduce genetic damage, stimulate cell-to-cell communication, enhance immune function, reduce cancer incidence, decrease risk of cardiovascular disease, and decrease risk of other degenerative diseases. Diets rich in various carotenoids have, for example, been related to a decreased risk for certain cancers including those of the digestive tract, prostate, and pancreas, as well as oral, pharynx or larynx cancers. A diet low in beta-carotene but adequate in other nutrients, including retinol, results in altered white-blood-cell and platelet indices. Lycopene, stored in the prostate, "cannot be converted to vitamin A, making it relatively more available in the tissue." The benefits come from the myriad of natural synergistic substances in food, not one isolated compound.
There are indications that the conversion of plant carotenoids to vitamin A VARIES inversely with vitamin A status - the higher the stores of vitamin A in the total body, the less conversion takes place. The amount of conversion is influenced "little or not at all" by serum (blood) retinol levels, but by total body stores. Plasma concentrations of several carotenoids correlate to levels of fruit and vegetable consumption. But such measurements do not tell the whole story. Since much remains to be learned about factors affecting serum levels of retinol and carotenoids, bioavailability, bioconversion, and the sensitivity of indicators of change in vitamin A status, "every effort should be made to increase the accessibility to and consumption of food sources of carotenoids, including dark-green leafy vegetables."
Can food sources of carotenoids adequately and positively affect the vitamin A levels in the body? In areas of the world notorious for low vitamin A status, the incorporation of carotenoid sources (such as dark green leafy vegetables, sweet potatoes, etc.) into the diet "significantly increased serum retinol concentrations." The greatest rise in retinol occurs when meals contain fat as well as the carotenoid-rich foods. When fat is ingested along with the carotenoid sources, higher concentrations of vitamin A are found in the liver. Community-based clinical trials and epidemiological studies show that where vitamin A deficiency is confirmed, carotenoids from food raise serum concentrations of retinol and "ward off or even correct clinical deficiency." Numerous studies from different parts of the world have demonstrated a positive health effect from vegetables and fruits rich in carotenoids.
For example, a study in which participants received sweet potato, kale, and tomato juice for lunch every day for three weeks experienced a boost in their immune response by 33% (measured by the ability of T cells to multiply). Another study showed that green and yellow vegetables "can provide adequate vitamin A nutrition in the diet" of children and protect them from becoming vitamin A deficient during seasons when retinol food sources are limited. Serum retinol increased when carrots and papaya were given to lactating women (whose vitamin A requirements are higher than pregnant women); both the vitamin A and iron status of these women improved. Prolonged cooking or frying of foods results in reduced effectiveness (lower potency) of carotenoids. iii
Outcomes from supplementing with isolated or synthetic carotenoids have been inconsistent, disappointing, and sometimes harmful. For example, data indicate "no overall benefit or harm" on cataracts after 12 years of beta-carotene supplementation. Numerous cardiovascular-disease intervention studies using beta-carotene found "few beneficial effects and some negative ones." After 12 years there were no significant differences between study participants given beta-carotene and those given placebo in the incidence of all cancers, incidence of lung cancer, number of deaths from cancer, deaths from cardiovascular disease, deaths from any cause, number of men with myocardial infarction, number of men with stroke, or number of men with any of the three major vascular disease endpoints (cardiovascular death, stroke, heart attack). Researchers of the Beta-Carotene and Retinol Efficacy Trial concluded that the combination of beta-carotene and retinol had no benefit on the risk of lung cancer of cardiovascular disease in current or former smokers or those who had experienced occupational exposure to asbestos. The supplements seem to have had an adverse effect similar to a trial of beta-carotene supplementation in Finland -- the risk for lung cancer increased. Study results suggest that beta-carotene supplementation may pose a risk in smokers and asbestos workers and is "of little benefit in preventing cancer in well-nourished populations." Yet population studies suggest clear benefits when diets are high in carotenoids.
Epidemiological studies have "consistently shown" that people who eat ample amounts of fruits and vegetables have lower rates of cardiovascular diseases and cancer than those who eat less of such foods. Studies have not shown any significant protective effects against cardiovascular disease or cancer when fabricated or segregated vitamin fractions are given. Instead, angina and cancer are increased in smokers, drinkers, and those exposed to asbestos. High dietary intake of carotenoid-containing foods reduces risk of age-related macular degeneration, cardiovascular disease, prostate cancer, breast cancer, head and neck cancers. But human intervention trials, limited to use of pharmacological doses of beta-carotene or other carotenoids, have not shown these protective effects. Results of epidemiologic studies conducted over the past 30 years or more have "consistently shown associations between dietary intake of fruit and vegetables and a reduced risk of several diseases." But in recent intervention trials "supranutritional [pharmacological] doses of synthetic B-carotene had unexpected and worrying results..." The combination of alcohol and synthetic beta-carotene is toxic to the liver. In smokers who also consume alcohol, fabricated beta-carotene supplementation promotes pulmonary cancer and possibly cardiovascular complications.
Beta-carotene supplementation "appears" to enhance natural killer cells, but does not enhance T cell-mediated immunity, even though food intake studies indicate it "should". An average of 12 years of beta-carotene supplementation does not affect the development of non-melanoma skin cancer, including basal cell carcinoma and squamous cell carcinoma. Beta-carotene made no significant difference in reducing the risk of type 2 diabetes, though several studies found that high intakes of vegetables and fruits rich in carotenoids reduce risk of type 2 diabetes. The serum level of beta-carotene and the degree of glucose intolerance have been directly and linearly correlated. Alas, study subjects "did not receive carrots - they received supplements" of isolated, synthetic beta carotene. No effects on biomarkers of oxidative stress were found with beta-carotene or lutein supplementation. Nursing mothers given beta-carotene do not experience an increase of beta-carotene in their breast milk. But women consuming red palm oil (a food source rich in carotenoids) show increased concentrations of alpha- and beta-carotene in breast milk and serum, and maintain breast-milk retinol concentrations.
"Although long-term doses of [synthetic, isolated] beta-carotene are not toxic in the general population, these doses may exacerbate or precipitate existing or borderline medical conditions." The assumption that the synthetic beta-carotene used in most studies is equivalent to beta-carotene in "a more natural milieu" (i.e., food) has yielded disastrous results. The "real lesson" is that real natural foods, with all their delicately-balanced proportions of "various isomers," are linked to reduced risks for diseases, but manufactured imitations are not. Scientists' tendency to isolate a naturally-occurring food ingredient, then to synthesize it and put it into a capsule or tablet has backfired many times. It does not work nutritionally. Taking excessive amounts of one carotenoid disrupts the balance of other carotenoids and possibly other nutrients and food factors. For example, isolated beta-carotene decreases plasma levels of lutein and zeazanthin. "Much of the evidence suggests an interaction between" beta-carotene and other carotenoids such as xanthaxanthin, lutein, and lycopene. It "could turn out" that the provitamin A activity of carotenoids depends on the content of other carotenoids and/or other natural substances in foods.
Studies with real humans and real foods suggest selective absorption, that the body chooses particular carotenoids in particular amounts needed at the time. Nature places nutrient ‘checks and balances' in foods, allowing the body to obtain exactly what it needs. When large amounts of separated or human-made compounds called "nutrients" are ingested, the body's biochemical balance can be disrupted, creating more problems.
As one scientist concluded, "there is no direct evidence that carotenoids themselves are responsible for" the protective and healthful affects of foods since the research cannot find a direct, linear, cause-and-effect link between an isolated chemical and a beneficial outcome. Scientists continue to search for "a biologic mechanism of action" while admitting that diets rich in fruits and vegetables and other natural whole foods "deliver the goods." With blinders firmly fixed, some attempt to "identify and quantify" segregated chemicals and their association with disease risk. Others grasp the concept that supplementation with solitary nutrient parts, especially if they are synthetic and given in large doses, can and will cause disturbances in the body's delicate equilibrium, disrupting the balance of nutrient and other biochemical interactions, potentially causing more harm than good.
Whole, natural foods contain a wide range of nutrients and other valuable substances in balance that work synergistically. The full spectrum of ingredients provides the real value of food. Obtaining carotenoids from foods means that all the balanced associated nutrients and other factors are also ingested which aid effectiveness and use as well as help prevent any "paradoxical reaction" that occurs with isolated and synthetic fractions. The advantages obtained from whole foods come from "beneficial interactions" among naturally-occurring carotenoids, phytochemicals, and other ingredients. "The nutrients and other healthful compounds in foods work in a fine balance which scientists are only beginning to understand." There has "never been any evidence" that carotenoids in foods pose any danger, partly because they come with many other components "that all work together". In fact, "virtually every study shows that foods" rich in carotenoids help keep people healthy and reduce risks for many health problems.
Studies actually emphasize the importance of food. "After all, it was on the basis of whole foods and integral meal patterns that the associations [between carotenoids and health benefits] were found." Attributing the helpful results to a specific "chemical" or a "pharmacologic" consequence of the diet detaches the relevance away from nutrition. Besides, food "has a physiological or psychological effect beyond the traditional nutritional effect." As one researcher opined, "epidemiologists should be forced to hang up as the motto on their campaign signs, "It's the foods, not the chemicals." iv
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Originally published as an issue of Nutrition News and Views, reproduced with permission by the author, Judith A. DeCava, CNC, LNC.