VITAMINS

Guenther von Eye, M.D., Cardiology. Associate Professor of Internal Medicine of the State University Medical School (UFRGS).

Overview

What are vitamins?

They’re nutritional elements essential to life (VITA) that have in their structure nitrogenated compounds (AMINES), which the organism isn’t able to synthesize and whose absence in the diet will cause manifestations of deficiency in the organism. The human body must receive vitamins through food, exogenous administration (orally or by injection), or by utilizing the vitamins formed by the intestinal flora (some vitamins can be produced in an individual’s intestines through the action of the intestinal flora on food remnants).

The lack of vitamins can be complete- avitaminosis- or partial – hypovitaminosis. In both situations, manifestations classified as deficiency diseases may arise.

The deficiency of vitamins can be caused by:

Decreased intake
Decrease absorption
Changes in the intestinal flora
Metabolism changes
Increased consumption.

The excess of vitamins – hypervitaminosis – can result from excessive intake or excessive administration of vitamins.

Classification of vitamins

Water-soluble

B1
B2
B6
B12
biotin
Pantothenic acid
Niacin, or Niacinamide, or PP factor (PP stands for pellagra-preventing)
Folic acid
C
Bioflavonoids.

Fat-soluble:

A
D
E
F
K

Vitamin F is no longer regarded as being a vitamin.

The first vitamin described was A. Later, vitamin B was discovered. Then an unfolding followed: vitamin B was made up by diverse elements; thus B1, B2, B3, and a few others emerged successively. Hence, the designation “B Complex”.

Important note: who must diagnose the lack or excess of vitamins is the physician. Indiscriminate vitamin intake may cause or even aggravate some diseases.

Reminder: no kind of tablet, pill or capsule can replace a healthy diet or make up for a bad diet. For good nutrition and health, the solution is simple: a diet rich in nutrients such as fruits, vegetables and grains.

WATER-SOLUBLE VITAMINS

VITAMIN C

History: scurvy is a disease caused by lack of vitamin C, and is known since the Crusades and diagnosed chiefly in Northern Europe’s inhabitants, where diet was low in green vegetables and fresh fruit in the winter. In the 17th century, with the introduction of potato into the northern Europeans’ diet, scurvy became rare. With the great navigations from the 16th century up to the 18th century, scurvy became the classic disease of sailors that spent long periods at high sea without ingesting fresh fruits or green vegetables.

In 1535, the natives of Canada taught navy’s captain Jacques Cartier that a tea made with Canada’s pine tree buds healed scurvy. Only in 1747, Lind, a physician of the English navy, undertook a study supplying different groups of sailors with different foods, aiming at treating scurvy. Of the groups, the first received mustard; the second, citron; the third, vinegar; the fourth, oranges and lemons; and the fifth group, sea water. In the end, he found that the group fed with lemons and oranges rapidly recovered from the disease. With this, the English navy introduced lemon juice into its sailors’ ration. In 1870, at Portsmouth’s Royal Naval Hospital alone, 1,457 scurvy cases were treated; in 1780, after the introduction of lemon juice, only 2 disease cases occurred. Afterwards, it was found that most animals synthesize vitamin C. However, guinea-pigs, non-human primates, Indian fruit bats and humans are unable to form ascorbic acid. Only in 1936, ascorbic acid was isolated and identified. Today, it’s produced industrially.

An English surgeon by the name of Crandon volunteered to a 161-day diet without vitamin C. After 41 days, vitamin C was no longer detectable in his plasma, disappearing from white blood cells at 121 days. After 120 days, perifollicular hyperkeratosis appeared, and at 161 days of diet subcutaneous bleedings manifested, and a wound was observed to have stopped scarring.

Alternative name: ascorbic acid

Recommended daily doses: 60 mg

Main functions: participates in the formation of catecholamines; increases intestinal iron absorption.

Main sources: fresh fruits and green vegetables.

Deficiency manifestations: collagen lesions. Scurvy, a traditional illness of long-distance cruising sailors, is nowadays a virtually unknown disease. A manifestation observed in the hair that may suggest vitamin C deficiency is when the hair becomes curly at sites where it used to be straight. See the historic data above.

Excess manifestations: formation of oxalate calculus in the kidneys. Note that the recommended daily dose is 60mg/d. Some commercial products contain up to 2000 mg per tablet, which means an intake 35 times as high as the recommended daily dose or higher.

Preventive or healing effect on viral diseases as the flu, cancer prevention, reduction in the risk for heart disease and cataract, increase in organic defenses, none of these has been proven as being a useful therapeutic effect of vitamin C.

The chances of deriving a health benefit from the use of high vitamin C doses are well below those of getting another disease.

Foods rich in vitamin C:

papaya: 1 middle sized unit (188 mg vitamin C)
broccoli: 1 cup (116 mg vitamin C)
orange juice: 1 glass (97 mg vitamin C)
strawberries: 1 cup (84 mg vitamin C)
navel orange: 1 unit (75 mg)
kiwi: 1 unit (74 mg)
melon: 1 cup (68 mg)
mango: 1 unit (57 mg)

VITAMIN B 1

History: vitamin B1 was the first in the B complex to be discovered. Its absence causes beriberi, disease whose incidence increased significantly in the 19th century, chiefly in Asia, when polished rice began being produced. In 1880, Japanese navy’s admiral Takaki proved that the cause of beriberi was alimentary by adding to the Japanese sailors’ diet fish, meat, barleycorn and vegetables. In 1897, Eijkman, a Dutch physician that worked in Java, observed that the powder derived from rice polishing, if diluted in water and administered to beriberi sufferers, healed that disease. In 1936, vitamin B1 was isolated and named thiamin.

Alternative name: thiamin.

Recommended daily doses: 1.5 mg. For breastfeeding mothers and the elderly, 3.0 mg.

Main functions: acts mainly on the energetic metabolism of sugars. Its function as a neurotransmitter has been disputed.

Main sources: meat, cereals, nuts, green vegetables and beer. Note: some fishes, crustacean and black teas may contain anti-thiamin factors.

Deficiency manifestations: the basic deficiency disease is beriberi, which manifests mainly in undernourished alcoholic people and people suffering from malnutrition in poor countries. The neurological manifestation of vitamin B1 deficiency is also designated dry beriberi, characterized by peripheral neuritis, sensitivity disorder with anesthesia or hyperesthesia zones, and loss of strength to limbs’ paralysis. In the brain, there may be depression, loss of energy, lack of memory, and even dementia syndromes as Korsakoff’s psychosis and Wernicke’s encephalopathy. Cardiac manifestations arising from lack of vitamin B1 are called wet beriberi, which manifests as shortage of air, heart enlargement, palpitations, tachycardia, changes to the electrocardiogram, including high-output heart failure.

In breastfed infants, the lack of vitamin B1 can arise on account of the mother’s milk being poor in thiamin, especially if the mother doesn’t receive vitamin B1 supplement.

In hyperthyroidism carriers, if there’s an increase in metabolism resulting from overactivity of the thyroid hormone, manifestations of vitamin B1 privation may arise due to increased consumption.

Excess manifestations: even at high doses, thiamin isn’t toxic. The occasional excessive intake of the vitamin is eliminated by the kidneys.

VITAMIN B 2

History: by 1879, a series of yellowish compounds had already been isolated from foods, being designated flavins. It was found that one part was heat-sensitive, which was called B1, while the other one, which was stable to heat, was denominated B2, later vitamin B2.

Alternative name: riboflavin

Recommended daily doses: 1.7 mg/d for men, and 1.6 mg/d for women.

Main functions: plays a significant role in energetic metabolism and as a protector for nerve sheaths. It’s an important factor to enzyme metabolism.

Main sources: milk, meat ,and green vegetables.

Note: sun radiation (UV) inactivates riboflavin.

Deficiency manifestations: very rare. They can appear in pregnant women, high-performance athletes, or in digestive disorders that change its absorption. The first manifestations of privation are tongue inflammations, cracks in the mouth corners, reddish lips, seborrheic dermatitis in the face, trunk and limbs, anemia and neuropathies. In the eyes, neoformation of vessels in the conjunctive can occur, in addition to cataract.

Deficiency of vitamin B2 usually accompanies the lack of other vitamins.

Excess manifestations: it isn’t toxic, even at high doses. The excess is eliminated by the kidneys.

VITAMIN B 6

History: in 1926, it was found that one of the consequences from vitamin B2 deficiency was dermatitis. In 1936, György isolated off vitamin B2 a water-soluble factor whose absence was the actual cause of dermatitis. This was designated vitamin B6. Several products have the same biologic property attributed to B6 (see alternative names).

Alternative names: pyridoxine, pyridoxol, pyridoxamine and pyridoxal.

Recommended daily doses: the daily need of pyridoxine is directly proportional to the dietary intake of proteins. For instance, who ingests 100 g/d of proteins needs to receive 1.5 mg/d pyridoxine. Pregnant women, tobacco and alcohol addicts need higher doses of vitamin B6.

Main functions: vitamin B6 is a coenzyme and interferes with the metabolism of proteins, fats and tryptophan. It acts on the production of hormones and stimulates the cells’ defensive functions. It plays a role in young individuals’ growth.

Main sources: cereals, meat, fruits and green vegetables. Cooking reduces food levels of B6.

Deficiency manifestations: they’re very rare, consisting of seborrheic lesions around the eyes, nose and mouth, accompanied by glossitis and stomatitis. As for the nervous system, the privation of vitamin B6 may lead to convulsions and edema in peripheral nerves, being suspected of causing carpal tunnel syndrome. Growth disorders and anemia are attributed to vitamin B6 deficiency.

Excess manifestations: pyridoxine has low acute toxicity, but doses of 200 mg/d, administered both orally and parenterally, can elicit neurological intoxications, with appearance of symptoms such as tingling in the hands and decreased hearing. Pyridoxine dependency cases have been reported.

VITAMIN B 12

History: vitamin B12, both in its history and functions, is closely related to folic acid and has two Nobel prize recipients in its résumé. Its story began in 1824 when Combe and Addison described megaloblastic anemia cases. Combe associated this anemia to digestive factors; however, only in 1860 Austin Flint described a severe gastric atrophy and talked about the possibility of a potential relation with the previously mentioned anemia.

In 1872, Biermer named it pernicious anemia. In 1925, Whipple observed that the liver contains a potent factor that corrects iron-deficiency anemia in dogs. Minot and Murphy, following and continuing with this line of observations, described the efficacy of liver in the diet for reversing pernicious anemia and were given Medicine’s most coveted award.

Shortly after, Castle observed the existence of a factor secreted by the stomach’s parietal cells, called intrinsic factor, which was needed for treating pernicious anemia and acted along with an extrinsic factor, similar to a vitamin, obtained from the liver. Only twenty years later, Rickes, Smith and Parker isolated and crystallized vitamin B12. Afterwards, Dorothy Hodgkin determined the crystal structure of vitamin B12, and also received a Nobel Prize hence.

In attempts to purify the extrinsic factor, Wills described a form of pernicious anemia in India, which responded to the liver-extracted factor, but didn’t respond to purified fractions that were known to be effective in the treatment of pernicious anemia. It became known as Wills’ factor, later designated Vitamin M, and nowadays is known as folic acid, which was isolated in 1941 by Mitchell.

Recent studies have shown that neither vitamin B12 nor folic acid purified and derived from food is the active enzyme for humans. During their derivation, volatile and active forms are converted into stable congeners of vitamin B12 and folic acid, cyanocobalamin and pteroilglutamic acid, respectively. These congeners must be converted in vivo so that they can be effective for the metabolism.

Alternative names: cobalamins, hydroxycobalamin, cyanocobalamin.

Recommended daily doses: 6 ug/d. Blood levels of vitamin B12 can be gauged and so diagnose its deficiency.

Main functions: vital for cell replication growth. Important to the formation of red blood cells.

Main sources: meat and liver. It’s also produced by the large intestine’s flora, but it isn’t absorbed there. Absorption occurs in the small intestine, after this is activated in the stomach, where it arrives through food ingestion. Vitamin B12 needs the so-called “intrinsic factor”, available in normal stomachs, to be absorbed. The vitamin B12 formed in the intestine is barely absorbed because it isn’t activated by the intrinsic factor.

Nearly 12% of people aged above 65 have plasma levels of cobalamin lower than 258 pmol/L stemming from a lower vitamin B12 absorption. Low levels of this vitamin are possibly associated with a greater risk for cancer and vascular diseases.

Vegetables, per se, don’t contain vitamin B12; this can lead vegetarians to present deficiency thereof. However, this doesn’t always occur because bacteria contaminating vegetables, or even those from the bowel tract, act on remnants of these vegetables and form vitamin B12; therefore, they partially fill the organism’s needs of those that don’t consume meat, liver, eggs, or milk and its derivatives.

Deficiency manifestations: macrocytic or pernicious anemia is the main manifestation. There’s evidence that low levels of vitamin B12 are associated with a higher incidence of vascular diseases and cancer. Cells of fast regeneration and replication (mucosae and cervix epithelium) also suffer with the lack of vitamin B12.

Vitamin B12 deficiency is common in people subjected to stomach surgery, when the part that produces the intrinsic factor accounting for vitamin B12 absorption is removed. Prone to show manifestations of vitamin B12 are strict vegetarians (who don’t consume meat, eggs, milk and its derivatives), intestinal parasitosis carriers, pancreas surgery patients, chronic inflammatory intestinal disease patients, and the elderly.

Deficiencies of vitamin B12 may cause irreversible lesions to the nervous system due to neuron death. The neurological symptoms are quite varying and result from death or function loss of cells affected at different segments of the brain and spinal cord. Neurological alterations may occur even without anemia being present.

Excess manifestations: not mentioned in medical literature.

WARNINGS:

Vitamin B12 is indicated by some to treat muscular or articular pains. Its efficacy as a pain-killer in these situations hasn’t been confirmed yet.
Cases of allergic reactions to the use of vitamin B12 have been reported, most notably if the vitamin is injected.
Doses above 100 ug/d aren’t utilized by the human body as they surpass the utilization capacity, being eliminated through urine hence.
In some intestinal diseases, impairment of vitamin B12 absorption may happen. In these cases, it must be administered parenterally, in general one dose every 30 days. If no bowel disease is present, the vitamin can be prescribed for oral administration.
Once macrocytic or pernicious anemia is diagnosed, vitamin B12 can be administered, but one shouldn’t fail to investigate the causes of its deficiency.
In patients with vitamin B12 and folic acid deficiency, administering polyvitaminic drugs with no or small doses of folic acid can improve anemia, while occurs an aggravation of neurological manifestations stemming from the deviation of folic acid to cure the pernicious anemia.
Replace vitamin B12 only under medical supervision and guidance.

PANTOTHENIC ACID

History: pantothenic acid was discovered by Williams in 1933 as a key substance for yeast growth. Its name comes from Greek, for which Panthos means everywhere. That’s because pantothenic acid is available in all places. It was found that a disease called chick pellagra was cured by liver extracts, but not by nicotinic acid. It was demonstrated by Wooley and Jokes that the factor healing the birds’ dermatitis was pantothenic acid. In 1947, Lipmann showed that the acetylation of sulfanilamide needed a co-factor containing pantothenic acid.

Alternative name: coenzyme A

Recommended daily doses: estimated at up to 10 ug. It’s hard to determine a minimum daily dose needed as deficiency states are virtually unknown.

Main functions: acts on the metabolism of most cells and the production of carbon hydrates, proteins and lipids. It interferes with the production of energy within the cells and hormone production.

Main sources: meat, eggs, fruits, cereals and green vegetables; it’s virtually available in every food.

Deficiency manifestations: are very rare. Privation may be experimentally generated with artificial foods, by using some antibiotics; in these cases, fatigue, sleeping and equilibrium disorders, cramps and digestive disorders, such as flatulence and crampy abdominal pain, appear. Individuals with normal diet have no deficiency of pantothenic acid.

Excess manifestations: intake excess (more than 10-20 mg/d) can cause diarrhea. As happens with further water-soluble vitamins, the excess is eliminated by the kidneys in the urine.

NIACIN AND NIACINAMIDE (PP FACTOR)

History: Pelle agra is an Italian term for rough skin, a disorder known for centuries in Italy, where people ate chiefly corn. In 1914, Funk postulated that pellagra was a deficiency disease. Shortly after, Goldberg demonstrated that pellagra could be cured with fresh meat, eggs and milk. Goldberg also observed that the humans’ poor diet was given to dogs, causing the black-tongue disease. Later, it was found to be also a water-soluble component, a stable element accompanying the B complex. In 1935, Warburg et al. isolated nicotinic acid from horse blood.

Alternative names: nicotinic acid, niacinamide and PP factor. Also termed “intelligence vitamins”.

Recommended daily dose: 15 mg.

Main functions: influences the formation of collagen and skin pigmentation caused by ultraviolet radiation. In the brain, niacin acts on the formation of messenger substances, such as adrenaline, influencing the nervous activity.

Main sources: meat and cereals. It originates from the metabolism of tryptophan: 60 mg tryptophan produces 1 mg niacin. People whose diet is mainly based on corn are prone to manifestations of niacin deficiency, as corn is very poor in tryptophan.

Deficiency manifestations: the 3 “D” disease, comprised of Diarrhea, Dementia and Dermatitis. The tongue may show a reddish color, ulcerations and edema. There may be excess salivation and enlargement of salivary glands. Dermatitis similar to skin burns may appear, as well as diarrhea, steatorrhea, nausea and vomiting. In the nervous system occur manifestations as headache, dizziness, insomnia, depression, loss of memory, and, in the most severe cases, hallucinations, dementia, and motrice and neurological alterations with periods of confusion and altered nervous sensations.

Excess manifestations: usually, niacin isn’t toxic, even at high doses, but it can cause itching, heat waves, hepatotoxicity, digestive tract disorders and activation of peptic ulcers.

Observation: the acronym PP stands for Pellagra -Preventing, manifestation found most notably in undernourished distilled alcohol addicts.

FOLIC ACID

History: see historic data for vitamin B12.

Alternative names: folacin, folates and pteroilglutamic acid are synonymous. Vitamin M and vitamin B9 are outdated terms. It’s also called “future mother’s vitamin”.

Recommended daily doses: 0.2 mg for children and 0.4 mg for adults. It’s indispensable for women prior to conception and at the first month of pregnancy in order to prevent congenital diseases in the baby, as anencephaly and spina bifida.

The habitual diet contains around 0.2 mg folic acid. Prolonged cooking of food can destroy up to 90% of its folic acid content.

Main functions: acts together with vitamin B12 on the transformation and synthesis of proteins. It’s necessary in the formation of red blood cells, tissue growth, and formation of deoxyribonucleic acid, which interferes with heredity.

Folic acid plays a role in the prevention of cardiovascular diseases, especially in metabolic disorder sufferers in whom there’s an increase in blood hemocysteine, where it acts as a reducer to this toxic substance.

Synthetic folic acid would be better absorbed by human organism, a claim supported mainly by the pharmaceutics industry.

Chinese medical literature claims that folic acid has the effect of preventing stomach cancer. There are authors who suggest that folic acid prevents large intestine and cervix cancers.

Regarding cancer, its etiology and prevention, there’s no unanimity among authors. There are those who support ideas that might represent individual vanities or commercial interests.

There are countries, among which are England and Chile, where folic acid is added to domestic-use wheat flour. In these countries, supplementation by other means is unnecessary.

Main sources: meat, dark green vegetables, cereals, black beans and potato. A 200-ml glass of beer contains 0.06 mg of folic acid.

Deficiency manifestations: the main manifestation of folic acid deficiency is the high incidence of children with congenital malformations in the nervous system born from mothers who were deprived of folic acid in early pregnancy. Also, there’s an increased incidence of cleft lip and cleft palate in this situation. It’s estimated that preventive administration of folic acid in this period and during the entire pregnancy would reduce the incidence of congenital malformations by 70%. The lack of folic acid increases the incidence of premature childbirths.

A risk factor lies in the fact that many women ignore they’re pregnant. It’s in the beginning of pregnancy that folic acid supplementation is important.

Folic acid deficiency is common in malnourished alcoholics, chronically undernourished people, people that don’t consume green vegetables, such as spinach, Swiss beet-chard, broccoli, and people that feed themselves chiefly with industrialized foodstuffs.

Folic acid deficiency, coupled with vitamin B12 deficiency, can lead people to experience vertigo, fatigue, memory loss, hallucinations and muscle weakness.

Excess manifestations: there is strong evidence that high doses of folic acid reduce the risk for coronary diseases and large intestine cancer. But such evidence isn’t definite, and the recommended dose is yet unknown.

There are studies suggesting that overadministration of folic acid during pregnancy increases the incidence of miscarriage. Further studies deny this claim for the reason that the number of pregnancies amongst women receiving high doses of folic acid that eventually have a miscarriage was similar to that of women that had received normal doses of folic acid – around 9.1%.

CARNITINE

History: in 1905, carnitine was identified as a nitrogenated constituent of the muscles, later being recognized as a growth factor for flour larvae. In 1950, investigators Fritz and Bremer observed the role of carnitine in the oxidation of fatty acids in mammals.

The name carnitine supposedly comes from “carne” (flesh).

Alternative names: L-carnitine, vitamin B11.

Recommended daily doses: a 15 mg/day dose of levo-carnitine administered orally is well-tolerated by man and doesn’t show any considerable side effect. The administration of DL-carnitine, by its turn, produces symptoms similar to myasthenia gravis.

Main sources: meat, fish and dairy products.

Main functions: L-carnitine is important for the oxidation of fatty acids, metabolism of sugars, and promoting the elimination of some organic acids. It acts on the endothelium of vessels, decreasing the levels of triglycerides and cholesterol. It acts by taking fats into the cells, producing energy, increasing fat consumption, having thereby a protective function for the liver. All of these functions and qualities of carnitine are controversial and disputed especially by vegetarians.

Deficiency manifestations: are rare and found mainly in hereditary metabolic disorders. Fatigue, muscle weakness, confusion and cardiac manifestations are the most common symptoms. Renal tubular lesions with renal insufficiency may arise.

Deficiency manifestations of carnitine are described in parenterally (intravenously) fed patients, but are easily corrected by supplementation.

In ischemic heart diseases and myocardiopathy, carnitine plays an important role, as the energy of the cardiac muscle largely originates from the oxidation of fatty acids.

Excess manifestations: are not described.

BIOTIN

History: in 1916, Bateman observed that mice fed with egg white as their sole source of protein developed neuromuscular disorders, dermatitis and hair thinning. This syndrome could be prevented if the egg white were cooked or either liver or yeast were added to the diet. In 1936, Kögl and Tönis isolated off the egg yolk a substance that was essential to yeast growth and designated it biotin. Later, it was found that this factor and the one preventing intoxication from cooked egg white were the same.

Alternative names: vitamin B8. From biotin derive 3 variants, namely, biocytin, lysine, biocytin dextro- and levo-sulfoxide. They’re useful for the growth of some microorganisms, and their utility for man is unknown.

Recommended daily doses: 100-200 ug.

Main sources: meat, yolk, milk, fish and nuts. Biotin is stable to cooking.

Main functions: important function in the metabolism of sugars and fats.

Deficiency manifestations: very rare and arise only if there’s destruction of intestinal bacteria, administration of biotin antimetabolics and diet with raw egg white leading to biotin deficiency. In these cases, atrophic glossitis, muscle pains, decreased appetite, flaccidity, dermatitis and changes in the electrocardiogram occur. Individuals that feed themselves for a long time with raw eggs only have shown these manifestations. Parenterally fed people may also present signs and symptoms of biotin privation. Skin lesions are characterized by severe exfoliative dermatitis and hair loss, which are reversible with administration of biotin.

Children with infant seborrhea and individuals with genetic defects are treated with 5 to 10 mg/d doses of biotin.

Excess manifestations: high doses of biotin can cause diarrhea.

CHOLINE

History: choline is not a vitamin, but it was considered as being one of the components of the B-complex.

In 1932, Best observed that pancreatectomized dogs maintained on insulin developed a fatty liver. This could be avoided by adding raw egg yolks, lecithin or pancreas to their diet. It was demonstrated that the substance that accounted for this effect was choline. This study kicked off subsequent investigations into lipotropic substances.

Alternative names: trimethylethanolamine. It’s similar to acetylcholine, having a similar, yet quite discreet, pharmacological action.

Recommended daily doses: 400-900 mg.

Main sources: yolk, liver, and peanuts.

Functions: mobilizes liver fats (lipotropic action) and is important in the formation of neurotransmitter acetylcholine, in addition to acting as a platelet-activating factor (PAF). It’s also important as a component of phospholipids. Choline supplies methyl radicals, essential to metabolic exchanges. It acts in combination with vitamin B12.

Deficiency manifestations: it leads to fat build-up in the liver, cirrhosis, increase in the incidence of liver cancer, hemorrhagic lesions of the kidneys, and lack of motor coordination.

Excess manifestations: are not described.

NOTE: the treatment of cirrhosis and hepatic steatosis arising from alcohol intake doesn’t respond to the use of choline. Similarly, it hasn’t been effective in the treatment of neurological diseases as Alzheimer’s, Friederich’s ataxia, dyskinesia, Huntington’s and Tourette’s diseases.

BIOFLAVONOIDS

In vegetables, there are substances denominated flavonoids, previously known as vitamin P. The flavonoids aren’t included amongst vitamins.

There are over 5,000 identified substances derived from plants that are recognized as flavonoids. Flavus is Latin for yellow, and on account of their yellow color when isolated, these substances are called accordingly. In vegetables, they’re supposedly responsible for their color and have the function of protecting the plant from the action of atmospheric oxygen. By analogy, a similar action is expected in the human organism when protecting the human body’s cells, mainly those of the vessels, from aggressions and degenerations resultant from the action of acid radicals on the tissues.

Alternative names: vitamin P, rutin.

Recommended daily doses: no data available.

Main functions: to protect the vascular endothelium from aggressions by acid radicals and, also, to diminish platelet adhesiveness, decreasing the risk of blood clot formation and consequent obstruction of arteries that may result in infarction.

Main sources: vegetables, being mainly found in their peels. Much talked about are the bioflavonoids of chocolate, wine, grape juice and other products derived from plants, even industrialized ones. The industry makes great efforts to promote concepts that enhance the value of these substances. However, from a nutritional perspective, fruits contain more flavonoids than industrialized products. Wine production,by its turn, owing to its anaerobic fermentation, preserves the flavonoids best.

Deficiency manifestations: are not described, but their deficiency is admitted to favoring early aging, in which its lack supposedly fails to provide the protective factor against degenerative vascular changes. Actually, aging delay, a very much desired event theoretically advocated, hasn’t been confirmed by serious long-term scientific studies as of yet. Vegetarians and some food fetishists vehemently embrace these claims of benefits.

Excess manifestations: the overadministration of flavonoids is associated with a greater incidence of leukemia in newborn babies from mothers that received high doses of flavonoids during certain pregnancy periods. Available in the market are products that contain high doses of flavonoids, and women at a fertile age should be warned of the limits they should observe as regards the intake of these products.

In some people, the intake of flavonoids triggers headache, wine consumers’ well-known migraine. Headache after excessive wine consumption, or even moderate, is usually attributed to alcohol by some, while others blame low-quality wine. However, there are authors that state flavonoids account for this unpleasant manifestation.

The consumption of a great amount of chocolate has some drawbacks, including obesity. Having too many shots of wine isn’t recommended either.

In summary, small amounts of chocolate and one or two glasses of wine (100 ml) per day are regarded as recommendable. If the purpose is to supply the organism with flavonoids, it’s better to consume fresh fruits and green vegetables.

FAT-SOLUBLE VITAMINS

VITAMIN A

Historic data: night blindness, the main manifestation of vitamin A privation, was already known by Egyptians over 3 thousand years ago. They ignored the reason for this manifestation, but treated it empirically with fried or cooked liver compresses on the eyes, Hypocrates already recommended, 2 thousand years ago, eating liver to treat night blindness. In 1865, in Brazil, ophthalmia brasilian was described, a disease that attacked undernourished slaves. Only in 1913, in an experimental study, it was described that animals affected by xerophthalmia (eye dryness) had this manifestation cured by the ingestion of yolk, milk, butter, and cod liver oil. During the 1914-1918 World War, it was observed that xerophthalmia in humans resulted from butter privation in the diet.

Alternative names: retinoids are substances like retinol and its derivatives, which have the biologic properties of vitamin A . Retinoids either occur in nature or are synthetically produced.

Recommended daily dose: 1 mg or 5,000 IU.

Main functions: important to the functions of retina, especially for night vision. It exerts a function in skin and mucosa cornification, reinforcement of the immune system, formation of bone, skin, hair and fingernails. It’s important in embryonic development. It influences immune responses and is likely to have effects on the prevention of some tumors.

Vitamin A has an antioxidant function, it binds with the so-called free radicals that originate from the oxidation of several elements. These free radicals have a noxious effect on cells and are considered as being the cause of arteriosclerosis, cataract, tumors, skin disorders, and rheumatic diseases.

Main sources for vitamin A , content in every 100 grams of food:

Liver – 25 mg
Chicken liver – 11 mg
Bovine liver – 8 mg
Pâté de foie gras– 2 mg
Carrots – 1 mg.

Note: in 1 g of polar bear liver is found 12 mg of retinol (40,000 IU).

Deficiency manifestations:

eyes

Keratomalacia (softening of the cornea), dry eyes, with ulcerations and xerosis of the conjunctiva and cornea are the earliest manifestations. Night blindness, the best known manifestation, is one of the first manifestations of vitamin A deficiency. Extreme vision difficulty, including complete blindness, is the most severe manifestation of its privation.

Respiratory system

The epithelium of the air ways undergoes changes, namely, keratinization, which favors an increase in infections. There may be a reduction in pulmonary elasticity, making it harder to breathe.

Skin

Keratinization and skin dryness lead to the eruption of papules that engulf the sebaceous follicles, mainly in the limbs’ ends.

Genitourinary system

Vitamin A deficiency leads to the formation of renal calculus. The epithelium of the urinary traits becomes rough, which favors crystal deposition and calculus formation. Changes in the formation of spermatozoa, degeneration of the testicles, miscarriages, anomalies and fetal death also occur.

Digestive system

There’s occurrence of changes to the intestinal epithelium and metaplasia in the pancreatic duct’s epithelium, which possibly account for the diarrhea attributed to the deficiency of vitamin A.

Sweat glands

They may atrophy and undergo keratinization. Alterations of sweat can worsen bodily smells.

Bones

In animals, experimentally, the lack of vitamin A elicits changes such as increase in bone porosity and thickness.

Nervous system

Changes to the smell, taste and hearing senses may occur. Lesions of nerves and increase in the production of liquor with hydrocephaly have been reported.

Blood

A reduction in the formation of red blood cells may take place.

Excess manifestations:

The excess of vitamin A, a frequent situation in people that deliberately consume vitamins, can cause unpleasant and even dangerous clinical manifestations.

Vitamin A intoxication can be either acute or chronic. Prolonged intake of 30mg/d of retinol for 6 months or more causes intoxications. Even on 10 mg/d some individuals already present with symptoms. In children, 7.5 to 15 mg/d for one month already produces manifestations of toxicity. For an acute intoxication to occur, an adult needs 500 mg; a young individual, 100 mg; and a child, 30 mg.

Owing to exaggerated intake, manifestations may arise, as dry, rough and scaly skin, lip fissures, follicular keratosis, bone and joint pains, headache, dizziness and nausea, hair loss, cramps, hepatic lesions and growth arrestment. There may be lack of appetite, edema, tiredness, irritability and bleeding as well. Enlargement of the spleen and liver, changes in hepatic function tests, drop in cholesterol and HDL cholesterol levels may also take place. Cases of fatal poisoning have been observed due to the ingestion of polar bear liver. Great attention must be paid to products containing retinoic acid used in acne treatment.

Recommended doses: 1 mg/d for normal people. For pregnant women, people with fat digestion disorders, diabetes, old people and alcoholics, doses 25-50% higher are recommended.

WARNINGS:

There are studies conducted with volunteers in which it was observed that the excessive and prolonged intake of vitamin A increased cancer incidence, most notably breast and large intestine cancer. This hasn’t been fully supported.
Excessive intake may lead to an increase in the incidence of femoral neck fractures.
An intake twice as high as that daily needed in pregnant women is associated to a greater incidence of specific congenital defects in children. This is another claim that still has to be confirmed.
Final suggestion – if you’re a normal person, with a normal diet, avoid vitamin A supplementation. In case you show some manifestation suggestive of deficiency thereof, consult with your doctor and ask for advice.

VITAMIN E

History: in 1922, Evans and Bischop observed that pregnant rats couldn’t maintain their pregnancy in the absence of an unknown factor. They would become pregnant and have a miscarriage afterwards. Also observed were changes to the testicles of rats deprived of this substance, considered as being anti-sterility, hence vitamin E. Evans isolated the vitamin and, in 1936, found it comprised a total of eight tocopherols, alpha-tocopherol being the most important.

Alternative name: tocopherol. Actually, there are eight similar substances gathered under the name of tocopherols.

Recommended daily dose: 10 to 30 IU.

Main functions: initially, it was regarded as the vitamin of fertility, being indicated to treat sexual impotence. To some people’s dismay, this has never been proven.

In animals (rats), the lack of vitamin E causes degenerative neurological alterations in the spinal cord. In humans, the lack of vitamin E causes neurological alterations such as decreased reflexes, decrease in the vibratory sensibility, in the proprioception, and ophthalmoplegia. Visual difficulties can be aggravated by pigmentary retinopathy, also caused by the lack of vitamin E.

There’s no proof demonstrating that vitamin E is useful in the treatment of menstrual disorders, vaginitis, menopausal changes, gravidic toxemia and reproductive difficulties.

Vitamin E helps in the treatment of necrotizing myopathy, but it isn’t useful in the treatment of muscular dystrophy.

Tocopherols act as antioxidants, protecting the cells from noxious effects of toxic substances, especially acid radicals. Currently, it is admitted that they protect from cancer, arteriosclerosis, joint inflammations and diabetes-related complications, since they block oxidative changes of low-density lipoproteins.

It’s disputable whether high vitamin E doses bring some benefit to the prevention of cardiovascular diseases. There are reports in which 400 IU/d of vitamin E was administered to patients suffering from ischemic heart disease.

In this group, the incidence of myocardial infarction was reduced by 50%, but the mean survival of these people was not extended. Another study showed that, in patients subjected to renal dialysis due to chronic renal insufficiency, the incidence of heart disease deaths dropped by 50% as compared to what was expected, when vitamin E was administered. However, in a study carried out in Italy, in the same clinical situation, no significant change was found in the incidence of cardiovascular diseases when high doses of vitamin E were administered. Nevertheless, the number of deaths from cardiac causes was significantly lower.

We must also underscore that the anti-free radical effect is achieved chiefly in the presence of flavonoids.

CONCLUSIONS

In the short run, in heart condition patients no evidence of obvious benefits from vitamin E supplementation has been found. No benefit, in the long run, has been determined either.

As for the benefits in cancer prevention, the results are controversial. Regarding breast cancer prevention, there’s no evidence supporting it. With respect to large intestine cancer, the results are in disagreement. A group that evaluated the association of alpha-tocopherol and beta-carotene noted a significant reduction in prostate cancer and no benefit in the prevention of other cancers. The same group of investigators observed that amongst smokers there was a significant increase in strokes when high doses of vitamin A and E were received.

There’s discreet evidence that high doses of vitamin E associated to Ginko biloba could slow down the progression of Alzheimer’s disease.

Main sources: vegetable oils, cereals and fresh green vegetables. Women’s milk contains enough vitamin E for the infant that’s being breastfed, as opposed to cow’s milk.

Deficiency manifestations: see main functions described above.

Excess manifestations: vitamin E, even at high doses, is not considered toxic, but if excessively consumed may compete in the absorption and reduce the availability of other fat-soluble vitamins, in addition to food-originated iron, and, thus, contribute to the triggering of anemia. It was also observed that high doses of vitamin E accelerate the progression of retinitis pigmentosa.

VITAMIN K

History: in 1929, Dam observed that chicks fed with certain rations had bleeding as a result from a drop in blood prothrombin levels. Six years later, he found that an unknown substance, which was fat-soluble, fought off blood loss. He named it vitamin K (Koagulations Vitamine). At the same time, other investigators, observing icteric patients and studying the causes of the reduction in blood coagulability, found that the decline in prothrombin was the factor accounting for that. In 1936, they observed that animals with biliary fistulas, in which the bile didn’t arrive in the intestine, had the same problem, and found out they could correct the disorder by feeding those animals with biliary salts.

Alternative names: vitamin K is comprised of 3 types, K1 (phytonadione), K2 (menaquinone-6), and K3 (menadione).

Recommended daily doses: the minimum daily doses necessary to keep clotting normal haven’t been determined yet. The necessary minimum is admitted to being 0.5 to 1 microgram/kg bodyweight. People with vitamin K deficiency are treated with 0.03 ug/d bodyweight. In adults, vitamin K2 is formed in the individual’s own intestine by the action of bacteria on the bowel content. Vitamin K1 comes from vegetables. In newborn babies, this doesn’t take place yet, being the reason why some pediatricians administer this vitamin to infants shortly after their birth in order to avoid the consequences from its deficiency (bleedings).

Main functions: vitamins K1 and K2 practically don’t have a pharmacodynamic activity in normal people. Vitamin K acts on the production of prothrombin, important factor in blood clotting. It acts, also, on the prevention of osteoporosis in the elderly and postmenopausal women.

Main sources: green vegetables and liver.

Deficiency manifestations: in adults, they’re extremely rare and may result from diseases in which there’s malfunctioning of the liver, intestinal malabsorption, changes in the intestinal flora (prolonged and intensive use of antibiotics), or undernourishment. The deficiency manifests through a tendency to bleeding.

Excess manifestations: vitamins K1 and K2 aren’t toxic, even at high doses; while high vitamin K3 doses may cause anemia and liver lesions.

An intravenous injection of phytonadione may cause chest pain, shock, and, seldom, death, which is attributed by some to the solvents used in injectable solutions. Menadione is irritating for the skin and lungs and can cause hemolytic anemia, and kernicterus in newborns, especially prematurely born infants. In people with liver disease, both menadione and phytonadione can depress even further the hepatic function.

VITAMIN D

History: vitamin D, actually, is the designation ascribed to two substances, cholecalciferol and ergocalciferol. Both have the property of preventing or curing rachitis, which was attributed to lack of fresh air and sunlight for children raised in urban areas. Other authors credited the disease to nutritional mistakes. In 1919, two authors, Mellanby and Huldschinsky, verified that all of them were right, since adding cod liver oil to the diet or exposing children to the sun prevented or cured the condition. In 1924, authors Heis, Steenbock and Black found that by irradiating animal rations with ultraviolet radiation rachitis was also cured or prevented.

Alternative name: calciferol.

Recommended daily doses: 400 IU

Main functions: vitamin D acts as a hormone on the regulation of calcium in the bones and blood.

Main sources: the human organism is able to synthesize vitamin D from cholesterol, hence, it could stop being considered a vitamin by definition. In regions where there’s little sun radiation, the human body needs to supplement its nutritional and/or environmental needs. The main sources are liver, fish oil, and yolk. Available in the market are vitamin D-“enriched” dairy products, something unnecessary in a sunny country as Brazil (see excess manifestations below).

Deficiency manifestations: vitamin D deficiency causes, in children, rachitis, and, in adults, osteomalacia (softening of the bones). In the elderly, it leads to osteoporosis.

Excess manifestations: a vitamin D overdose elicits hypercalcemia (excess calcium in the blood), which favors calcium deposition in the vessels (arteriosclerosis) and the increased elimination of calcium in the urine, which, by its turn, favors the formation of urinary calculus. The high blood calcium content changes the functions of the heart and nerves.

Both excess and privation of vitamin D change bone formation.

VITAMIN F

Alternative names: the term vitamin F is an outdated designation that encompasses essential non-saturated fatty acids (not formed in the human organism), such as linoleic acid, oleic acid and linolic acid. They’re not amines; hence, they ceased to be considered as vitamins.

Main functions: skin protection and interfere with the human body’s growth. Essential fatty acids are used mainly in cosmetics of topic application and serve to render the skin soft due to their anti-keratinizing effect. They’re widely used to treat dry, cracked and aged skin.

Main sources: the name vitamin F stems from the fact that essential fatty acids are found in fats. Fat is “Fett” in German. It is found most notably in oils from corn, sunflower, soy, grape seed, wheat germ, and olive, as well as in fish oils, especially cold-water fish.

Deficiency manifestations: changes to the skin and body growth.

Excess manifestations: not described.

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