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Subsections
Vitamins
Vitamins are essential substances which act in very small quantities.
Under- or oversupply of vitamins bears serious dangers.To avoid misuse in food production there were limits established by each country.
Germany has a limit for vitamin A of 1000 and for vitamin D 2,5 microgramms/100g food.
At the beginning of the research concerning vitamins no one knew their chemical structure and therefore proper scientific names could not be given. The vitamins were therefore designated by a letter of the alphabet.
Some of the substances cited below are nowadays not considered as vitamins any more. However they are listed here as a reference to readers of old books searching historical development of the knowledge of vitamins.
Important vitamins are:
Vitamin A (retinol)
Vitamin B-complex group
B1 (thiamine)
B2 (riboflavin)
B3 (niacin, niacinamide)
B4 (adenine)
B5 (pantothenic acid)
B6 (pyridoxine)
B10 also called Bx or PABA (para-aminobenzoic acid)
B11 (growth factors, vitamin B11
B12 (cobalamin, Cyanocobalamin)
B13 (orotic acid)
B15 (pangamic acid)
B17 (amygdalin)
Bc (folic acid)
Bt (carnitine) It is a non-essential aminoacid,
and is not a vitamin.
Choline
Inositol
C (ascorbic acid)
D (calciferol, viosterol, ergosterol)
E (tocopherol)
F (fatty acids)
Linoleic acid and linolenic acid were classified as vitamin F. Today this classification is not being used any more. G (riboflavin)
H (biotin)
K (menadione)
L (necessary for lactation)
M (folic acid)
P (bioflavonoids)
Rutin, hesperidin, Citrin and other bioflavonoids were grouped under the name of vitamin P. They are not vitamins in its deep meaning because it is not possible to produce deficiency sympotms with bioflavonoid-free nutrition. Pp (niacinamide)
P4 troxerutin
T (growth-promotion substances, termitin, torutinin)
Vitamin T was decribed by Goetsch in 1946. In 1955 it has been prooved that vitamin T was a mixture of vitmamin B1, B2, B6, nicotinic acid, pantothenic acid, folic acid, biotin, choline, para-aminobenzoic acid and small amounts of vitamin B12.
Vitamin T was told to be responsible for building "giants" of ants and soldiers among the termites whith great heads. Without vitamin T the termites would retain a small head. The unspecific growth-promotion could not be observed in human.[1] U (extracted from cabbage juice)
Fruits and vegetables, protective factors
There are no evidences that isolated or in combination given antioxidants have a preventive activity against cancer or cardiac infarction
The protective activity which is being found in natural food must therefore be active only in a natural system or in combinations with other active compounds presenting synergic effects.
One should however not forget the preventive effect of folic acid during pregnancy preventing neural tube defects of the newborn (spina bifida and hydrocephalus). (400microg folic acid/day) [2].
Folate deficiency in early pregnancy is linked to increased risk of neural tube defects or spina bifida and anencephaly in infants. Since 1998 all US all grain products are fortified with folic acid. There is an ongoing debate in UK to fortify flour with folic acid. The Ireland's National Committee on Folic Acid Fortication recommended that most white, brown and wholemeal breads sold in the country be fortified with 120 micrograms of folic acid per 100g of bread. Food Standards Australia New Zealand made a proposal top fortify all bread-making flour with folic acid. [3]
Van Guelpen and colleagues found that plasma
folate concentrations were strongly positively related to colorectal cancer CRC risk.
They concluded that their findings suggest a decreased CRC risk in subjects with low folate status. This possibility of a detrimental component to the role of folate in carcinogenesis could have implications in the ongoing debate in Europe concerning mandatory folate fortification of foods.
The UK Food Standards Agency recommended that bread or flower to be fortified
with folic acid to reduce the number of cases of neural tube defects (spina
bifida) (March 2007). [4]
The Institute of Food Research (IFR) warns of possible adverse effects of
fortifying food with folic acid. According to Anthony Wright and colleagues,
folates are metabolised in the gut, and folic acid is metabolised in the
liver, which could easily become saturated. Supplementation may result in
unmetabolised folic acid to enter the systemic circulation, since human
liver's low capacity for reduction may eventually give rise to saturation.
[5]
The FDA published in 1996 regulations requiring the addition of folic acid to
enriched breads, cereals, flours, corn meals, pastas, rice, and other grain products.
The Foof Standards Agency considered mandatory fortification in 2002. However,
the Scientific Advisory Committee on Nutrition (SACN) opposed to the
fortification and issued an advice on the introduction of mandatory
fortification of flour with folic acid at current states saying that it beside
reducing the risk of NTD-affected pregnancies in the UK, it would also increase
the proportion of people in the population at risk of exceeding folic acid
intakes above the UL/day and the number of people aged 65 years and over with
low vitamin B12 status at risk of consuming more than 1mg/day of folic acid.
The advice was linked to the condition that there be controls on voluntary
fortification, and clear guidance be given on the appropriate use of
supplements containing folic acid. [6]
According to Kim and Solomons 2007, recent studies suggest that folic acid supplementation and fortification may promote the progression of already
existing, undiagnosed, preneoplastic and neoplastic lesions. These observations
are based on the increase in colon cancer diagnoses in the US and Canada.
[7]
Unmetabolised folic acid accelerates cognitive decline in the elderly with low vitamin B12 status. Dietary folates have a protect against cancer, but folic acid
supplementation may increase the incidence of bowel cancer and breast cancer
in postmenopausal women. [8] [4] is a generic term for a family of B-group vitamins. There
are large numbers of naturally occurring folates but methyl- and formyltetrahydropteroylpolyglutamates are the main forms found in foods. (pteroylmonoglutamic acid) is a synthetic form used in
supplements and food fortification. Sometimes it is colled Vitamin B9. The reference nutrient intake (RNI) is the amount of a nutrient that is considered sufficient to meet the requirements of 97.5% of the population. The lower reference nutrient intake (LRNI) is the
amount of a nutrient that is considered sufficient to meet the requirementsof 2.5% of the population.
For adults, the RNI for folate is 200microg/day and the LRNI is 100microg/day. For infants and children, the RNIs are: 0-12 months, 50microg/day; 1-3 years, 70microg/day; 4-6 years, 100microg/day; 7-10 years, 150microg/day; the RNI for children 11 years and above is the same as that for adults. The LRNIs for infants and children are: 0-12 months, 30microg/day; 1-3 years, 35microg/day; 4-6 years, 50microg/day; 7-10 years, 75microg/day; the LRNI for children 11 years and above is the same as that for adults. [6]
For guidance purposes only, in the general population a supplemental dose of 1 mg/day (equivalent to 0.017 mg/kg bw/day in a 60 kg adult) would not be expected to cause adverse effects. Assuming a maximum intake from food of approximately 0.49 mg/day, a total dose of 1.5 mg/day (equivalent to 0.025 mg/kg bw/day in a 60 kg adult) would not be expected to have any adverse effects. [9] [10]
Preconceptional folate supplementation for at least 1 year may halve number of premature birthsFolic acid reduces neural tube defects (spina bifida) and anencephaly. Foli acid is already being added to cereal products in U.S. and Canada starting in 1998.
Radek Bukowski and colleagues in a study concerning folate supplementation and
pregnancy found that supplementation for at least 1 year before conception was
associated with a 70% decrease in the incidence of spontaneous preterm
delivery between 20 and 28 weeks and 50% decrease in the incidence of
spontaneous preterm delivery between 28 and 32 weeks.
Radek Bukowski and colleagues recommend that women of childbearing age take a
daily dose of 400 micrograms starting at least 1 year before conception. The
study was presented at the 28th Annual Society for Maternal-Fetal Medicine
(SMFM) 2008 meeting. [11]
According to a Health Food Manufacturer's Association (HFMA) Report, the
average intake of folic acid per day per person in the UK is 200 µgram. But
periconceptional requirement of folic acid per day is 400 µgram.
Supplementation in postconceptional period proved to be less effective in
preventing NTD. Folic acid given in the periconceptional period prevents
childhood leukaemia, decreases the incidence of Coronary Heart Disease and
Stroke. The decrease in plasma homocysteine levels reduces the number of deaths
due to stroke and Ischemic heart disease, and low levels of folate and Vitamin
B12 were linked to depression.
In its paper Dhruvashree Somasundara also stresses that elderly are at risk
primarily because they are commonly deficient in Vitamin B12. He calls to
fortify food with both folic acid and Vitamin B12. [12]
According to Mark A. Lawrence concerns about the safety implications of
mandatory folic acid fortification include possible increased risk of cancer
particularly colorectal cancer, decreased cognitive function, increased risk of
compromised immunity and lack of evidence of protection against coronary heart disease.
Concern has also been raised regarding an increased proportion of
methylenetetrahydrofolate reducatase homozygote births in women using folic acid
supplements to prevent NTDs. This genotype is reliant on a high intake of folate
to maintain health and is negatively associated with increased risk of several
chronic diseases if diet quality is not maintained. Further it must be excluded
that other phenotypic changes in offspring may take place when folic acid is
supplemented in utero.
[13]
Robert Clarke (1998) advocated that daily supplementation with both 0.5-5 mg
folic acid and about 0.5mg vitamin B-12 would be expected to reduce blood
homocysteine concentrations by about a quarter to a third (for example, from
about 12 µmol/l to 8-9 µmol/l).
The author called for large scale randomised trials to determine whether lowering
blood homocysteine concentrations reduces the risk of vascular disease. This
publication initiated a high amount of research on the effect of homocysteine
blood level. [14]
In 2008 Linda Dodds and colleagues found that increased total homocysteine
(tHcy) was associated with placental-mediated adverse pregnancy outcomes.
Increased tHcy concentrations increased risk of pregnancy loss or preeclampsia compared with subjects with lower tHcy concentrations, but it was not
associated with increased risk of developing gestational hypertension or having
an small for gestational age infant.
The authors concluded that high tHcy in early pregnancy is a risk factor for
pregnancy loss and preeclampsia and results in abnormalities of the placental
vasculature. [15]
Roi Miodini Nilsen and colleagues reported in 2007 a strong risk reduction of
placental abruption when both folic acid and multivitamin were supplemented.
The authors conclude that folic acid and other vitamin supplementation during
pregnancy may be associated with reduced risk of placental abruption. [16]
Leane Hoey and colleagues studied the effect of fortified foods on blood levels
of biomarkers of folate, vitamin B and homocysteine. They wrote that mandatory
folic acid fortification of food is effective in reducing neural tube defects
and may even reduce stroke-related mortality, but it remains controversial
because of concerns about potential adverse effects. Europe has therefore only a voluntary fortification.
The authors found that voluntary food fortification increased dietary intake and
biomarker status of folate and metabolically related B vitamins with potential
beneficial effects on health. In this research the authors stress that those who
do not consume fortified foods regularly may have insufficient B vitamin status
and will not participate of these benefits. [17]
High plasma homocysteine levels are a risk factor for mortality and vascular
disease in observational studies of patients with chronic kidney disease. Folic
acid and B vitamins decrease homocysteine levels in this population but whether
they lower mortality is unknown.
Treatment with high doses of folic acid and B vitamins did not improve survival
or reduce the incidence of vascular disease in patients with advanced chronic
kidney disease or end-stage renal disease. [18]
Allen J. Wilcox and colleagues found in a study published in 2007 that folic
acid supplementation during early pregnancy (>400 µg/day) was associated
with a reduced risk of isolated cleft lip with or without cleft palate.
The finds suggest that diets rich in fruits, vegetables, and other high folate
containing foods reduced the risk somewhat, however, folic acid supplements and
multivitamins added to a folate rich diets is the best protection. Folic acid
provided no protection against cleft palate alone. [19]
Shi Wu Wen and colleagues
studied the effect of folic acid supplementation in early second trimester
and reduction of risk of developing preeclampsia. The authors found that the
supplementation of multivitamins containing folic acid was associated with
increased serum folate (on average 10.51 µmol/L), decreased plasma
homocysteine (on average 0.39 µmol/L), and reduced risk of preeclampsia.
They concluded that supplementation of multivitamins containing folic acid in
the second trimester is associated with reduced risk of preeclampsia.
According to the authors these finding may become a new prevention strategy
for pre-eclampsia. [20]
Yoshihiro Sato and colleagues
2002 studied the changes in total plasma homocysteine concentration that
occurred in the first, second, and third trimesters of normal pregnancy in
comparision with nonpregnant controls.
The authors found that homocysteine decrease during pregnancy compared with
nonpregnant controls. Homocysteine levels were decreased with folic acid
supplementation. Homocysteine correlated with albumin levels, which decreased
during pregnancy and with folic acid supplementation.
Vitamin K
[21]
Vitamin K is an essential fat-soluble micronutrient, which is needed for a unique post-translational chemical modification in a small group of proteins with calcium-binding properties, collectively known as vitamin K-dependent proteins or Gla proteins. Thus far, the only unequivocal role of vitamin K in health is in the maintenance of normal coagulation.
Nutritional vitamin K deficiency is a bleeding tendency caused by the relative inactivity of the procoagulant proteins.
Vitamin K dependent proteins synthesized by other tissues include the bone protein osteocalcin and matrix Gla protein, though their functions remain to be clarified. [22]
Vitamin K denotes a group of 2-methilo-naphthoquinone derivatives. They are human lipophilic vitamins linked to blood coagulation, bone health and liver cancer.
Vitamin K2 (menaquinone, menatetrenone) is normally produced by bacteria n the intestines and dietary deficiency is extremely rare unless the intestines are heavily damaged.
Vitamin K is a group name for a number of related compounds, which have in common a methylated naphthoquinone ring structure, and which vary in the aliphatic side chain attached at the 3-position. Phylloquinone(also known as vitamin K1 invariably contains in its side chain four isoprenoid residues, one of which is unsaturated.
Menaquinones have side chains composed of a variable number of unsaturated isoprenoid residues; generally they are designated as MK-n where n specifies the number of isoprenoids.
Naphthoquinone is the functional group. The mechanism of action is therefore similar for all K-vitamins but intestinal absorption, transport, tissue distribution, and bio-availability may differ due to different lipophilicity of the various side chains, and by the different food matrices in which they occur.
The German Association for Nutrition (Deutsche Gesellschaft für Ernährung e.V.) recommend the consumption of vitamin K for Women 65 microg and for man 80 microg /day.
There are two main forms of vitamin K:
The vitamin K1 It is the most important and is known as phylloquinone
or phytonadione . It is present in green leafy vegetables such as lettuce, broccoli and spinach, and can be synthesised in the gut by microflora.
Vitamin K-n
A group of compound called menaquinones (MK-n) is can also be found in foods, where " n "stands for a number of prenyl side chains. MK4 is found in meat. Fermented food like cheese and natto are rich in MK7, MK8, and MK9.
Sarah Cockayne and colleagues in a meta-analysis of human clinical trials using MK-4 supplements for bone health conclude that this systematic review suggests that supplementation with phytonadione and menaquinone-4 reduces bone loss. In the case of the latter, there is a strong effect on incident fractures among Japanese patients. [23]
MK4 from natto and other forms of vitamin K were reported to reduce bone loss. [24]
Naoko Tsugawa and colleagues state in a researche communication that vitamin K deficiency is associated with low bone mineral density and increased risk of bone fracture. Phylloquinone (K1) and menaquinone 4 (MK4) and 7 (MK7) are generally observed in human plasma; however, data are limited on their circulating concentrations and their associations with bone metabolism or with gama-carboxylation of the osteocalcin molecule.
They conclude that submaximal gama-carboxylation being related to the prevention of fracture or bone mineral loss, circulating vitamin K concentrations in elderly people should be kept higher than those in young people. [21]
According to WHO vitamin K deficiency in infants up to around age 6 months, although rare, represents a significant public health problem throughout the world. It is now being termed vitamin K deficiency bleeding (VKDB). In adults, primary vitamin K-deficient states that manifest as bleeding are almost unknown. [25]
The Danish Osteoporosis Prevention Study
(DOPS), however, found vitamin K1 to have no effect on the bone mineral density (BMD)reporting that reports that vitamin K1 intake had no impact on BMD and fracture risk of peri-menopausal women. This supports the statement of WHO/FAO that the only unequivocal role of vitamin K in health is in the maintenance of normal coagulation. citeWHObleeding [26]
Makiko Yoshida and colleagues 2008 in a study concerning the beneficial effect
of vitamin K on insulin resistance, found that supplementation with 500 µg/day
phylloquinone for 36 months improves the insulin resistance in older men and
women. Insulin resistance was measured by homeostasis model assessment
(HOMA-IR) at 36 months as primary outcome, and fasting plasma insulin and
glucose were examined as the secondary outcomes.
The authors concluded that Vitamin K supplementation for 36 months at doses
attainable in the diet may reduce progression of insulin resistance in older men,
but not in women.
[27]
The BMD, or Bone mineral density score is determined by methods using X-ray
Absorptiometry, Computed Tomography or Quantitative Ultrasound to determine osteopenia (low bone mass) or osteoporosis. The Dual Energy X-ray
Absorptiometry or DXA is most frequently used in these cases.
According to Cheung and colleagues 2008 vitamin K, aside of its role in blood
coagulation, the deficiency of vitamin K1 may play a role in low BMD and
risk for fractures.
The authors found in a study that daily 5 mg vitamin K1 supplementation for 2
to 4 years increased serum vitamin K1 levels by 10-fold, and decreased the
percentage of undercarboxylated osteocalcin and total osteocalcin levels (bone
formation marker), but did not change C-telopeptide levels (bone resorption
marker). Women which received supplementation of vitamin K had a reduced
number of clinical fractures and cancers.
The authors concluded that daily 5 mg of vitamin K1 supplementation f does not
protect against age-related decline in BMD, but may protect against fractures and
cancers in postmenopausal women with osteopenia. The authors call for more
studies oin this matter.
Provitamin A can be modified by the body to vitamin A.This happens only to the extent of need. Therefore one says provitamin A to be a safe source of vitamin A bearing no danger of overfeeding. [28]
Phototransduction is a process by which light is converted into electrical signals in the rod cells, cone cells and photosensitive ganglion cells of the retina of the eye.
The retina is formed by rods and cone cells. These cells contain a chromophore, which are formed by membrane protein called opsin, connected with the aldehyde of Vitamin A1 (11-cis retinal). Retinol cannot be synthesised by humans and must be supplied by vitamin A in the diet. Deficiency of all-trans retinol can lead to night blindness.
Rod cells deal with low light level and do not mediate colour vision. Cone cells can code the color of an image. There are three different types of cones. Each cone type responds best to certain wavelengths, or colours, of light because each type has a slightly different opsin. Opsins transform a photon of light into an electrochemical signal, triggering the visual transduction cascade. Another opsin found in the mammalian retina, melanopsin, is involved in circadian rhythms and pupillary reflex but not in image-forming. Opsins can change their conformation from a resting state to a signalling state upon light absorption, which activates the G protein, thereby resulting in a signalling cascade that produces physiological responses. [29] [30]
Vitamin A deficiency in children increases vulnerability to infections like diarrhoea and measles and may also lead to blindness. Globally, the World Health Organisation estimates that 190 million children under the age of 5 may be vitamin A deficient. But, despite widespread efforts, vitamin A programmes do not reach all children who could benefit.
Mayo-Wilson et al 2011, say that vitamin A supplements reduce child mortality by 24% in low and middle income countries. It may also reduce mortality and disability by preventing measles, diarrhoea and vision problems, including night blindness. Vitamin A supplementation may save over 600,000 each year and 20 million disability-adjusted life years would be gained. The authors urge policymakers to provide vitamin A supplementation for children under 5 in deficient areas. [31]
The WHO stresses that for pregnant women in high-risk areas, vitamin A deficiency occurs especially during the last trimester when demand by both the unborn child and the mother is highest, seen as night blindness during this period.
To combat vitamin A deficiency, the WHO pursues short-term interventions and proper infant feeding backed up by long-term sustainable solutions, which includes a combination of breastfeeding and vitamin A supplementation, coupled with enduring solutions, such as promotion of vitamin A-rich diets and food fortification. Between 6 months and 6 years of age can reduce overall child mortality by a quarter in areas with significant vitamin A deficiency.. However, because breastfeeding is time-limited and the effect of vitamin A supplementation capsules lasts only 4-6 months, they are only initial steps towards ensuring better overall nutrition and not long-term solutions.
In 1998 WHO and its partners UNICEF, the Canadian International Development Agency, the United States Agency for International Development and the Micronutrient Initiative - launched the Vitamin A Global Global Alliance for Vitamin A (GAVA), which is an informal partnership between the Canadian International Development Agency, Helen Keller International, Micronutrient Initiative, UNICEF, USAID, and the World Bank. About 75 per cent of the vitamin A required for supplementation activity by developing countries is supplied by the Micronutrient Initiative.
Vitamin Angels was launched in 2007 and will cover 18 countries. The program gives children two high dose vitamin A and anti-parasitic supplements (twice a year for four years), which provides children with enough of the nutrient during their most vulnerable years in order to prevent them from going blind and suffering from other life-threatening diseases caused by Vitamin A Deficiency. [32]
The light sensing process so far had been exclusively linked to retinal. Holmes et al. 2011 discovered a second form of phototransduction light sensing in cells. This light sensing system uses cryptochromes coupled to a B2 vitamin derivate. Cryptochromes are blue-light photoreceptors found in circadian and arousal neurons.
The research targeted the CRYPTOCHROME (CRY) gene of large lateral ventral arousal neurons (l-LNv) in Drosophila melanogaster. The authors report that cry-null lines are light unresponsive, but light response is restored when CRY expression is reactivated, requiring a flavin redox-based mechanism which also depends on potassium channel conductance, but is independent of the classical circadian CRY-TIMELESS interaction. Neurons not light responsive could be activated when they were genetically induced to express cryptochrome.
Hipervitaminosis of vitamin B1 may lead to nervousness and headache.
There is no maximum limit for vitamin B2.Even in high dose there are no undesired reactions.
Accentuated hipervitaminosis of vitamin B6 causes alterations of the mobility,numbness and psychical alterations.Alterations similar to contergan in neonates were also observed.
The UK Committee on Toxicity of Chemicals in Food recommend not to exceed 10 mg per day.
A sufficient supply of vitamin B6 is guaranteed with consumption of meat,fish,eggs, and some vegetables. Some food supplements contain up to 100 mg.The Committee tries to organise a voluntary producer limit of vitamin B6 in food supplements and include more informations on label.The commission is concerned about possible damage of the nervous system in case of high dose.
There are no major problems noted by excessive consumption of vitamin B12. A predisposition to thrombosis is possible.
Niacin is a global denomination of nicotinic acid and her acid amid denominated as nicotinamide, also called niacinamide.Both vitamins have same properties.
Nicotinamide is important to the transport of electrons in cells and is engaged in the following reactions:
- Anaerobic glicolysis
- In the cycle of cancer (oxidative phosphorilation)
- In the synthesis of fatty acids.
Nicotinic acid and nicotinamide can be assimilated directly or are created by hydrolysis of coenzyme. Adenine is transformed in NAD(P) in the liver. NAD(P) stands for Nicotinamide-AdenineDinucleotide-Phosphate.
To synthesises NAD in human cells 60 mg of tryptophane corresponding to 1 mg equivalents of nicotinamide are necessary.For this reason the unit " niacin equivalent " was created.
1 niacin equivalent = 1 mg niacin = 60 mg tryptophane
Niacin is not deposited. Poisonings resulting from excessive addition of niacin to food are documented.Symptoms are ictericia, failures of liver, icteric skin with burning flushes. Toxic reactions were not noted after daily intake of 3 to 6 grams of nicotinic acid trying to inhibit the production of hepatic VLDL causing parallel dilatation of the peripheric vascular system producing the red flush which disappears after some days.
Nicotinamide does not produce flush and does not reduce cholesterol.
It is therefore that nicotinamide is being used in treatment of insufficiency of niacin, using dose between 50 to 250 mg/day.
Niacin is present mainly in animal food (meat)as coenzymes.
Absorption of Niacin from meat is near 100%.The amount of niacin in plants is very low.
In cereals niacin is being found in the aleurone coat (external coat of the grain). Niacin is lost during polishing of grains to obtain white flour.
In cereal niacin is bound as a complex in macromolecules niacitine, therefore only 30% of vegetable niacin can be assimilated.
Triptophane is sometimes much higher as free niacin, therefore the equivalent of niacin is being used. In vivo conversion of triptophane in niacin depends on coexistence of vitamin B6.
| Food |
mg niacin in 100 g |
|---|
| Meat |
5 to 11 |
| Fish |
3 to 4 |
| Sardine |
9,7 |
| Tuna |
8,5 |
| Mackerel |
7,5 |
| Milk |
0,09 |
| Butter |
0,03 |
| Cheese |
1,2 |
| Black bread |
3,3 |
| White bread |
0,9 |
| Lentil |
2 |
| Soya meal |
2,2 |
| Sunflower seed |
4 |
| Yeast, dry |
45 |
| Yeast, fresh |
17 |
| Fruits |
0,65 |
| Vegetables 0,6 to 2,0 |
|
| Coffee, ground |
13,7 |
| Group |
babies |
children |
men |
women |
| Under 4 month |
5 |
|
|
|
| From 4 to 12 month |
6 |
|
|
|
| From 1 to 4 years |
|
9 |
|
|
| Over 4 and under 7 years |
|
12 |
|
|
| From 7 to under 10 years |
|
13 |
|
|
| From 10 to 13 years |
|
|
15 |
14 |
| From 13 to under 15 years |
|
|
20 |
16 |
| From 15 to under 19 years |
|
|
20 |
16 |
| From 19 years and up |
|
|
18 |
15 |
| Pregnant |
|
|
|
17 |
| During lactation |
|
|
|
20 |
[33]
Transglutaminase is an enzyme which polymerizes proteins with the result of a network like structures. This effect is used in the production of meat, sausages, cheese, yogurt and related products, ice creams and production of gelatin improving consistency and cream character of the products. As sun incidence and the amount of natural vitamins in
different geographical regions throughout the world vary, each country has its own regulations.
France being nearer to the Equator and having thus a higher sun incidence as Germany has a limit of vitamin A which is very low. Vitamin D is there not allowed in order to avoid an oversupply. [34]
Michael Holick and colleagues found that vitamin D2 daily was as effective as
the same amount of vitamin D3 in maintaining serum 25-hydroxyvitamin D
levels and did not negatively influence serum 25-hydroxyvitamin D3 levels.
Therefore, vitamin D2 is equally as effective as vitamin D3 in maintaining
25-hydroxyvitamin D status. This study was performed in response to two
reports suggested that vitamin D2 is less effective than vitamin D3 in maintaining vitamin D status.
The European Union advises not to exceed 1000 mg of complementary vitamin C in a daily personal feeding.
Other specific legislations exists and should be observed for each vitamin and each kind of food. [35]
According to US surveys the intake of vitamin D is insufficient. Additional food fortification as well as dietary and supplement guidance are needed for the general population.
Vitamin D status differs by latitude and race and variation of the sunlight during seasons, especially the winter month. Individuals with more skin pigmentation are at increased risk of deficiency. It is synthesised in the body on exposure to sunlight. Food can not supply sufficient amounts.
To reduce cancer risk, exposure to sunlight or artificial UVR sources should be accompanied by abundant fruit and vegetables intake and/or antioxidants, not smoking in order to help combat the free radicals generated from UVR exposure. [36]
According to the study published by Garland, a scientist of the University of California Moores Cancer Centre, the vitamin D status differs by latitude and race, with residents of the northeastern United States and individuals with more skin pigmentation being at increased risk of deficiency.
The increased skin pigmentation of African-Americans reduces their ability to synthesize vitamin D, turning them more susceptible to breast cancer, colon, prostate and ovarian cancers as white women.
Vitamin D fortified foods are consumed to reduce the risk of osteoporosis. The cancer risk reduction may become another important reason for the demand of this vitamin The authors suggest that efforts to improve vitamin D status, for example by vitamin D supplementation, could reduce cancer incidence and mortality at low cost, with few or no adverse effects. [37]
Harald Dobnig and colleagues 2008 say that low 25-hydroxyvitamin D and
1,25-dihydroxyvitamin D levels are independently associated with all-cause and
cardiovascular mortality.
Thes authors write that these findings base on the correlation of low
25-hydroxyvitamin D levels of inflammation indicators (C-reactive protein
and interleukin 6 levels), oxidative burden (serum phospholipid and
glutathione levels), and cell adhesion (vascular cell adhesion molecule 1 and
intercellular adhesion molecule 1 levels).
The authors point out that urbanization, demographic shifts, decreased
outdoor activity, air pollution and global dimming, and decreases in the
cutaneous production of vitamin D with age may account for 50% to 60% of
people to have low vitamin-D status.
The minimum desirable serum level of 25-hydroxyvitamin D has been suggested to
be 20 to 30 ng/mL, and levels lower than this are clearly related to
compromised bone-mineral density, falls, and fractures and more recently have
also been linked to cancer and immune dysfunction, as well as cardiovascular
disease, hypertension, and metabolic syndrome, the authors report.
The study used data from the Ludwigshafen Risk and Cardiovascular Health
(LURIC) study which investigated the effect of genetic polymorphisms and
plasma biomarkers on cardiovascular health status.
[38]
However, they stress that aside of the effect of low vitamin D status, other
factors may be associated with mortality including matrix metalloproteinases.
[39]
Edward Giovannucci and colleagues in a study in 2008 found an association of low levels of 25(OH)D with higher risk of myocardial infarction. [40]
Researchers found new evidence from the Northern Manhattan Study connecting low vitamin D levels to atherosclerosis. Silverberg et al. 2011, report that D levels 25-hydroxyvitamin D levels were associated with increased intima-media and maximal carotid thickness in those with plaque.
The authors studied 203 adults from the Northern Manhattan Study (NOMAS) which is a research study of stroke and stroke risk factors in the Northern Manhattan community. [41]
The authors assessed levels and effects of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, calcium, phosphorus, and parathyroid hormone. They found that 25-hydroxyvitamin D was inversely associated with both intima-media thickness and maximal carotid plaque thickness. Plaque number was associated with phosphorus levels (beta, 0.39 per 1-mg/dL increase) and calcium-phosphorus product (beta, 0.36 per 10-U).
25-hydroxyvitamin D accounted for 13% of the var
iance in both intima-media thickness and maximal carotid plaque thickness. Calcium, parathyroid hormone, and 1,25-dihydroxyvitamin D levels were not associated with carotid measures. There are still insufficient data on the effect of vitamin D. The precise nature of this association and the optimum levels of vitamin D for vascular health remain unknown, say the authors. [42]
The Institute of Medicine (IOM) recommended 600 international units (IU) per day for people aged 1 to 70 and 800 IU per day for those aged 71 and older, and an acceptable upper limit of daily intake to 4000 IU for adults. Extremely high intakes of vitamin D can lead to too much calcium in the blood and damage the kidney and heart, but whether moderately high doses of vitamin D have side effects is not yet clear. The IOM says that vitamin D has bone benefits but it is unknown whether vitamin D supplements prevent diseases cancer, heart disease, stroke, or other chronic diseases.
Because of this uncertainty, the IOM called for more research to determine whether higher doses of vitamin D can lower the risk for cancer, heart disease, stroke, and other chronic illnesses and whether such doses pose any health risks. The VITAL Study, also known as the Vitamin D and Omega-3 Trial, is designed to answer the scientific questions regarding vitamin D.
[43]
Foregoing vitamin D studies said it could only reduce fracture risk in
combination with calcium. However, according to Heike A. Bischoff-Ferrari and
colleagues 2009 the prevention of nonvertebral fractures with vitamin D is
dose-dependent for individuals aged 65 years or older. The authors found that
a high supplemental vitamin D dose (482-770 IU/d) should reduce nonvertebral
fractures by at least 20% and hip fractures by at least 18%. The use of
low-dose vitamin D with or without calcium in the prevention of fractures
among older individuals is not being recommended by the authors, and greater
benefits may be achieved if vitamin D supplementation starts earlier. [44]
Bruce Ames and Joyce McCann in a critical review write that there is evidence
to suggest an important role for vitamin D in brain development and function.
The authors comment previous studies in both human and animal models which indicate that inadequate levels of vitamin D may also produce cognitive or
behavioural consequences, although the evidence is not conclusive for the moment.
The authors conclude that despite residual uncertainty, recommendations for
vitamin D supplementation of at-risk groups, including nursing infants, the
elderly, and African-Americans appear warranted to ensure adequacy. [45]
Marian Evatt and colleagues 2008 report that Fifty-five per cent of patients
with Parkinson's disease had insufficient levels of plasma 25-hydroxyvitamin D
(25[OH]D). The authors wrote that low vitamin D levels may contribute to the
risk of developing Parkinson's disease.
The group with Parkinson's disease in this study presented a vitamin D serum
level of 31.9 ng/ml compared with 34.8 ng/ml of a group of Alzheimer's
disease and 37.0 ng/ml of healthy groups. The authors concluded that vitamin
D insufficiency may have a unique association with Parkinson's.
The researchers continue their study to see if a dietary supplement, or increased
exposure to sunlight may help alleviate symptoms or even retard progression of
the disease. [46]
Llewellyn and colleagues 2010 studied the connection between cognitive decline
and low levels of serum 25-hydroxyvitamin D (25[OH]D) using data of the
InCHIANTI study [47] conducted in Italy between 1998 and 2006.
The Mini-Mental State Examination (MMSE) [48] was used
to evaluate cognitive decline. Severe serum 25(OH)D deficiency were found
with levels <25 nmol/L), levels >25 to <50 nmol/L were considered as
insufficient, whereas levels of 25(OH)D >/=75 nmol/L were considered as
sufficient.
Evaluating their data, the authors state that low levels of vitamin D are
associated with substantial cognitive decline in the elderly population, and
status of vitamin D should be considered en treatment and prevention.
Data from the Third National Health and Nutrition Survey (NHANES III) [49] also show that vitamin D deficiency is associated with
an increased risk for cognitive impairment in older persons. According to Dr.
Llewellyn vitamin D seems to play a role in processes that may be important
for dementia risk, including vascular health and amyloid clearance from the brain.
Controversies
McGrath and colleagues 2007 also using data from NHANES III did not find an
association between vitamin D levels and cognitive performance. Llewelly says
that results of McGrath study may be related to methodology which used only
delayed verbal memory from the Mini-Mental State Examination (MMSE) and the
East Boston Memory Test. [50]
Andrew Grey, MD, and Mark Bolland, in an editorial comment the study of
Llewellyn and colleagues, pointing out that it is unlikely that a single
vitamine could play such a substantial role in preventing diseases. The
authors say that it is more likely that low vitamin D is not the cause, but
only a marker of overall poor health, low sunlight exposure, low physical
activity, high adiposity. [51] [52]
Overall, individuals with ≥1000 IU/day oral Vitamin D had 50% lower
incidence of colorectal cancer compared to reference values. Cedric F. Garland
urges for a prompt public health action to increase intake of Vitamin D3
to 1000 IU/day, and to raise 25-hydroxyvitamin D by encouraging a modest
duration of sunlight exposure. [53]
A study leaded by Esther M. John found that the risk of prostate cancer was
reduced by 50 percent in men who had high levels of sun exposure during their
lifetimes, compared with men who had low lifetime levels. The findings of this
study support the hypothesis that sun exposure and vitamin D receptor (VDR)
polymorphisms together play important roles in the aetiology of prostate cancer.
The best source of vitamin D is from 20-30 minutes sun exposure. Long sun exposure is discouraged due to the risk of skin cancer. Other authors find 5 to 10 minutes sun exposure on our face and arms during the summer time sufficient to obtain the required daily amount of Vitamin D. [54]
Vitamin D supplementation in winter necessary
[55] [56] [54]
Dr Julie Wallace and researchers from the Northern Ireland Centre for Food and Healthtogether with with colleagues from University College Cork to investigate what level of dietary vitamin D is needed in winter.
According to Dr. Wallace higher levels of vitamin D fortification and supplementation are needed. Large population groups are at risk of having not sufficient supply of vitamin D. Foods which are good sources of vitamin D like oily fish are not consumed regularly. The best source could be from fortified foods and supplements.
Some authors point out that Asian children suffer insufficient levels of vitamin D with , risk of osteoporosis.
Vitamin D2 is as effective as vitamin D3 Michael Holick and colleagues found that vitamin D2 daily was as effective as
the same amount of vitamin D3 in maintaining serum 25-hydroxyvitamin D
levels and did not negatively influence serum 25-hydroxyvitamin D3 levels.
Therefore, vitamin D2 is equally as effective as vitamin D3 in maintaining
25-hydroxyvitamin D status. This study was performed in response to two
reports suggested that vitamin D2 is less effective than vitamin D3 in
maintaining vitamin D status.
[57]
Gordon and colleagues 2008 found that a low degree of vitamin D insufficiency
is widespread in US. The authors also stress that breastfed infants in winter
who did not receive vitamin D supplementation were the most severely vitamin D deficient.
The authors enforce the recommendations for health care providers and parents
to ensure that breastfed infants receive daily vitamin D supplementation for
the duration of breastfeeding
In this study older age, winter season, higher body mass index, black
race/ethnicity, and elevated parathyroid hormone concentrations were also
associated with lower vitamin D status. One-third of vitamin D-deficient
participants exhibited demineralization.
[58]
Rovner and O'Brien 2008 found that there
is still insufficiency on vitamin D in children in the United States. The
authors efforts call for efforts to improve the vitamin D status of children.
[59]
According to Kremer and colleagues 2010 vitamin D insufficiency
(25-hydroxyvitamin D) is linked to increased muscle fat and decreased muscle
strength. Approximately 59% of subjects were 25OHD insufficient (higher or
equal to 29 ng/ml). Serum 25OHD wasa found to inversely related to percent
muscle fat. The relation between 25OHD and muscle adiposity was independent
of body mass or visceral fat. The authors concluded that vitamin D
insufficiency is associated with increased fat infiltration in muscle young
women but stress that more studies are necessary before a supplementation can
be recommended.
In a study of 2009 the group around Kremer found that vitamin D insufficiency
is associated with increased body fat and decreased height but not changes in
peak bone mass. [60] [61]
Lu Wang and colleagues 2008 investigated the associations of intake of dairy
products, calcium, and vitamin D with the incidence of hypertension trend. The
risk of hypertension decreased with high dietary calcium intake, but did not
change with calcium or vitamin D supplements, or with high-fat dairy products
for which the saturated fats in high-fat dairy products may my be responsible
for. High calcium intake facilitates weight loss and enhances insulin
sensitivity, which also contribute to blood pressure reduction.
The study concluded that intakes of low-fat dairy products, calcium, and
vitamin D reduced the risk of hypertension in middle-aged and older women,
suggesting their potential roles in the primary prevention of hypertension and
cardiovascular complications.
The study supports the 2005 Dietary Guideline from the US Department of
Agriculture recommending the intake of milk and milk products to three
servings per day and stresses the importance of low-fat dairy products.
[62]
According to Cannell and colleagues 2008 the metabolic product of vitamin D is
a potent, pleiotropic,repair and maintenance, secosteroid hormone. Vitamin D
deficiencies are common, standing for a host of diseases other than cancer.
Daily ingestion of 1100 IU of colecalciferol (vitamin D) over a 4-year period
were suggested to reduced the incidence of non-skin cancers. The authors
stress that official recommendations were never designed and are not effective
in preventing or treating vitamin D deficiency.
Diagnosis of vitamin D deficiency
The authors say that assessing serum 25-hydroxy-vitamin D is the only way to
make the diagnosis and to assure that treatment is adequate and safe.
They recommend that the of serum levels of 25-hydroxy-vitamin D should be
raised >40 ng/ml, year around, which is the level found in humans living
naturally in a sun-rich environment. Sunlight, artificial ultraviolet B
radiation or supplementation are being suggested by the authors which say that
benefits of all treatment modalities outweigh potential risks.
Cannell and colleauges suggest a supplementation of ≤ 5000 IU (125
microg) of vitamin D/day for obese, aged and/or dark-skinned patients to
maintain adequate levels during the winter at many temperate latitudes [63]
Both forms of vitamin D (D2 and D3) used in supplementation had been regarded as equivalent and interchangeable.
However, according to Lisa A Houghton and Reinhold Vieth, ergocalciferol (Vitamin D2 should not be regarded as a nutrient suitable for supplementation or fortification because it is less efficient in raising serum 25-hydroxyvitamin D, its metabolites have a diminished binding to vitamin D binding protein in plasma, and a nonphysiologic metabolism and shorter shelf life compared with cholecalciferol (vitamin D3).
Consumer should look at the ingredient list of fortified foods such as margarine, cereals and probiotics for good cholecalciferol (vitamin D)
[63] [64]
The 25-(OH)D is the major circulating vitamin D metabolite found in human
serum and is determined by diet and exposure to sun. Several recent studies
advocate a high level of vitamin D to reduce risk of coronary and other
diseases, such as pancreatic cancer. Pancreatic cells express 25-(OH)
D(3)-1alpha-hydroxylase that generates the biologically active
1,25-dihydroxy(OH)(2) D form, and a high vitamin D status may affect the cells
of the pancreas. Stolzenberg-Solomon 2009, however, cites a nested
case-control study conducted in a population of male Finnish smokers which
showed a 3-fold increased risk for pancreatic cancer with high vitamin D
status. This study was conducted in male smokers, limiting therefore its
conclusions to this group. The author writes that there are more studies necessary to make a final conclusion on the association of vitamin D and
pancreatic cancer.
[65]
In a nested case-control study in the Prostate, Lung, Colorectal, and Ovarian
Screening Trial cohort of men and women prediagnostic serum 25(OH)D
concentrations study Stolzenberg-Solomon and colleagues found no association
of Vitamin D with pancreatic cancer overall. This study could not support the
strong positive association of 25(OH)D and pancreatic cancer of the foregoing
Finnish study. However, increased risk of pancreatic cancer was found in
persons with low solar exposure, but not in those with moderate to high
annual exposure, which is similar to the Finish study.
[66] [55] [56] [54]
Several recent epidemiological studies demonstrate reduced bone density and increased rates of bone loss in individuals habitually consuming low protein diets.
In short term studies Women's Health Research at Yale found that a low animal and plant protein diet caused levels of certain hormones (calcitropic parathyroid hormone (PTH) ) to rise, which act to stimulate bone breakdown to compensate for the calcium it was not getting from the diet.
The calcitropic hormones were NcAMP, Midmolecule PTH, Intact PTH and calcitriol.
Replacing all meat and animal proteins with soy foods, the low soy protein diet seemed to interfere with intestinal calcium absorption to an even greater extent than did the low mixed source protein diet. Should this be confirmed in ongoing studies, inclusion of additional calcium when consuming soy foods will prove to be necessary. [67]
Preeclampsia is a pregnancy induced hypertension in association with significant
amounts of protein in the urine. There can be many different causes for the
syndrome. While blood pressure elevation is the most visible sign of the disease,
it involves generalized damage to the maternal endothelium and kidneys and liver,
with the release of vasopressive factors only secondary to the original damage.
Many strategies to reduce the risk of preeclampsia are being studied using
vitamine or minerals as supplements: [68]
According to Lisa M. Bodnar and colleagues 2007 maternal vitamin D deficiency may
be an independent risk factor for preeclampsia. The authors suggest vitamin D
supplementation in early pregnancy to prevent preeclampsia and promote neonatal
well-being.
Sources of Vitamin D
Vitamin D is formed in the skin during exposure to sunlight. It is found in
fatty fish, however, diet alone without supplementation may lead to an under
supply. Urbanisation, demographic shifts, decreased outdoor activity, air
pollution and global dimming, and increasing age are told to be responsible
for wide population groups to be deficient in vitamin D. [69]
Hypovitaminosis D is prevalent in youth worldwide, but the safety of vitamin D
at doses exceeding 200 IU/day is unknown in this age group. We assessed the
safety of high doses of vitamin D3 administered to apparently healthy school children.
Ghada El-Haff Fuleihan and colleagues 2008 in a study with adolescents, gave
vitamin D3 in 200 and 2.000 IU/day for one year. No vitamin D intoxication
was detected with biochemical variables monitoring.
The authors concluded that vitamin D3 at doses equivalent to 2,000 IU/day for
one year is safe in adolescents and results in desirable vitamin D levels.
According to Michael Holick, vitamin D deficiency remains common in children
and adults. In utero and during childhood, vitamin D deficiency can cause
growth retardation and skeletal deformities and may increase the risk of hip
fracture later in life.
Holick states that curret recommendations of 200 IU per day for children and
adults up to 50 years of age for vitamin D need to be increased to 800 - 1000
IU vitamin D3.
About 60 per cent of northern populations may be vitamin D deficient.
increasing the risk of osteopenia, osteoporosis, muscle weakness, fractures,
common cancers, autoimmune diseases, infectious diseases and cardiovascular
diseases. [70]
According to Vieth and colleagues 2007, human diets do not provide sufficient
vitamin D, which is confirmed by low serum 25(OH)D concentrations.
Vieth concludes that correction of low 25(OH)D concentrations can happen only
if some or all of the following are implemented: the encouragement of safe,
moderate exposure of skin to ultraviolet light; appropriate increases in food
fortification with vitamin D; and the provision of higher doses of vitamin D
in supplements for adults. [71]
Holik and Chen 2008 recommends a circulating level of 25-hydroxyvitamin D of >75
nmol/L, or 30 ng/mL, to maximize vitamin D's beneficial effects for health. In
the absence of adequate sun exposure, at least 800-1000 IU vitamin D3/d may be
needed to achieve this in children and adults. Vitamin D2 may be equally
effective for maintaining circulating concentrations of 25-hydroxyvitamin D when
given in physiologic concentrations. [72] [73]
According to Suzanne Judd and colleagues 2008, point out that recent clinical
trials and animal studies have suggested that vitamin D insufficiency may be
associated with elevated blood pressure. In their study, the authors found that
systolic blood pressure (SBP) is inversely associated with serum vitamin D
concentrations in nonhypertensive white persons in the United States. The
authors call for studies on the potential effects of vitamin D supplementation as
a method to reduce SBP in persons at risk of hypertension. [74]
A novel sunscreen-antioxidant was developed by Damiani and colleagues contains the UVB absorber, 2-ethylhexyl-4-methoxycinnamate (OMC) combined with the piperidine nitroxide TEMPOL, which has antioxidant properties. This sunscreen could reduce the risk of melanoma caused by sun exposure.
[75]
According to DeAnn Lazovic and colleagues 2010 the use of indoor tanning devices
increases the risk of melanoma by 74 percent if tanning beds are used for any
amount of time. Frequent uses of tanning beds increases melanoma risk 2.5 to 3
times compared with persons who never use it. Frequent users of indoor tanning
beds ( 50 plus hours, more than 100 sessions, or for 10-plus years.) are 2.5 to 3
times more likely to develop melanoma than those who never use tanning devices.
The risk was directly related to the time spent tanning. These findings were
independent of the type of tanning device, gender or age, contradicting previous
studies of Cokkinides and the position of the American Cancer Society which
say that indoor tanning before the age of 35 years increases the risk of
melanoma. The study of Cokkinides and colleagues 2010
refers to the meta analysis which says that indoor tanning use before the age
of 35 years increases the risk of melanoma. These believes leaded to state
legislation restricting minors' access to indoor tanning.
[76] The American Cancer Society
says that using a tanning bed before age 35 increases a person's risk of
developing melanoma by 75 percent. Physicians hope that recent actions by the
FTC, along with TMA-supported state legislation placing age restrictions on
minors' use of tanning beds, will spur the tanning industry to operate more
responsibly and stop spreading false information to the public.
[77]
Public health implication of tanning beds
[78]
Tanning bed proponents claim that vitamin D supplementation supports indoor
tanning health effect. They support the theory that reduced vitamin D levels
or certain vitamin D receptor polymorphisms may increase melanoma risk.
Woo and Eide 2010 clarify that ultraviolet A is used by most tanning devices.
This light is relatively ineffective in stimulating vitamin D synthesis. Health
benefits from this association is therefore significant. The authors stress,
therefore, the importance of education of the general public and a stricter
indoor tanning legislation to reduce public health risks. [79]
The proposed Tanning Bed Cancer Control Act intends to regulate the use of
tanning beds. It proposes a limit on the amount of UV rays emitted by a tanning
bed and how long someone can be exposed to them, along with an age limit of over
18. [80]
Incidence rates of skin cancer are rising in Great Britain. Some occupations are
exposed to sunlight, such as farmers, construction workers and some public
service workers. Young 2009 found a clear association between solar radiation and
skin cancer and calls for protective measures to reduce the burden of
occupational skin cancer in Great Britain. [81]
According to Dr. Anthony Norman of the University of California, Riverside and there are evidences that vitamin D, when converted into a hormone, promotes the normal growth of cells and has anticancer properties rising the interest to develop the vitamin D hormone or analogues for use in cancer treatment vitamin D hormone to decrease the proliferation of cells and control malignant cell growth. [82]
According to the paediatrician Dr. Tamer Adham the children over eight years old in the United Arab Emirates (UAE) need 15-20 minutes of exposure to sunlight per day because they often have a high level of vitamin D deficiency due to lack of exposure to sunlight in this region. This may be due to clothing habit of the region.
Other authors recommend 2000 IU, equal to the so-called upper safe limit, however, scientists do not recommend taking high doses of the vitamin warning against increased calcium blood levels and kidney problems. [83]
Bo-Ying Bao from the University of Rochester and Taipei Medical University found evidences that indicate that vitamin D, in the form of the highly active 1 alfa, 25-dihydroxyvitamin D3 (1,25-VD) suppresses prostate cancer progression by inhibition of tumour growth and metastasis. Vitamin D acts inhibiting the function of protease enzymes that are involved in tumour invasion.
These findings support the idea that vitamin D-based therapies might be beneficial in the management of advanced prostate cancer.
Bo-Ying Bao found that 1,25-Vitamin D decreased matric metalloproteinases (MMP-9) and cathepsins (CPs), while it also increased the activity of their counterparts, tissue inhibitors of metalloproteinase-1 (TIMP-1) and cathepsin inhibitors. 1,25-VD did not suppress MMP-9 expression at the transcriptional level, but reduced its mRNA stability. [84]
Elina Hypponen and Chris Power in a British study found significantly higher
concentrations of vitamin D in persons which used vitamin D supplements or
oily fish, but were not significantly higher in participants who consumed
vitamin D-fortified margarine than in those who did not. The authors conclude
that the prevalence of hypovitaminosis D in the general population was
alarmingly high duringthe winter and spring, which warrants action at a
population level rather than at a risk group level.
Julia Knight and colleagues found, in an epidemiological study, that reduced
breast cancer risks were associated withincreasing sun exposure cod liver oil
use and increasing milk consumption for more than 10 glasses per week from
ages 10 to 19 but less in ages 20 to 29, no evidence was found for ages 45
to 54. The authors conclude that vitamin D could help to prevent breath cancer
in early life, particularly during breast development, but found reduced and
even no such effect in higher ages. [85]
Evidences for a better survival of patients with non-small-cell lung cancer
due to vitamin D were reported by Wei Zhou and colleagues (2007). The
researchers investigated the results of circulating 25-hydroxyvitamin D
(25(OH)D) levels on overall survival (OS) and recurrence-free survival (RFS)
in early-stage non-small-cell lung cancer (NSCLC).
For the joint effects of 25(OH)Dlevel and vitamin D intake, the combined high
25(OH)D levels and high vitamin D intake were associated with better survival
than the combined low 25(OH)D levels and low vitamin D intake.. Similar
effects of 25(OH)D levels and vitamin D intake were observed for RFS. The
authors concluded that vitamin D may be associated with improved survival of
patients with early-stage NSCLC. [86]
Evaluation of most relations of health and disease that involve vitamin D
leads to the conclusion that a desirable 25(OH)D concentration is >75 nmol/L
(30 nanog/mL). [87] [88]
Supplemental intake of 400 IU vitamin D/d has only a modest effect on blood
concentrations of 25(OH)D, raising them by 7-12 nmol/L, depending on the
starting point. To raise 25(OH)D from 50 to 80 nmol/L requires an additional
intake of about 1700 IU vitamin D/d.
The most advantageous serum concentrations of 25(OH)D begin at 75 nmol/L (30
ng/mL), and the best are between 90 and 100 nmol/L (36-40 ng/mL).
In most persons, these concentrations could not be reached with the current
recommendation of the Institute of Medicine of intakes are 200 IU/d from
birth through age 50 years, 400 IU for those aged 51-70 years, and 600 IU for
those aged >70 years.
Bischoff-Ferrari and colleagues suggest therefore in 2006 that an intake for
all adults of >1000 IU (40 microg) vitamin D (cholecalciferol)/d is needed
to bring vitamin D concentrations in no less than 50% of the population up
to 75 nmol/L. The authors stress that the implications of higher doses for
the entire adult population should be addressed in future studies.
[87]
Based on these facts Reihold Veight an colleagues call for international
agencies such as the Food and Nutrition Board and the European Commission's
Health and Consumer Protection Directorate-General to reassess as a matter of
high priority their dietary recommendations for vitamin D, because the formal
nationwide advice from health agencies needs to be changed. [89]
[90]
A report of the DIPART (Vitamin D Individual Patient Analysis of Randomized
Trials) Group says that Vitamin D
plus calcium, but not vitamin D alone in doses of 10 to 20 µg, reduces the
risk for fractures and hip fractures. The link between vitamin D plus calcium
and a reduced risk for fractures is not affected by age, sex, fracture
history, or hormone replacement therapy. A better undestanding of the effect
od vitamin D is essential because fragility fractures are a significant source
of morbidity and mortality in older persons. Clinical trials focused on vitamin E were not successful to lower cholesterol. Das et al 2012 assessed the LDL reducing role of isomers of vitamin E, the tocotrienols. Rabbits were submitted to cholesterol-rich diet supplemented with tocotrienols.
The authors report that left ventricular function including aortic flow, the developed pressure, and the myocardial infarct size exhibited significantly improved recovery with tocotrienol-gama and -alpha but not with tocotrienol-delta. The authors explain that tocotrienol-gama and -alpha lower hypercholesterolemic proteins, such as the matrix metalloproteinase MMP2, MMP9(cholesterol regulates MMP2 and MMP9 expression), ET-1 which is increased by hypocholesterolemia, and SPOT 14 which is linked with hypercholesterolemia. The cholesterol suppressing TGF-beta was upregulated. Tocotrienol-delta had no effect.
Cardioprotection of red palmoil tocotrienols [92]
The tocotrienol-rich fraction (TRF) from red palm oil are being suggested by Das et al.2008 as cardioprotective. Tocotrienol were also found to act neuroprotective against stroke. TRF of palm oil consists of three isoforms of tocotrienols (alpha, gama, and delta) as well as alpha-tocopherol. The optimal concentration for TRF was determined by the authors being 3.5% TRF and 0.3 mg/kg body wt of tocotrienol given to rats for 4 weeks.
TRF as well as all the isomers of tocotrienol used in our study provided cardioprotection, as evidenced by their ability to improve postischemic ventricular function and reduce myocardial infarct size. The gamma-isoform of tocotrienol was the most cardioprotective of all the isomers followed by the alpha- and delta-isoforms.
The cardioprotection of tocotrienol isoforms were assessed by controlling their abilities to stabilize the proteasome, allowing it to maintain a balance between prodeath and prosurvival signals. Tocotrienol isoforms generated a survival signal by reducing c-Src and increasing the phosphorylation of Akt.
Proteasomes are very large protein complexes located in the nucleus and the cytoplasm. They degrade unneeded or damaged proteins. of particular proteins and degrade misfolded proteins by proteolysis C-src tyrosine kinase, also known as CSK, is a human protein and gene. It includes an SH2 domain, an SH3 domain, and a tyrosine kinase domain. This protein specifically phosphorylates Tyr-504 residue [93].
According to Professor Peter Jüni, several thousand deaths per year in Germany may be caused by vitamin supplements consumption. Peter Jüni is the Head of the Division of Clinical Epidemiology and Biostatistics and the Director of CTU Bern, the University hospital's clinical trials unit (Switzerland). He based his projections on studies which focus on vitamin dietary supplementation.
The BfR at Berlin cautions that a one-sided, imbalanced diet cannot be corrected by taking food supplements. Food supplements are superfluous for healthy individuals on a normal diet. In a balanced diet the body has all the nutrients it needs. Normally, the additional intake of individual nutrients is not, therefore, necessary. In some situations targeted supplementation with individual nutrients may make sense.
Unlike medicinal products food supplements do not have to be registered with the Federal Office of Consumer Protection and Food Safety (BVL). There are currently no binding maximum levels for the ingredients (nutrients or other substances with nutritional or physiological action) of supplements on either the national or the European level. An EU-wide regulation on valid maximum levels for vitamins and minerals is in the process of being elaborated.
Food supplements are foods and are intended to supplement the diet and must be safe. However, the mere fact that a food supplement is on the market does not mean that the purchaser can assume that this is a worthwhile or valuable food. Food supplements may also be on the market when their nutritional-physiological value is questionable.
During pregnancy and breastfeeding there is an elevated need for specific nutrients. The intake of essential nutrients by older people may also be insufficient for instance as a consequence of chewing or swallowing disorders or a loss of appetite. In these cases, dietary supplementation may be necessary or advisable. This should be done under medical supervision.
Data on nutrient intake indicate that the intake of a small number of vitamins and minerals like vitamin D, calcium, folic acid and iodine by some groups in the population is not in line with the intake recommendations of the German Nutrition Society (DGE e.V.). However this cannot generally be equated with insufficient intake or even a deficiency.
In the same way, both an insufficient and excessive supply of micro-nutrients, i.e. vitamins, minerals and trace elements, secondary plant substances can result in adverse health effects.
Nevertheless, the best nutritional strategy is still a balanced, diverse diet with plenty of fruit and vegetables. Food supplements are not substitutes of equal value.
Pd Dr. Diana Rubin of the BfR reports that almost one third of Germans consume vitamins supplements aiming to stay healthy. Rubin says this is an ominous mistake, because vitamins may even be life-threatening, according to a broadcast program at NDR in July 2011.
Rubin stated that vitamins are no youth or beauty fountain, do not protect against cancer or heart diseases. On the contrary, some studies say that special vitamins like vitamin E and Vitamin A increase cancer risk. Too much is dangerous when vitamins are taken in synthetic form as capsules or pils. Therefore most experts warn against doing so.
Prof. Karl Lauterbach calls for a proactive education of health officials, pharmacists and consumer concerning the health risks of vitamin supplements and have no mercy on the lobby of the supplement industry, according to Spiegel Online. Lauterbach is a German scientist and member of the Bundestag (SPD). He is professor of health economics and epidemiology at the University of Cologne.
Tendal et al 2011 looked at the multiplicity of data in trial reports and assessed the impact of multiplicity on Cochrain meta-analysis results published from issue 3 in 2006 to issue 2 in 2007.
The authors selected 19 Cochrain meta-analyses for their analysis. They found that 18 meta-analysis presented multiplicity of data.
The authors stressed that such multiplicity of data can affect the findings of systematic reviews and meta-analyses. They reinforce the need of reviews and meta-analyses to comply with prespecified protocols which identify time points, intervention groups, and scales of interest.
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Römp, Hermann:Vitamine,Chemie Lexikon,fünfte Auflage 1962.
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Wolfram,G.: Bedarfsermittlung für wirksame Stoffe, Ableitung von Referenzwerten/Verzehrsempfehlungen; Funktionelle Lebensmittel- Lebensmittel der Zukunft, Erwartungen, Wirkungen, Risiken; Band 25 der Schriftenreihe Lebensmittechemie, Lebensmittelqualität. (Hrsg) Lebensmittelchemische Gesellschaft-Fachgruppe in der GDCH.Behrs Verlag, page 64 and 66.
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