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Shilajit

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Latin Name:Asphaltum

English Name:Mineral Pitch and Shilajit
Sanskrit/Indian Name:Shilajit

The name
Shilajit is a Sanskrit word meaning “conqueror of mountains and destroyer of weakness.” It is also spelt as Shilajeet, and is known by various other names like Shilajita Mumiyo; Mineral pitch, Mineral wax or Ozokerite in English; Black Asphaltum; and Asphaltum punjabianum in Latin.

Description:
Shilajit is used in the Ayurveda, the traditional Indian system of medicine. Shilajit is a rasayana herb and is an adaptogen. Shilajit contains at least 85 minerals in Ionic form as well as humic acid and fulvic acid. Clinical researches have been in progress and the ancient claims of the drug’s several properties, including anti-aging properties.A similar exudate from the Caucasus Mountains is called Mumiyo but is not considered as strong as the Himalayan Shilajit.

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Origin
Ancient Indian yogis, and practitioners of Aurvedic medicine, on understanding several potent qualities of Shilajit, had attributed divine powers to Shilajit. In essence Shilajit is a natural concentrate of plants of the regions of the Himalayas, and is found in the Himalayan ranges in India, Nepal, Pakistan, China, Tibet, and part of Central Asia and Scandinavia. The flora of the Himalayas is rich and varied, and for thousand of years the plants have come to life, absorbed nutrients from the soil, and then died out. This is a process which has been repeated again and again countless times, and continued for millennia. It is believed that Shilajit found in the Himalayas are the fossilized form of those plants, and the particular biosphere of the Himalayas created them and bestowed medicinal qualities to them. Shilajit, found in the higher altitudes of the Himalayas, are collected during summer months when the ice melts, and Shilajeet lumps are sometimes spotted and collected from the crannies of rocks, and similar places. Shilajit so collected are processed by several drug manufactures and presented in capsule form for human consumption.

Puri (2006) in his book has devoted one chapter to Shilajit. He has given in detail about the study of Shilajit in the last two centuries and the various speculated sources of Shilajit. The Indian workers considered dendroid Euphorbia” as the source but in Ladakh faeces of mountain mouse were considered the source. In Russian literature, it is said to have formed by compaction of Junipers. Scientific studies reveal that it is a humus like compound. Dr Peter Zahler (1998 and 2002) has commented on the relationship of the occurrence of salajit and the Woolly Flying Squirrel and Dr Carman (unpublished) has reported his observations of mammal pellets (Woolly Flying Squirrel and Afghani Pika) in association with salajit deposits in northern Pakistan. These pellets are the so called “pallets’ in photomicrographs described by Faruqi (1997).

Modern discovery:Winston, David & Maimes, Steven. “Adaptogens: Herbs for Strength, Stamina, and Stress Relief,” Healing Arts Press, 2007. Contains a monograph on shilajit and health benefits.

Over sixty years of clinical research have shown that shilajit has positive effects on humans. It increases longevity, improves memory and cognitive ability, reduces allergies and respiratory problems, reduces stress, and relieves digestive troubles. It is anti-inflammatory, antioxidant, and eliminates free radicals. The research proves that shilajit increases immunity, strength, and endurance, and lives up to its ancient reputation as the “destroyer of weakness.”

Technically, shilajit is an exudate that is pressed out from layers of rock in the most sacred and highest mountains in Nepal and other areas. It is composed of humus and organic plant material that has been compressed by layers of rock. Humus is formed when soil microorganisms decompose animal and plant material into elements usable by plants. Plants are the source of all our food and humus is the source of plant food. Unlike other soil humus, shilajit humus consists of 60-80% organic mass.

Click to see:->Shilajit-The True Story of An Ayurvedic Formula

Shilajit is truly an amazing medicine.

Shilajit: Antiaging and Aphrodisiac herb

SHILAJIT -FULVIC ACID Rejuvenation elixir.

Sacred Soma of the Alchemists

The most powerful anti-aging substance and Rejuvenator even known to mankind.Feel the power of growing young.

Resources:
http://en.wikipedia.org/wiki/Shilajit
http://www.ayurvediccure.com/shilajit.htm

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Suppliments our body needs

Dimethylaminoethanol (DMAE)

chemical structure of dimethylaminoethanol (DMAE)
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Definition:
Dimethylaminoethenol (DMAE) is a metabolite, a product produced by the body’s metabolic process of procaine. It is a central nervous system stimulant that has a mild impact. It’s effect is similar to an amphetamine, but it is not such a drug. The term DMAE is actually an abbreviation for dimethylaminoethanol, a naturally occurring chemical produced by the human brain. It is a choline molecule that has one methyl group missing from the nitrogen, and it may be for this reason that it can cross the blood-brain barrier more easily than choline. While choline is known to be the precursor of acetylcholine, a recognized neurotransmitter, DMAE may prove to offer a more direct approach to this function by moving into the brain, being acted on by an enzyme (methylation), and thereby undergoing conversion into choline directly where it is needed.

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Although free-radicals are a natural result of the human body’s activity, the human equilibrium may be upset because of modern diet and environmental conditions that add further stressors to the system. These conditions cause a need for additional antioxidants in order for the body to cope with industrialized life. Antioxidants seem to reinforce one another, and for this reason it seems prudent to combine the use of several rather than to rely on only one type.

Dimethylaminoethanol, also known as DMAE or dimethylethanolamine, is an organic compound. This compound also goes by the names of N,N-dimethyl-2-aminoethanol, beta-dimethylaminoethyl alcohol, beta-hydroxyethyldimethylamine and Deanol. It is a liquid with a color that ranges from clear to pale yellow.

DMAE is known chemically as dimethyl-amino-ethanol. DMAE has been known in Europe by the product name Deanol for more than three decades. DMAE has two methyl groups and is chemically similar to choline. DMAE has been popular for many years in those interested in improving mental alertness and clarity of thinking.

Industrial uses
Dimethylaminoethanol is used as a curing agent for polyurethanes and epoxy resins. It is also used in mass quantities for water treatment, and to some extent in the coatings industry. It is used in the synthesis of dyestuffs, textile auxiliaries, pharmaceuticals, emulsifiers, and corrosion inhibitors. It is also an additive to paint removers, boiler water and amino resins.

Biochemical precursor
Dimethylaminoethanol is related to choline and is a biochemical precursor to the neurotransmitter acetylcholine, and found naturally in fish like sardines and anchovies. It is reported to have nootropic effects, although research on this chemical has found both positive and negative potential results.

It is believed that dimethylaminoethanol is methylated to produce choline in the brain[1]. It is known that dimethylaminoethanol is processed by the liver into choline; however, the choline molecule is charged and cannot pass the blood-brain barrier.

Research
Short term studies have shown an increase in vigilance and alertness, with a positive influence on mood. Long term studies are equivocal. Some showed dimethylaminoethanol to increase the lifespan of animals in which it was tested, while others indicate a possible reduction in the average life span of quail.  With the uncertainty of whether this could be extrapolated to humans, dimethylaminoethanol supplementation is not generally recommended. It is possible that dose is a major determining factor in the overall effects of dimethylaminoethanol – a high dose could produce effects opposite to those sought and contribute to life-shortening.

DMAE Research for Alzheimer’s, memory loss, age related mental decline
Studies with DMAE go back to the 1950s. One double blind, placebo-controlled trial performed in twenty-seven patients with severe Alzheimer’s disease did not show significant benefits (Fisman 1981). Another study on twenty-one patients with memory deficits was also discouraging since no improvement was found in memory (Caffarra 1980). However, DMAE was found helpful in patients with age related mental decline. DMAE was given for four weeks to fourteen older patients (Ferris 1977). Ten patients improved and four were unchanged. The patients on DMAE had reduced depression, less anxiety, and increased motivation, but they had no improvement in memory. The researchers say, “the results thus suggest that although DMAE may not improve memory, it may produce positive behavioral changes in some senile patients.” Dementia is a term that is now substituted for senility and is sometimes used to denote a severe case of age related cognitive decline.

DMAE has been touted as an anti-aging nutrient but there have not been any human studies evaluating the claim that DMAE slows aging.

DMAE Positive effects – Benefit of DMAE – DMAE Enhances Mood and Alertness
Most people notice being more alert and focused within a couple of hours after taking DMAE. The DMAE benefit of alertness and focus can last most of the day. A few report a higher sense of wellbeing. DMAE is recommended to be taken in the early part of the day. I also like the mind boosting effect of Acetyl-l-carnitine, but my favorite is a combination of several nutrients and herbs, including DMAE bitartrate, found in Mind Power Rx.

There are dozens of herbs and nutrients available in health food stores that influence mental function. One that has been popular for many years is DMAE, which stands for dimethyl-amino-ethanol. A recent German study evaluated the brain’s electrical reaction during presentation of videoclips of 7 minute duration in 80 subjects with borderline emotional disturbance. The researchers recorded the different emotional states by having the subjects watch these film excerpts. Half of the subjects were then started on a daily dose of DMAE and the testing was repeated after 6 and 12 weeks. The testing included showing the videoclips, filling out mood questionnaires, and also evaluating the brain’s electrical reaction through EEGs (electrodes placed on the scalp that measure brain activity) . The results showed that those who took the DMAE daily had a decrease in theta and alpha1 brain electrical activity indicating that they were more alert. Furthermore, the questionnaires revealed that those on DMAE had a better mood. The researchers conclude, “DMAE can be interpreted to induce a psychophysiological state of better feeling of wellbeing on both levels of analysis mood and electrical pattern of brain activity in subjects suffering from borderline emotional disturbance.”

Dr Sahelian says: Most people notice being more alert and focused within a couple of hours after taking DMAE. DMAE is available in dosages ranging from 100 to 400 mg. It is best to start with a low dose, such as 50 to 150 mg of actual DMAE since high doses can cause anxiety, restlessness, and muscle tenseness in the neck and shoulders. DMAE taken late in the day may cause insomnia.

Efficacy of dimethylaminoethanol (DMAE) containing vitamin-mineral drug combination on EEG patterns in the presence of different emotional states. Dimpfel W. Forschung und Entwicklung -, Kurt-Schumacher-Str. 9, D-35440 Linden, Germany. Eur J Med Res. 2003 May 30;8(5):183-91.

The psychophysiological model of provoking different emotional states by watching film excerpts with various emotional contents was used to characterize drug action in 80 subjects (male /f emale = 50%) with threshold emotional disturbance within a randomized, group-parallel, double-blind, placebo-controlled study. Analyzing the brain’s electrical reaction during presentation of 5 videoclips of 7 min duration followed by 3 minutes pause revealed a content specific representation of topographical frequency changes. This procedure was repeated after 6 and 12 weeks of daily intake of a vitamin-mineral drug combination containing dimethylaminoethanol (DMAE) or placebo. Subjects taking DMAE supplement for 3 months developed significant less theta and alpha1 power in sensomotoric areas of the cortex. Since decreases in theta and alpha1 electrical power have been associated with increased vigilance and attention, subjects taking DMAE combination obviously were more active and felt better. Therefore the vitamin-mineral combination containing DMAE can be interpreted to induce a psychophysiological state of better feeling of wellbeing on both levels of analysis mood and electrical pattern of brain activity in subjects suffering from borderline emotional disturbance.

DMAE Side effects
DMAE is available in varying dosages. It is best to start with a low dose, such as 50 to 150 mg of actual DMAE to avoid DMAE side effects. High doses can cause anxiety, restlessness, and muscle tenseness or stiffness in the neck, jaw, and shoulders. DMAE taken late in the day may cause insomnia. Other DMAE side effects on high dosages include irritability, headache, and overstimulation.

DMAE Availability
DMAE is usually sold by the name of DMAE bitartrate. A 350 mg pill of DMAE bitartrate yields 130 mg of actual DMAE. It is also available as DMAE liquid. One product contains 35 mg of DMAE per drop. Most users notice an effect from 50 to 150 mg of actual DMAE or 150 to 350 mg of DMAE bitartrate.

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DMAE Summary
DMAE can be helpful in the elderly who have cognitive decline. This nutrient can also be taken by an adult of any age who needs to be more focused and alert.

DMAE and Skin
A recent study shows DMAE cream is able to increase firmness of skin. Perhaps DMAE cream has anti-wrinkle potential. See below for the abstract.

The role of dimethylaminoethanol in cosmetic dermatology.
Am J Clin Dermatol. 2005;6(1):39-47. Grossman R.
Johnson and Johnson Consumer Products Worldwide, Skillman, NJ 08558
Skincare formulations for the improvement of aging skin are increasingly important consumer products. Here, we review available data on one such agent – 2-dimethylaminoethanol ( DMAE ) or deanol – that has recently been evaluated in a placebo-controlled trial. DMAE is an analog of the B vitamin choline and is a precursor of acetylcholine. Although the role of acetylcholine as a neurotransmitter is well known, growing evidence points to acetylcholine as a ubiquitous cytokine-like molecule that regulates basic cellular processes such as proliferation, differentiation, locomotion, and secretion in a paracrine and autocrine fashion. Indeed, this modulatory role may contribute to the cutaneous activity of DMAE. In a randomized clinical study, 3% DMAE facial gel applied daily for 16 weeks has been shown to be safe and efficacious in the mitigation of forehead lines and periorbital fine wrinkles, and in improving lip shape and fullness and the overall appearance of aging skin. Conclusions: Thus, the benefits of DMAE in dermatology include a potential anti-inflammatory effect and a documented increase in skin firmness with possible improvement in underlying facial muscle tone. Studies are needed to evaluate the relative efficacy of DMAE compared with other skin-care regimens (e.g., topical antioxidant creams, alpha-hydroxy acids).

Split face study on the cutaneous tensile effect of 2-dimethylaminoethanol (dmae) gel.
Skin Res Technol 2002 Aug;8(3):164-7
Beyond subjective assessments, the effect of skin tensors is difficult to assess. The present 2-phase randomized double-blind split face study was designed to compare the effect of a gel containing 3% 2-dimethylaminoethanol (deanol, DMAE) with the same formulation without DMAE. METHODS: In a first pilot study, sensorial assessments and measures of the skin distension under suction were performed in eight volunteers. In a second study conducted in 30 volunteers, shear wave propagation was measured. RESULTS: Large interindividual variations precluded any significant finding in the first study. The DMAE formulation showed, however, a significant effect characterized by increased shear wave velocity in the direction where the mechanical anisotropy of skin showed looseness. The DMAE formulation under investigation increased skin firmness.

Resources:
http://en.wikipedia.org/wiki/Dimethylethanolamine
http://www.raysahelian.com/dmae.html
http://www.dmae.org/

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Vitamin E

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Definition:
Vitamin E is the collective name for a set of 8 related tocopherols and tocotrienols, which are fat-soluble vitamins with antioxidant properties Of these, ?-tocopherol (also written as alpha-tocopherol) has been most studied as it has the highest bioavailability, with the body preferentially absorbing and using this form.
………..RRR alpha-tocopherol  (Vitamin E).……………
It has been claimed that ?-tocopherol is the most important lipid-soluble antioxidant, and that it protects cell membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction.This would remove the free radical intermediates and prevent the oxidation reaction from continuing. The oxidised ?-tocopheroxyl radicals produced in this process may be recycled back to the active reduced form through reduction by other antioxidants, such as ascorbate, retinol or ubiquinol.

The functions of the other forms of vitamin E are less well-studied, although ?-tocopherol (also written as gamma-tocopherol) is a nucleophile that may react with electrophilic mutagens, and tocotrienols may have a specialized role in protecting neurons from damage.[6] However, the roles and importance of the various forms of vitamin E are presently unclear,[7][8] and it has even been suggested that the most important function of vitamin E is as a signaling molecule, and that it has no significant role in antioxidant metabolism.

Most studies about Vitamin E have supplemented only alpha-tocopherol, but doing so leads to reduced serum gamma- and delta-tocopherol concentrations. For more info, read article tocopherol.

1 IU of vitamin E is the biological equivalent of about 0.667 mg d-alpha-tocopherol (2/3 mg exactly), or of 1 mg of dl-alpha-tocopherol acetate.

The term vitamin E describes a family of 8 antioxidants, 4 tocopherols and 4 tocotrienols. alpha-tocopherol (a-tocopherol) is the only form of vitamin E that is actively maintained in the human body and is therefore, the form of vitamin E found in the largest quantities in the blood and tissue.

It is an anti-oxidant vitamin that protects us from damage to our cells, and prevents and dissolves blood clots. Vitamin E has also been used by doctors in helping prevent sterility, muscular dystrophy, fibrocystic breast disease, calcium deposits in blood walls and heart conditions.
A deficiency of vitamin E may lead to a rupture of red blood cells, loss of reproductive powers, lack of sexual vitality, degenerative changes in the changes in the heart and other muscles.

Since vitamin E is oil soluble, we store it in our bodies. High supplemental amounts may interfere with blood clotting. Vitamin E should not be taken along with iron. Supplemental doses over 400 IU may cause temporarily high blood pressure.

The Recommended Daily Allowance for adult males is 10 mg and 8 mg for adult females.

Food sources of Vitamin E


Particularly high levels of vitamin E can be found in the following foods:

*Almonds

*Asparagus

*Avocado

*Nuts

*Olives

*Red Palm Oil

*Seeds

*Spinach and other green leafy vegetables

*Vegetable oils — Canola, corn, sunflower, soybean, cottonseed

*Wheat germ

*Dandelion

*Broccoli

*Mango

*Turnip
Because most of the food sources of vitamin E are foods that aren’t consumed in large amounts, a therapeutic level of vitamin E may be achieved only with supplements.

Benefits Of Vitamin E


Vitamin E is an important nutrient that helps your body in a variety of ways. You should get enough from a healthy, balanced diet. However, high amounts (400 IU) may be harmful.

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The benefits of vitamin e for the overall good health of individuals are substantial. In particular, vitamin e is very important in healthy and proper skin care.Click to learn more about BENEFITS OF VITAMIN E

Vitamin E acts as a powerful antioxidant by neutralizing free radicals in the body that cause tissue and cellular damage. Vitamin E also contributes to a healthy circulatory system and aids in proper blood clotting and improves wound healing. Some studies have shown that vitamin E decreases symptoms of premenstrual syndrome and certain types of breast disease.

Other studies have shown that taking large doses of Vitamin E has decreased the risk of Coronary Artery Disease (CAD). Animal studies have suggested that vitamin E does slow the development of atherosclerosis, but the American Heart Association doesn’t recommend using supplements until the effects are proven in large-scale, carefully controlled clinical trials.

Nutritionists categorize vitamins by the materials that a vitamin will dissolve in. There are two categories: water-soluble and fat-soluble vitamins. Fat-soluble vitamins—vitamins A, D, E and K—are stored in the fat tissues of the body for a few days to up to six months. If you get too much of a fat-soluble vitamin, it can be stored in your liver and may sometimes cause health problems. Vitamin E is a fat-soluble vitamin.

Some people take mega-doses of fat-soluble vitamins, which can lead to toxicity. Eating a normal diet of foods rich in these vitamins won’t cause a problem. Remember, you only need small amounts of any vitamin.

Some health problems can make it hard for a person’s body to absorb these vitamins. If you have a chronic health condition, ask your doctor about whether your vitamin absorption will be affected.

Vitamin E Controversy – Cause or Correlation?
A study published in the Annals of Internal Medicine stated that high doses of vitamin E are dangerous and should be avoided. This study considered doses of vitamin E in excess of 400 IU per day to be high and doses of vitamin E less than 400 IU per day to be low. Is it true that high doses of vitamin E are dangerous? Does the danger out weigh the benefit of vitamin E supplements?
Click to learn more from Office of Dietary Supplements • National Institutes of Health

Click to learn more from Micronutrient Information Center

Side Effects:
In November, 2004, the American Heart Association stated that high amounts of vitamin E can be harmful. Taking 400 IU per day, or higher, may increase the risk of death.

Taking smaller amounts, such as those found in a typical multivitamin, was not harmful.

Recommendations :

Specific recommendations for each vitamin depend on age, gender, and other factors (such as pregnancy). The Food and Nutrition Board at the Institute of Medicine report the following dietary reference intakes for vitamin E:

0 to 6 months: 4 mg/day
7 to 12 months: 5 mg/day
1 to 3 years: 6 mg/day
4 to 8 years: 7 mg/day
9 to 13 years: 11 mg/day
14 and older: 15 mg/day
Women who are producing breast milk (lactating) may need slighly higher amounts. Check with your doctor.

Resources:
http://en.wikipedia.org/wiki/Vitamin_E
http://www.nlm.nih.gov/medlineplus/ency/article/002406.htm#top

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Vitamin D

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Definition:Vitamin D is a fat-soluble steroid hormone precursor that contributes to the maintenance of normal levels of calcium and phosphorus in the bloodstream.
Strictly speaking, it is not a vitamin since human skin can manufacture it, but it is referred to as one for historical reasons.It is often known as calciferol.
Vitamin D is a group of fat-soluble prohormones, the two major forms of which are vitamin D2 (or ergocalciferol) and vitamin D3 (or cholecalciferol). The term vitamin D also refers to metabolites and other analogues of these substances. Vitamin D3 is produced in skin exposed to sunlight, specifically ultraviolet B radiation.

Vitamin D plays an important role in the maintenance of organ systems.

Vitamin D regulates the calcium and phosphorus levels in the blood by promoting their absorption from food in the intestines, and by promoting re-absorption of calcium in the kidneys, which enables normal mineralization of bone and prevents hypocalcemic tetany. It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts.

Absent vitamin K or with drugs (particularly blood thinners) which interfere with Vitamin K metabolism, Vitamin D can promote soft tissue calcification.

It inhibits parathyroid hormone secretion from the parathyroid gland.
Vitamin D affects the immune system by promoting phagocytosis, anti-tumor activity, and immunomodulatory functions.

Vitamin D deficiency can result from inadequate intake coupled with inadequate sunlight exposure, disorders that limit its absorption, conditions that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders, or, rarely, by a number of hereditary disorders.Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and possibly contributes to osteoporosis.

Vitamin D regulates the expression of genes associated with cancers and autoimmune disease by controlling the activation of the vitamin D receptor (VDR), a type 1 nuclear receptor and DNA transcription factor. Research has indicated that vitamin D deficiency is linked to colon cancer and more recently, to breast cancer. Conflicting evidence links vitamin D deficiency to other forms of cancer.

Forms:
Several forms (vitamers) of vitamin D have been discovered. The two major forms are vitamin D2 or ergocalciferol, and vitamin D3 or cholecalciferol.

Vitamin D1: molecular compound of ergocalciferol with lumisterol, 1:1
Vitamin D2: ergocalciferol or calciferol (made from ergosterol)
Vitamin D3: cholecalciferol (made from 7-dehydrocholesterol in the skin).
Vitamin D4: 22-dihydroergocalciferol
Vitamin D5: sitocalciferol (made from 7-dehydrositosterol)
Chemically, the various forms of vitamin D are secosteroids; i.e., broken-open steroids.[8] The structural difference between vitamin D2 and vitamin D3 is in their side chains. The side chain of D2 contains a double bond between carbons 22 and 23, and a methyl group on carbon 24.

Vitamin D2 is derived from fungal and plant sources, and is not produced by the human body. Vitamin D3 is derived from animal sources and is made in the skin when 7-dehydrocholesterol reacts with UVB ultraviolet light at wavelengths between 270–300 nm, with peak synthesis occurring between 295-297 nm. These wavelengths are present in sunlight at sea level when the sun is more than 45° above the horizon, or when the UV index is greater than 3. At this solar elevation, which occurs daily within the tropics, daily during the spring and summer seasons in temperate regions, and almost never within the arctic circles, adequate amounts of vitamin D3 can be made in the skin after only ten to fifteen minutes of sun exposure at least two times per week to the face, arms, hands, or back without sunscreen. With longer exposure to UVB rays, an equilibrium is achieved in the skin, and the vitamin simply degrades as fast as it is generated.

In humans, D3 is as effective as D2 at increasing the levels of vitamin D hormone in circulation; However, in some species, such as rats, vitamin D2 is more effective than D3. Both vitamin D2 and D3 are used for human nutritional supplementation, and pharmaceutical forms include calcitriol (1alpha, 25-dihydroxycholecalciferol), doxercalciferol and calcipotriene.

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Biochemistry:
Vitamin D is a prohormone, meaning that it has no hormone activity itself, but is converted to the active hormone 1,25-D through a tightly regulated synthesis mechanism. Production of vitamin D in nature always appears to require the presence of some UV light; even vitamin D in foodstuffs is ultimately derived from organisms, from mushrooms to animals, which are not able to synthesize it except through the action of sunlight at some point in the synthetic chain. For example, fish contain vitamin D only because they ultimately exist on calories from ocean algae which synthesize vitamin D in shallow waters from the action of solar UV.

Production in the skin:
The skin consists of two primary layers: the inner layer called the dermis, composed largely of connective tissue, and the outer, thinner epidermis. The epidermis consists of five strata; from outer to inner they are: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale.

Vitamin D3 is produced photochemically in the skin from 7-dehydrocholesterol. The highest concentrations of 7-dehydrocholesterol are found in the epidermal layer of skin, specifically in the stratum basale and stratum spinosum. The production of pre-vitamin D3 is therefore greatest in these two layers, whereas production in the other layers is less.

Synthesis in the skin involves UVB radiation which effectively penetrates only the epidermal layers of skin. While 7-Dehydrocholesterol absorbs UV light at wavelengths between 270–300 nm, optimal synthesis occurs in a narrow band of UVB spectra between 295-300 nm. Peak isomerization is found at 297 nm. This narrow segment is sometimes referred to as D-UV. The two most important factors that govern the generation of pre-vitamin D3 are the quantity (intensity) and quality (appropriate wavelength) of the UVB irradiation reaching the 7-dehydrocholesterol deep in the stratum basale and stratum spinosum.

A critical determinant of vitamin D3 production in the skin is the presence and concentration of melanin. Melanin functions as a light filter in the skin, and therefore the concentration of melanin in the skin is related to the ability of UVB light to penetrate the epidermal strata and reach the 7-dehydrocholesterol-containing stratum basale and stratum spinosum. Under normal circumstances, ample quantities of 7-dehydrocholesterol (about 25-50 µg/cm² of skin) are available in the stratum spinosum and stratum basale of human skin to meet the body’s vitamin D requirements, and melanin content does not alter the amount of vitamin D that can be produced. Thus, individuals with higher skin melanin content will simply require more time in sunlight to produce the same amount of vitamin D as individuals with lower melanin content. As noted below, the amount of time an individual requires to produce a given amount of Vitamin D may also depend upon the person’s distance from the equator and on the season of the year.

Mechanism of action:
Once vitamin D is produced in the skin or consumed in food, it is converted in the liver and kidney to form 1,25 dihydroxyvitamin D, (1,25(OH)2D) the physiologically active form of vitamin D (when “D” is used without a subscript it refers to either D2 or D3). Following this conversion, the hormonally active form of vitamin D is released into the circulation, and by binding to a carrier protein in the plasma, vitamin D binding protein (VDBP), it is transported to various target organs.

The hormonally active form of vitamin D mediates its biological effects by binding to the vitamin D receptor (VDR), which is principally located in the nuclei of target cells. The binding of calcitriol to the VDR allows the VDR to act as a transcription factor that modulates the gene expression of transport proteins (such as TRPV6 and calbindin), which are involved in calcium absorption in the intestine.

The Vitamin D receptor belongs to the nuclear receptor superfamily of steroid/thyroid hormone receptors, and VDR are expressed by cells in most organs, including the brain, heart, skin, gonads, prostate, and breast. VDR activation in the intestine, bone, kidney, and parathyroid gland cells leads to the maintenance of calcium and phosphorus levels in the blood (with the assistance of parathyroid hormone and calcitonin) and to the maintenance of bone content.

The VDR is known to be involved in cell proliferation, differentiation. Vitamin D also affects the immune system, and VDR are expressed in several white blood cells including monocytes and activated T and B cells.

Nutrition:
Only fish is naturally rich in vitamin D, so much vitamin D intake in the industrialized world is from fortified products including milk, soy milk and breakfast cereals or supplements.

A blood calcidiol (25-hydroxy-vitamin D) level is the accepted way to determine vitamin D nutritional status. The optimal level of serum 25-hydroxyvitamin D is 35–55 ng/mL; with some debate among medical scientists for the slightly higher value. Suplementation of 100 IU (2.5 mcg) vitamin D3 raises circulating 25(OH)D by 2.5 nmol/l (1 ng/ml).

The 2005 Dietary Guidelines for Americans recommend that older adults, people with dark skin, and those exposed to insufficient ultraviolet radiation (i.e., sunlight) consume extra vitamin D from vitamin D-fortified foods and/or supplements. Individuals in these high-risk groups should consume 25 µg (1000 IU) of vitamin D daily to maintain adequate blood concentrations of 25-hydroxyvitamin D, the biomarker for vitamin D status.

The Canadian Pediatric Society recommends 2,000 IU daily for pregnant and breastfeeding women.

In food
Season, geographic latitude, time of day, cloud cover, smog, and sunscreen affect UV ray exposure and vitamin D synthesis in the skin, and it is important for individuals with limited sun exposure to include good sources of vitamin D in their diet.

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Milk and cereal grains are often fortified with vitamin D.

In some countries, foods such as milk, yogurt, margarine, oil spreads, breakfast cereal, pastries, and bread are fortified with vitamin D2 and/or vitamin D3, to minimize the risk of vitamin D deficiency. In the United States and Canada, for example, fortified milk typically provides 100 IU per glass, or one quarter of the estimated adequate intake for adults over the age of 50

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Fatty fish, such as salmon, are natural sources of vitamin D.
Fatty fish, such as salmon, are natural sources of vitamin D.Fortified foods represent the major dietary sources of vitamin D, as very few foods naturally contain significant amounts of vitamin D.

Natural sources of vitamin D include:
Fish liver oils, such as cod liver oil, 1 Tbs. (15 mL) provides 1,360 IU
Fatty fish species, such as:
Herring, 85g (3 oz) provides 1383 IU
Catfish, 85g (3 oz) provides 425 IU
Salmon, cooked, 3.5 oz provides 360 IU
Mackerel, cooked, 3.5 oz, 345 IU
Sardines, canned in oil, drained, 1.75 oz, 250 IU
Tuna, canned in oil, 3 oz, 200 IU
Eel, cooked, 3.5 oz, 200 IU
One whole egg, 20 IU
Deficiency:
Vitamin D deficiency can result from: inadequate intake coupled with inadequate sunlight exposure, disorders that limit its absorption, conditions that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders, or, rarely, by a number of hereditary disorders. Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and contributes to osteoporosis

Diseases caused by deficiency:
The role of diet in the development of rickets was determined by Edward Mellanby between 1918–1920. In 1921 Elmer McCollum identified an anti-rachitic substance found in certain fats could prevent rickets. Because the newly discovered substance was the fourth vitamin identified, it was called vitamin D. The 1928 Nobel Prize in Chemistry was awarded to Adolf Windaus, who discovered the steroid 7-dehydrocholesterol, the precursor of vitamin D.

Vitamin D deficiency is known to cause several bone diseases including:

Rickets, a childhood disease characterized by impeded growth, and deformity, of the long bones. The earliest sign of subclinical vitamin D deficiency is Craniotabes, abnormal softening or thinning of the skull.
Osteomalacia, a bone-thinning disorder that occurs exclusively in adults and is characterized by proximal muscle weakness and bone fragility.

Osteoporosis, a condition characterized by reduced bone mineral density and increased bone fragility.
Prior to the fortification of milk products with vitamin D, rickets was a major public health problem. In the United States, milk has been fortified with 10 micrograms (400 IU) of vitamin D per quart since the 1930s, leading to a dramatic decline in the number of rickets cases.

Zinc and Iron are often found to be poorly regulated or even deficient in Vitamin D deficiency. Vitamin D enhances the activities of Vitamin A, and Zinc reduces the toxicity of Vitamin A, while Iron reduces the toxicity of Zinc. These four are seen as part of the pathology of Alzheimer’s, Parkinson’s and some peripheral neuropathies including Restless legs syndrome

Vitamin D malnutrition may also be linked to an increased susceptibility to several chronic diseases such as high blood pressure, tuberculosis, cancer, periodontal disease, multiple sclerosis, chronic pain, depression, schizophrenia, seasonal affective disorder, peripheral artery disease and several autoimmune diseases including type 1 diabetes .

Groups at greater risk of deficiency
Vitamin D requirements increase with age, while the ability of skin to convert 7-dehydrocholesterol to pre-vitamin D3 decreases. In addition the ability of the kidneys to convert calcidiol to its active form also decreases with age, prompting the need for increased vitamin D supplementation in elderly individuals. One consensus concluded that for optimal prevention of osteoporotic fracture the blood calcidiol concentration should be higher than 30 ng/mL, which is equal to 75 nmol/L. One billion people in the world are currently Vitamin D deficient, if 75 nmol/L is used as cutoff value for insufficiency.

Because inflammation leads to the increased conversion of 25D into 1,25 D and because studies typically only measure 25D to determine deficiency, it is important to differentiate symptoms caused by insufficient 25D from those conditions which themselves cause lower levels of 25D, which presents as insufficiency.

The American Pediatric Association advises vitamin D supplementation of 200 IU/day (5?g/d) from birth onwards. (1 IU Vitamin D is the biological equivalent of 0.025 ?g cholecalciferol/ergocalciferol). The Canadian Paediatric Society recommends that pregnant or breastfeeding women consider taking 2000 IU/day, that all babies who are exclusively breastfed receive a supplement of 400 IU/day, and that babies living above 55 degrees latitude get 800 IU/day from October to April. Health Canada recommends 400IU/day (10?g/d). While infant formula is generally fortified with vitamin D, breast milk does not contain significant levels of vitamin D, and parents are usually advised to avoid exposing babies to prolonged sunlight. Therefore, infants who are exclusively breastfed are likely to require vitamin D supplementation beyond early infancy, especially at northern latitudes. Liquid “drops” of vitamin D, as a single nutrient or combined with other vitamins, are available in water based or oil-based preparations (“Baby Ddrops(R)” in North America, or “Vigantol(R) oil” in Europe). However, babies may be safely exposed to sunlight for short periods; as little as 10 minutes a day without a hat can suffice, depending on location and season. The vitamin D used for in supplements and infant formula is not distinguishable in efficacy from that produced by the body naturally. The risk of overdose is not present with natural exposure to sunlight, because the skin’s capacity to produce vitamin D is self-limiting (skin production is thought to reflect the dose of vitamin D to which our evolution optimized human biology). In contrast, care should be given to limit oral intake for infants to no more than 1000 IU (25 mcg) daily, or for adults no more than 10,000 IU (250 mcg) daily.

Obese individuals may have lower levels of the circulating form of vitamin D, probably because of reduced bioavailability, and are at higher risk of deficiency. To maintain blood levels of calcium, therapeutic vitamin D doses are sometimes administered (up to 100,000 IU or 2.5 mg daily) to patients who have had their parathyroid glands removed (most commonly renal dialysis patients who have had tertiary hyperparathyroidism, but also to patients with primary hyperparathyroidism) or with hypoparathyroidism. Patients with chronic liver disease or intestinal malabsorption disorders may also require larger doses of vitamin D (up to 40,000 IU or 1 mg (1000 micrograms) daily).

The use of sunscreen with a sun protection factor (SPF) of 8 inhibits more than 95% of vitamin D production in the skin. Recent studies showed that, following the successful “Slip-Slop-Slap” health campaign encouraging Australians to cover up when exposed to sunlight to prevent skin cancer, an increased number of Australians and New Zealanders became vitamin D deficient. Ironically, there are indications that vitamin D deficiency may lead to skin cancer. To avoid vitamin D deficiency dermatologists recommend supplementation along with sunscreen use.

The reduced pigmentation of light-skinned individuals tends to allow more sunlight to be absorbed even at higher latitudes, thereby reducing the risk of vitamin D deficiency. However, at higher latitudes (above 30°) during the winter months, the decreased angle of the sun’s rays, reduced daylight hours, protective clothing during cold weather, and fewer hours of outside activity, diminish absorption of sunlight and the production of vitamin D. Because melanin acts like a sun-block, prolonging the time required to generate vitamin D, dark-skinned individuals, in particular, may require extra vitamin D to avoid deficiency at higher latitudes. In June 2007, The Canadian Cancer Society began recommending that all adult Canadians consider taking 1000 IU of vitamin D during the fall and winter months (when typically the country’s northern latitude prevents sufficient sun-stimulated production of vitamin D). At latitudes below 30° where sunlight and day-length are more consistent, vitamin D supplementation may not be required. Individuals clad in full body coverings during all their outdoor activity, most notably women wearing burquas in daylight, are at risk of vitamin D deficiency. This poses a lifestyle-related health risk mostly for female residents of conservative Muslim nations in the Middle East, but also for strict adherents in other parts of the world.

Overdose:
Vitamin D stored in the human body as calcidiol (25-hydroxy-vitamin D) has a large volume of distribution and a half-life of about 20 to 29 days. However, the synthesis of bioactive vitamin D hormone is tightly regulated and vitamin D toxicity usually occurs only if excessive doses (prescription forms or rodenticide analogs) are taken. Although normal food and pill vitamin D concentration levels are far too low to be toxic in adults, because of the high vitamin A content in codliver oil, it is possible to reach toxic levels of vitamin A (but not vitamin D) via this route, if taken in multiples of the normal dose in an attempt to increase the intake of vitamin D. Most historical cases of vitamin D overdose have occurred due to manufacturing and industrial accidents.

Exposure to sunlight for extended periods of time does not cause vitamin D toxicity. This is because within about 20 minutes of ultraviolet exposure in light skinned individuals (3–6 times longer for pigmented skin) the concentration of vitamin D precursors produced in the skin reach an equilibrium, and any further vitamin D that is produced is degraded. Maximum endogenous production with full body exposure to sunlight is 250 µg (10,000 IU) per day.

The exact long-term safe dose of vitamin D is not entirely known, but dosages up to 250 micrograms (10,000 IU) /day in healthy adults are believed to be safe., and all known cases of vitamin D toxicity with hypercalcemia have involved intake of or over 1,000 micrograms (40,000 IU)/day[38]. The U.S. Dietary Reference Intake Tolerable Upper Intake Level (UL) of vitamin D for children and adults is 50 micrograms/day (2,000 IU/day), although this is widely presumed to be below actual physiological daily requirements. In adults, sustained intake of 2500 micrograms/day (100,000 IU) can produce toxicity within a few months. For infants (birth to 12 months) the tolerable UL is set at 25 micrograms/day (1000 IU/day), and vitamin D concentrations of 1000 micrograms/day (40,000 IU) in infants has been shown to produce toxicity within 1 to 4 months. In the United States, overdose exposure of vitamin D was reported by 284 individuals in 2004, leading to 1 death. The Nutrition Desk Reference states “The threshold for toxicity is 500 to 600 micrograms [vitamin D] per kilogram body weight per day.” The US EPA published an oral LD50 of 619 mg/kg for female rats.

Serum levels of calcidiol (25-hydroxy-vitamin D) are typically used to diagnose vitamin D overdose. In healthy individuals, calcidiol levels are normally between 32 to 70 ng/mL (80 to 175 nmol/L), but these levels may be as much as 15-fold greater in cases of vitamin D toxicity. Serum levels of bioactive vitamin D hormone (1,25(OH2)D) are usually normal in cases of vitamin D overdose.

Some symptoms of vitamin D toxicity are a result of hypercalcemia (an elevated level of calcium in the blood) caused by increased intestinal calcium absorption. Vitamin D toxicity is known to be a cause of high blood pressure. Gastrointestinal symptoms of vitamin D toxicity can include anorexia, nausea, and vomiting. These symptoms are often followed by polyuria (excessive production of urine), polydipsia (increased thirst), weakness, nervousness, pruritus (itch), and eventually renal failure. Other signals of kidney disease including elevated protein levels in the urine, urinary casts, and a build up of wastes in the blood stream can also develop. In one study, hypercalciuria and bone loss occurred in four patients with documented vitamin D toxicity. Another study showed elevated risk of ischaemic heart disease when 25D was above 89 ng/mL.

Vitamin D toxicity is treated by discontinuing vitamin D supplementation, and restricting calcium intake. If the toxicity is severe blood calcium levels can be further reduced with corticosteroids or bisphosphonates. In some cases kidney damage may be irreversible.

Role in immunomodulation:
The hormonally active form of vitamin D mediates immunological effects by binding to nuclear vitamin D receptors (VDR) which are present in most immune cell types including both innate and adaptive immune cells. The VDR is expressed constitutively in monocytes and in activated macrophages, dendritic cells, NK cells, T and B cells. In line with this observation, activation of the VDR has potent anti-proliferative, pro-differentiative, and immunomodulatory functions including both immune-enhancing and immunosuppressive effects.

Effects of VDR-ligands, such as vitamin D hormone, on T-cells include suppression of T cell activation and induction of regulatory T cells, as well as effects on cytokine secretion patterns. VDR-ligands have also been shown to affect maturation, differentiation, and migration of dendritic cells, and inhibits DC-dependent T cell activation, resulting in an overall state of immunosuppression.

VDR ligands have also been shown to increase the activity of natural killer cells, and enhance the phagocytic activity of macrophages. Active vitamin D hormone also increases the production of cathelicidin, an antimicrobial peptide that is produced in macrophages triggered by bacteria, viruses, and fungi. Vitamin D deficiency tends to increase the risk of infections, such as influenza and tuberculosis. In a 1997 study, Ethiopian children with rickets were 13 times more likely to get pneumonia than children without rickets.

These immunoregulatory properties indicate that ligands with the potential to activate the VDR, including supplementation with calcitriol (as well as a number of synthetic modulators), may have therapeutic clinical applications in the treatment of; inflammatory diseases (rheumatoid arthritis, psoriatic arthritis), dermatological conditions (psoriasis, actinic keratosis), osteoporosis, cancers (prostate, colon, breast, myelodysplasia, leukemia, head and neck squamous cell carcinoma, and basal cell carcinoma), and autoimmune diseases (systemic lupus erythematosus, type I diabetes, multiple sclerosis) and in preventing organ transplant rejection. However the effects of supplementation with vitamin D, as yet, remain unclear, and supplementation may be inadvisable for individuals with sarcoidosis and other diseases involving vitamin D hypersensitivity.

A 2006 study published in the Journal of the American Medical Association, reported evidence of a link between Vitamin D deficiency and the onset of Multiple Sclerosis; the authors posit that this is due to the immune-response suppression properties of Vitamin D.

Role in cancer prevention and recovery:
The Canadian Cancer Society recommends that adults should consider supplementeing with 1,000 IU of vitamin D per day during the fall and winter. They base this recommendation on the growing evidence for a link between vitamin D and a reduced risk for colorectal, breast and prostate cancers.

The vitamin D hormone, calcitriol, has been found to induce death of cancer cells in vitro and in vivo. Although the anti-cancer activity of vitamin D is not fully understood, it is thought that these effects are mediated through vitamin D receptors expressed in cancer cells, and may be related to its immunomodulatory abilities. The anti-cancer activity of vitamin D observed in the laboratory has prompted some to propose that vitamin D supplementation might be beneficial in the treatment or prevention of some types of cancer.

A search of primary and review medical literature published between 1970 and 2007 found an increasing body of research supporting the hypothesis that the active form of vitamin D has significant, protective effects against the development of cancer. Epidemiological studies show an inverse association between sun exposure, serum levels of 25(OH)D, and intakes of vitamin D and risk of developing and/or surviving cancer. The protective effects of vitamin D result from its role as a nuclear transcription factor that regulates cell growth, differentiation, apoptosis and a wide range of cellular mechanisms central to the development of cancer. In 2005, scientists released a metastudy which demonstrated a beneficial correlation between vitamin D intake and prevention of cancer. Drawing from a meta-analysis of 63 published reports, the authors showed that intake of an additional 1,000 international units (IU) (or 25 micrograms) of vitamin D daily reduced an individual’s colon cancer risk by 50%, and breast and ovarian cancer risks by 30%.[62] Research has also shown a beneficial effect of high levels of calcitriol on patients with advanced prostate cancer. A randomized intervention study involving 1,200 women, published in June 2007, reports that vitamin D supplementation (1,100 international units (IU)/day) resulted in a 60% reduction in cancer incidence, during a four-year clinical trial, rising to a 77% reduction for cancers diagnosed after the first year (and therefore excluding those cancers more likely to have originated prior to the vitamin D intervention). In 2006, a study at Northwestern University found that taking the U.S. RDA of vitamin D (400 IU per day) cut the risk of pancreatic cancer by 43% in a sample of more than 120,000 people from two long-term health surveys.

A 2006 study using data on over 4 million cancer patients from 13 different countries showed a marked difference in cancer risk between countries classified as sunny and countries classified as less–sunny for a number of different cancers. Research has also suggested that cancer patients who have surgery or treatment in the summer — and therefore make more endogenous vitamin D — have a better chance of surviving their cancer than those who undergo treatment in the winter when they are exposed to less sunlight.

A scientific review undertaken by the National Cancer Institute found no link between baseline vitamin D status and overall cancer mortality. They did find that vitamin D was beneficial in preventing colorectal cancer, which showed an inverse relationship with blood levels “80 nmol/L or higher associated with a 72% risk reduction”.

Role in cardiovascular disease prevention
Research indicates that vitamin D may play a role in preventing or reversing coronary disease. Vitamin D deficiency is associated with an increase in high blood pressure and cardiovascular risk. When researchers monitored the vitamin D levels, blood pressure and other cardiovascular risk factors of 1739 people, of an average age of 59 years for 5 years, they found that those people with low levels of vitamin D had a 62% higher risk of a cardiovascular event than those with normal vitamin D levels.

A report from the National Health and Nutrition Examination Survey (NHANES) found that low levels of vitamin D were associated with an increased risk of peripheral artery disease (PAD). Researchers divided 4,839 participantes in NHANES into quartiles (four groups) based on their blood levels of vitamin D, and found that increasing levels of vitamin D were associated with a lower prevalence of PAD. The authors adjusted for other factors which could influence the development of PAD (such as smoking and high cholesterol) and found that among participants with the lowest vitamin D levels (<17.8 ng/mL) PAD was 80% more common than in individuals with the highest levels (>29.2 ng/mL) of vitamin D.

Researchers publishing in the Journal of Circulation studied the blood levels of vitamin D in 1739 middle-aged children of partipants in the Framingham Heart Study in Framinhgam, Massachussetts (their mean age was 59 years; 55% were women; all were white) who did not have any prior history of cardiovascular disease. These subjects were followed for a mean of 5.4 years. The authors adjusted for other conventional risk factors for cardiovascular disease which could have confounded the results and still found that among the 120 individuals in this group who suffered a first cardiovascular event, those who had the lowest levels of vitamin D were most likely to have had an event. Individuals with lowest levels of vitamin D (<15 ng/mL) had a 62% increased risk (95% confidence interval 1.11 to 2.36, P=0.01) for having a first cardiovascular event compared with those with vitamin D levels of 15 ng/mL. This effect was evident in participants with hypertension, but not in those without hypertension.

In a study of 34 middle-aged men, researchers found that low levels of vitamin D were associated with hypertension, elevated VLDL triglycerides, and impaired insulin metabolism.

As with cancer incidence, a qualitative inverse correlations was found between coronary disease incidence and serum vitamin D levels of 32.0 versus 35.5 ng/mL. Cholesterol levels were found to be reduced in gardeners in the UK during the summer months. Heart attacks peak in winter and decline in summer in temperate but not tropical latitudes.

The issue of vitamin D in heart health has not yet been settled. Exercise may account for some of the benefit attributed to vitamin D, since vitamin D levels are higher in physically active persons. Moreover, there may be an upper limit after which cardiac benefits decline. One study found an elevated risk of ischaemic heart disease in Southern India in individuals whose vitamin D levels were above 89 ng/mL. These sun-living groups results do not generalize to sun-deprived urban dwellers. Among a group with heavy sun exposure, taking supplemental vitamin D are unlikely to result in blood levels over the ideal range, while urban dwellers not taking supplemental vitamin D may fall under the levels recognized as ideal, and being below the preferable levels may cause adverse affects on the health of each group.

Role in all-cause mortality:
Low vitamin D levels are associated with cancer, diabetes, and hypertension, and in increased mortality among patients undergoing dialysis. Using the National Health and Nutrition Examination Survey Melamed and coworkers at the Albert Einstein College of Medicine evaluated whether low serum vitamin D levels were associated with mortality in the general population. The researchers studied the association of low vitamin D levels with all-cause mortality, cancer, and cardiovascular disease (CVD) mortality among 13,331 diverse American adults who were 20 years or older. Vitamin D levels of these participants were collected over a 6-year period (from 1988 through 1994), and individuals were passively followed for mortality through the year 2000. The researchers found that being older, female, nonwhite, having diabetes, a current smoker, and having a higher body mass index were all independently associated with a greater risk of being vitamin D deficient, while greater physical activity, vitamin D supplementation, and evaluating subjects in a non-winter season (greater exposure to sunshine) were all associated with higher levels. During a median of 8.7 years of follow-up, there were 1806 deaths, including 777 (43%) from CVD. The authors divided the participants into 4 groups (quartiles) based on their serum vitamin D levels, and adjusted for baseline demographics, season, and CVD risk factors. Being in the lowest quartile (vitamin D levels <17.8 ng/mL) was associated with a 26% increased rate of all-cause mortality (mortality rate ratio, 1.26; 95% CI, 1.08-1.46). The adjusted models of CVD and cancer mortality revealed a higher risk, but it was not statistically significant. The authors concluded that having low levels of vitamin D (<17.8 ng/mL) was independently associated with an increase in all-cause mortality in the general population.

Among many factors that may be responsible for vitamin Ds apparent beneficial effect on all-cause mortality is its effect on telomeres and its potential effect on slowing aging. Richards and coworkers examined whether vitamin D concentrations would slow the rate of shortening of leukocyte telomeres (a marker of aging). The authors stated that vitamin D is a potent inhibitor of the proinflammatory response and slows the turnover of leukocytes. Leukocyte telomere length (LTL) predicts the development of aging-related disease, and length of these telomeres decreases with each cell division and with increased inflammation (more common in the elderly). Researchers measured serum vitamin D concentrations in 2160 women aged 18-79 years (mean age: 49.4) from a large population-based cohort of twins. This study divided the group into thirds [tertiles http://en.wiktionary.org/wiki/tertile] based on vitamin D levels, and found that increased age was significantly associated with shorter LTL (r = -0.40, P < 0.0001). Higher serum vitamin D concentrations were significantly associated with longer LTL (r = 0.07, P = 0.0010), and this finding persisted even after adjustment for age (r = 0.09, P < 0.0001) and other variables that independently could affect LTL (age, season of vitamin D measurement, menopausal status, use of hormone replacement therapy, and physical activity). The difference in LTL between the highest and lowest tertiles of vitamin D was highly significant (P = 0.0009), and the authors stated that this was equivalent to 5.0 years of aging. The authors concluded that higher vitamin D levels, (easily modifiable through nutritional supplementation), were associated with longer LTL, which underscores the potentially beneficial effects of vitamin D on aging and age-related diseases.

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Resources:

http://en.wikipedia.org/wiki/Vitamin_D

http://www.sciencedaily.com/articles/v/vitamin_d.htm

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Suppliments our body needs

Vinpocetine

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Definition:
Vinpocetine (pronounced vin-poe-ce-teen) is a synthetic compound derived from vincamine, a substance found naturally in the leaves of the lesser periwinkle plant (Vinca minor). Vinpocetine was developed in the late 1960s.

Vinpocetine (brand names: Cavinton, Intelectol; chemical name: ethyl apovincaminate) is a semisynthetic derivative alkaloid of vincamine (sometimes described as “a synthetic ethyl ester of apovincamine”), an extract from the periwinkle (plant) Vinca minor.

Vinpocetine is reported to have cerebral blood-flow enhancing and neuroprotective effects, and is used as a drug in Eastern Europe for the treatment of cerebrovascular disorders and age-related memory impairment.

Vinpocetine is widely marketed as a supplement for vasodilation and as a nootropic for the improvement of memory. There exists anecdotal report of uncomfortable adverse reactions to vinpocetine in a small subset of users. A low initial dosage is often recommended.

Vinpocetine is available as a prescription drug in Europe and Japan. In the the United States and Canada. It is sold in health food stores and online as a dietary supplement.

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Possible Nootropic Properties
A number of studies on healthy volunteers have demonstrated vinpocetine may elicit improvement on some aspects of memory. The degree which the nootropic effects of vinpocetine are mediated by mechanisms beyond vasodilation is currently unknown.

 

Mechanism of Action:
Vinpocetine has been shown to selectively inhibit voltage-sensitive Na+ channels, resulting in a dose-dependent decrease in evoked extracellular Ca+ ions in striatal nerve endings. The Na+ channel inhibiting properties of vinpocetine are thought to contribute to a general neuroprotective effect through blockade of excitotoxicity and attenuation of neuronal damage induced by cerebral ischemia/reperfusion.

Vinpocetine is also a phosphodiesterase (PDE) type-1 inhibitor, (with an IC50 of approximately 10-5 M.) leading to increases in intracellular levels of cyclic guanosine 3’5′-monophosphate (cGMP), an action that has been attributed to the vasorelaxant effects of vinpocetine on cerebral smooth muscle tissue.

Increases in neuronal levels of DOPAC, a metabolic breakdown product of dopamine, have been shown to occur in striatal isolated nerve endings as a result of exposure to vinpocetine. Such an effect is consistent with the biogenic pharmacology of reserpine, a structural relative of vinpocetine, which depletes catecholamine levels and may cause depression as a side-effect of the cardiovascular and anti-psychotic effects.

Use Of Vinpocetine:
Vinpocetine widely used in the body building community as an antivasoconstrictor. However, no studies have been conducted on the effectiveness of vinpocetine on performance enhancement during exercise

Vinpocetine is naturally occurring from the plant Crioceras Longiflorus and also can be obtained from Vincamine.

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Vinpocetine derived from Tabersonine, an alkaloid extracted from seeds of the Voacana tree that is native to West Africa.

Vinpocetine is a cerebral metabolic activator and a neuronal protector. Clinical studies indicate that vinpocetine helps increase blood flow; cerebral vasodilation produces an immediate increase in the cerebral oxygenation and this results finally in the activation of the cerebral metabolism, the increase of glucose and the improvement of certain neurotransmitters´utilization . Another benefit that has been observed by using vinpocetine is its neuronal protection effects which increase resistance of the brain to hypoxia and ischemia , reduce platelet aggregation, and improve red blood cells deformability allowing oxygen to feed neurons through microcapillaries . Evidence also shows that Vinpocetine has antioxidant properties.
The are more than 100 clinical studies on Vinpocetine performed on over 30,000 patients proving its safety and effectiveness. Vinpocetine has many different effects of varying importance on cognitive functions such as increase of attention, concentration, and memory .

Almost anyone can benefit from taking vinpocetine. From people who have already cognitive deterioration, through baby boomers who are starting to suffer the symptoms of memory loss to young people and students who want to enhance their memory to increase their intellectual intelligence as well as to get good results at exams.
Stroke and vascular dementia
Vinpocetine is thought to increase blood circulation in the brain, which may explain why some preliminary studies suggest that it may reduce brain impairment and dementia after an ischemic stroke. Although promising, well-designed human studies are needed.

Alzheimer’s disease
Vinpocetine is also being explored as a complementary treatment for people with Alzheimer’s disease. It’s thought to enhance the brain’s use of oxygen, protect brain cells against damage, and increase blood flow to the brain by inhibiting an enzyme called phosphodiesterase.

Although preliminary studies on the use of vinpocetine for Alzheimer’s disease showed promise, a critical review of previously published studies found that the evidence as a whole was too weak to rely on, due to limitations in the design of the studies. More research is needed.

Tinnitus
Studies suggest that vinpocetine may help with tinnitus after trauma to the ear.

To boost brain function
Vinpocetine is marketed in North America as a supplement that can boost memory and brain function in healthy people, but there is no real evidence yet that it can help.

Dosage
It is recommended that first-time users ingest only 2-5 mg of vinpocetine to make sure they are not hypersensitive to it. Users may then increase the dosage to 10-30 mg a day (which may, although very rarely, cause some side-effects).


Side Effects and Safety Concerns

No adverse reactions to vinpocetine have been reported in human trials. Due to the small sample size of existing trials the prevalence of adverse reactions is still unknown although thought to be rare. Anecdotal evidence has suggested that a small subset of users may experience adverse reactions. Due to the possibility of adverse reactions, a low initial dose is typically recommended. The small size of existing studies precludes conclusion on the prevalence or severity of possible adverse reactions in vinopocetine usage.

The safety of vinpocetine in pregnant women has not been evaluated.

Vinpocetine has been implicated in one case to induce agranulocytosis, a condition in which granulocytyes – an important type of white blood cell, are markedly decreased. Some people have anecdotally noted that their continued use of vinpocetine reduces immune function. Commission E warned that vinpocetine reduced immune function and could cause apoptosis in the long term.

Side effects of vinpocetine may include indigestion, nausea, dizziness, anxiety, facial flushing, insomnia, headache, drowsiness and dry mouth. Vinpocetine may also cause a temporary drop in blood pressure.

Vinpocetine shouldn’t be taken by pregnant or nursing women. The safety of vinpocetine in people with liver or kidney damage isn’t known. People with bleeding disorders, low blood pressure or seizure disorders shouldn’t use vinpocetine. It also shouldn’t be used two weeks before or after a surgical or dental procedure.

There is one case report of agranulocytosis associated with the use of vinpocetine.

Possible Drug Interactions
Vinpocetine shouldn’t be taken by people who are taking drugs or herbs that “thin” the blood (anticlotting or antiplatelet medications), such as aspirin, Plavix (clopidogrel), Ticlid (ticlopidine), (Trental) pentoxifylline, vitamin E, garlic or ginkgo. It should not be used with Coumadin (warfarin).

Disclaimer:The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:
http://en.wikipedia.org/wiki/Vinpocetine
http://altmedicine.about.com/od/herbsupplementguide/a/vinpocetine.htm
http://www.vinpocetine.com/

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