Archive for the ‘Vitamins’ Category

Obesity can lead to vitamin D deficiency

Wednesday, February 6th, 2013

obesityTUESDAY Feb. 5, 2013 — Obesity can lead to vitamin D deficiency, a new study indicates.

British researchers looked at data from about 165,000 people, and found that a 10 percent rise in body-mass index (BMI) was linked with a 4 percent drop in concentrations of vitamin D in the body. BMI is a measurement of body fat based on height and weight.

The link between BMI and vitamin D levels was found in men and women, as well as in younger and older people, the investigators noted.

The findings suggest that a higher BMI leads to lower levels of vitamin D circulating in the body, while a lack of vitamin D has only a small effect on BMI, according to the authors of the study, published Feb. 5 in the journal PLoS Medicine.

Efforts to tackle obesity may also help reduce levels of vitamin D deficiency, said lead investigator Dr. Elina Hypponen, of University College London’s Institute of Child Health.

Previous studies have linked vitamin D deficiency with obesity, but it wasn’t clear whether a lack of vitamin D triggered weight gain or whether obesity led to vitamin D deficiency, the study authors noted in a university news release.

Vitamin D, which is essential for healthy bones and other functions, is produced by the skin when exposed to sunlight. It can also be obtained through foods and supplements.

“Vitamin D deficiency is an active health concern around the world. While many health messages have focused on a lack of sun exposure or excessive use of suncreams, we should not forget that vitamin D deficiency is also caused by obesity,” Hypponen said.

“Our study highlights the importance of monitoring and treating vitamin D deficiency in people who are overweight or obese, in order to alleviate adverse health effects caused by a lack of vitamin D,” she added.

Although the study reported that higher BMI leads to lower levels of vitamin D circulating in the body, it did not prove a cause-and-effect relationship.

More information

The U.S. National Institutes of Health, Office of Dietary Supplements, has more about vitamin D.

Know your vitamin Ds – 3 beats 2

Saturday, May 26th, 2012

From Reuters Health Information

Vitamin D3 Beats D2 for Raising Serum Levels: Meta-Analysis

NEW YORK (Reuters Health) May 18 – Vitamin D3 (cholecalciferol) is more effective than vitamin D2 (ergocalciferol) at raising serum levels of 25 hydroxyvitamin D – and that’s regardless of dosage, frequency or route of administration, according to a systematic review and meta-analysis of randomized controlled trials.

Vitamin D3 “could potentially become the preferred choice for supplementation,” the authors concluded in a paper online May 2nd in the American Journal of Clinical Nutrition.

However, they say more work is needed to examine the metabolic pathways involved in oral and intramuscular administration of vitamin D and the effects across age, sex, and ethnicity, which their review was unable to verify.

First author Dr. Laura Tripkovic, from the UK’s University of Surrey in Guildford, and colleagues say there is a “widespread perception” that both vitamins D2 and D3 are equally effective in raising serum 25(OH)D levels, when in fact there is a “lack of clarity” in the literature on this issue.

They performed a comprehensive literature search for relevant studies in adults that directly compared vitamins D2 and D3, eventually selecting 10 studies for review (1,016 subjects total), seven of which were included in their meta-analysis.{{{0}}}

In these studies, vitamins D2 and D3 were used in varying ways. One study used a single bolus orally of 50,000 IU; one study used a single large bolus of vitamin D2 or D3 (300,000 IU) and compared IM with oral administration. Six studies tested daily oral supplementation strategies by using dosages between 1000 and 4000 IU. One study chose a weekly intervention of 50,000 IU. Another compared daily with monthly intervention by using 1600 and 50,000 IU, respectively. The final study compared a single IM injection of 300,000 IU of vitamin D2 vs a single oral dose of 300,000 IU of vitamin D3.

Treatment follow-up times varied from 28 days to 24 weeks for the bolus-intervention studies, whereas the daily and weekly study designs had intervention periods that ranged from 14 days to 12 months. The researchers say a “concern for all studies” was the lack of consensus in the analysis of serum 25(OH)D concentrations.

With these caveats in mind, the researchers report that vitamin D3 supplementation produced a significantly greater absolute increase from baseline of serum 25(OH)D in eight studies, no matter what the dose, frequency or route of administration. Two studies found vitamin D2 and D3 equally efficacious.

Likewise, in the seven-study meta-analysis, vitamin D3 supplementation had a significantly greater effect in raising serum 25(OH)D concentrations over time compared with vitamin D2 supplementation, with a weighted mean difference of 15.23 (p=0.001).

“When the frequency of dosage administration was compared, there was a significant response for vitamin D3 when given as a bolus dose (p=0.0002) compared with administration of vitamin D2, but the effect was lost with daily supplementation,” the authors report.

Nevertheless, they say “regardless of whether supplementation with vitamin D was in small daily doses or in larger and more infrequent bolus dosages, the favoring toward cholecalciferol was still evident.”

Based on their findings, the authors say, “It is clear that there are stark differences in the metabolic fates of ergocalciferol and cholecalciferol that should not be ignored. When the evidence from the studies that focused on vitamin D metabolism at the cellular level is compared with the evidence from clinical trials, it is clear that, overall, there was consistency in the results that shows cholecalciferol appears to have advantageous biological qualities that allow it to sustain its systemic influences for far longer and at far greater concentrations than does ergocalciferol.”

Limitations of the analysis include the small number of studies available for review and the “high” heterogeneity between studies. The investigators also point out that all studies used doses of ergocalciferol and cholecalciferol “far above” the currently recommended daily allowance of 600 IU for males and females aged 1 to 70 years.

These factors “limit the ability to extrapolate the outcomes of this review toward realistic public health recommendations when referring to ergocalciferol and cholecalciferol supplementation,” the authors say.


Am J Clin Nutr 2012.


Getting enough B’s? – Vit B1,2,3,6 and 12

Tuesday, December 29th, 2009

Metametrix’s Organic Acids, Comprehensive Metabolic Profile and Adrenal Stress panel can reveal B-Complex Insufficiency especially when

-Either Organic Acids test or CMP test, shows concurrent elevations of all 5 keto acids ie pyruvate, alpha-ketoglutarate,alpha-ketoisocaproate, alpha-ketoisovalerate and alpha-keto-beta-methylvalerate.

Adrenal Stress test shows low cortisol/DHEA.

Vitamin B1 (Thiamine) Deficiency

Thiamine derivatives and thiamine-dependent enzymes are present in all cells of the body, thus, a thiamine deficiency would seem to adversely affect all of the organ systems. However, the nervous system and the heart are particularly sensitive to thiamine deficiency, because of their high oxidative metabolism.

Thiamine deficiency can lead to myriad problems including neurodegeneration, wasting and death. It is thought that many people with diabetes have a deficiency of thiamine and that this may be linked to some of the complications that can occur.
Well-known syndromes caused by thiamine deficiency include beriberi and Wernicke-Korsakoff syndrome, diseases also common with chronic alcoholism.

Insufficient absorption of B1 results in a disease called beriberi affecting the peripheral nervous system and/or the cardiovascular system, with fatal outcome if not cured by thiamine administration.

In less severe deficiency, nonspecific signs include malaise, weight loss, irritability and confusion, fatigue, loss of appetite, gastrointestinal upsets, nausea and weakness.

Signs of a severe deficiency include mental confusion, muscular weakness, paralysis of the extremities, heart problems and loss of reflexes.

Food Sources of Vitamin B1
Thiamine is found in a wide variety of foods at low concentrations. Yeast and pork are the most highly concentrated sources of thiamine. Cereal grains, however, are generally the most important dietary sources of thiamine, by virtue of their ubiquity. Of these, whole grains contain more thiamine than refined grains, as thiamine is found mostly in the outer layers of the grain and in the germ (which are removed during the refining process). For example, 100g of whole wheat flour contains 0.55 mg of thiamine, while 100 g of white flour only contains 0.06 mg of thiamine.

Sources: Oysters, green peas, brewer’s yeast, organ meats, lean cuts of pork, dried beans and peas, oranges, wheat germ, breads and cereals whole grain, peanuts and peanut butter. Some other foods rich in thiamine are oatmeal, flax and Sunflower seeds, brown rice, whole grain rye, asparagus, kale, cauliflower, potatoes, liver (beef, pork and chicken) and eggs.

Possible Causes of Deficiency
A lack of thiamine can be caused by
• malnutrition,
• a diet high in thiaminase-rich foods (raw freshwater fish, raw shellfish, ferns)
• and/or foods high in anti-thiamine factors (tea, coffee, betel nuts)
• and by grossly impaired nutritional status associated with chronic diseases, such as
o alcoholism,
o gastrointestinal diseases,
o HIV-AIDS, and persistent vomiting

Vitamin B-2

Vitamin B-2 (Riboflavin) is necessary for the normal release of energy from carbohydrate, protein and fat in food. It’s also important for normal growth and development, the production and regulation of certain hormones, and the formation of red blood cells.

Sources: Dairy products, cheese, meat, poultry, fish, enriched and fortified grains, cereals and bakery products, legumes, mushrooms, green vegetables such as broccoli, asparagus and spinach. Exposure to light will degrade riboflavin. Riboflavin is generally stable during the heat processing and normal cooking of foods if light is excluded

Signs of Deficiency: Soreness of the mouth, lips and tongue, burning and itching of the eyes, loss of vision, sensitivity to light. As the deficiency progresses, the inside of the mouth, and the eyes and skin become inflamed, and depression and/or hysteria develop.

Any excess at nutritionally relevant doses is excreted in the urine, imparting a bright yellow color when in large quantities. In humans, there is no evidence for riboflavin toxicity produced by excessive intakes.

Vitamin B-3

Vitamin B-3 (Niacin) is essential for the release of energy from carbohydrates. It aids in the breakdown of protein and fats, in the synthesis of fats and certain hormones, and in the formation of red blood cells.

Niacin is involved in both DNA repair, and the production of steroid hormones in the adrenal gland.

Sources: Meat, poultry, fish, enriched cereals and grains, and nuts. Although milk and eggs contain very little niacin, they provide tryptophan, which is converted into niacin by the body.

Signs of Deficiency: Weakness, loss of appetite, indigestion, skin inflammation, and lethargy. A severe deficiency results in the disease pellagra, which causes scaly skin, swollen tongue, tremors and damage to the central nervous system.

Common psychiatric symptoms of niacin deficiency include irritability, poor concentration, anxiety, fatigue, restlessness, apathy, and depression. Mild niacin deficiency has been shown to slow metabolism, causing decreased tolerance to the cold.

High-dose niacin may also elevate blood sugar, thereby worsening diabetes mellitus. Hyperuricemia is another side-effect of taking high-dose niacin, and may exacerbate gout.Niacin at doses used in lowering cholesterol has been associated with birth defects in laboratory animals, with possible consequences for infant development in pregnant women.
Niacin at extremely high doses can have life-threatening acute toxic reactions. Extremely high doses of niacin can also cause niacin maculopathy, a thickening of the macula and retina which leads to blurred vision and blindness. This maculopathy is reversible after stopping niacin intake.

The following metametrix tests and the results which reveals Niacin deficiency are as follows:
-The CMP and Organic Acids test when pyruvate is high and lactate and picolinate are low.
-Fatty Acids are high
-Cardio profile revealing hypertriglyceridemia.

Vitamin B-6

Vitamin B-6 (Pyridoxine) helps the body build and break down carbohydrates, fats, and proteins. It plays a key role in the processing of amino acids, the building blocks of protein, and the nutrient aids in the formation and maintenance of the nervous system.

Pyridoxine assists in the balancing of sodium and potassium as well as promoting red blood cell production. It is linked to cardiovascular health by decreasing the formation of homocysteine. In addition, pyridoxine can help balance hormonal changes in women and aid in immune system. Lack of pyridoxine may cause anemia, nerve damage, seizures, skin problems, and sores in the mouth.

It is required for the production of the monoamine neurotransmitters serotonin, dopamine, norepinephrine and epinephrine, as it is the precursor to pyridoxal phosphate: cofactor for the enzyme aromatic amino acid decarboxylase.

Sources: Chicken, fish, kidney, liver, pork, eggs, unmilled rice, soy beans, oats, wholewheat products, peanuts and walnuts. Another very good source of pyridoxine is dragon fruit from South East Asia. Pyridoxine is not normally found in plants and plants are not the principal source of this vitamin. This vitamin is made by certain bacteria. Some vegetarians may get adequate pyridoxine simply from eating plants that have traces of soil (like potato skins). Most people get their supply of this vitamin from either milk or meat products.

Signs of Deficiency: Depression, vomiting, increased susceptibility to disease and infection, skin and nerve inflammation, anemia, nausea and lethargy.


However, vitamin B6 can cause neurological disorders, such as loss of sensation in legs and imbalance, when taken in high doses (200 mg or more per day – 10,000% of US RDA) over a long period of time. Vitamin B6 toxicity can damage sensory nerves, leading to numbness in the hands and feet as well as difficulty walking. Symptoms of a pyridoxine overdose may include poor coordination, staggering, numbness, decreased sensation to touch, temperature, and vibration, and tiredness for up to six months.

The following metametrix tests and the results which reveals B6 deficiency are as follows;
-CMP and Organic Acids indicating that both Xanthurenate and Kynurenate are High
-Amino Acids tests showing multiple essential amino acids- High (leucine, isoleucine, valine, phenylalaine,tryptophan or glutamine.
-Homocysteines tests indicating HIGH levels
– RBC Essential elements test indicating low RBC magnesium.

Vitamin B12 is a water soluble vitamin with a key role in the normal functioning of the brain and nervous system, and for the formation of blood. It is one of the eight B vitamins. It is involved in the metabolism of every cell of the body, especially affecting DNA synthesis and regulation, but also fatty acid synthesis and energy production.
Vitamin B12 enhances the phase-response of circadian melatonin rhythm to a single bright light exposure in humans. Sleep disturbances may occur because B12 may be involved in the regulation of the sleep wake cycle by the pineal gland (through melatonin).
Symptoms and damage from deficiency

Vitamin B12 deficiency can potentially cause severe and irreversible damage, especially to the brain and nervous system. At levels only slightly lower than normal, a range of symptoms such as fatigue, depression, and poor memory may be experienced.
However, these symptoms by themselves are too nonspecific to diagnose deficiency of the vitamin.
During the course of disease, mental disorders can occur which include: irritability, focus/concentration problems, depressive state with suicidal tendencies, paraphrenia complex. These symptoms may not reverse after correction of hematological abnormalities, and the chance of complete reversal decreases with the length of time the neurological symptoms have been present.

High levels of homocysteine are related to the early development of heart and blood vessel disease. In fact, it is considered an independent risk factor for heart disease. High homocysteine is associated with low levels of vitamin B6, B12, and folate and renal disease. Homocysteine is a common amino acid found in the blood and is acquired mostly from eating meat.

Food Sources of B12
Vitamin B12 is naturally found in meat (especially liver and shellfish), milk and eggs. Eggs are often mentioned as a good B12 source, but they also contain a factor that blocks absorption.

Gastric acid is needed to release vitamin B12 from protein for absorption.

According to the U.K. Vegan Society, the present consensus is that any B12 present in plant foods is likely to be unavailable to humans and so these foods should not be relied upon as safe sources, as the B12 analogues can compete with B12 and inhibit metabolism. Also, vegan humans who eat only plant based foods must ordinarily take special care to supplement their diets accordingly. The only reliable vegan sources of B12 are foods fortified with B12 (including some soy products and some breakfast cereals), and B12 supplements.
While lacto-ovo vegetarians usually get enough B12 through consuming dairy products, vitamin B12 may be found to be lacking in those practicing vegan diets who do not use multivitamin supplements or eat B12 fortified foods. Examples of fortified foods often consumed include fortified breakfast cereals, fortified soy-based products, and fortified energy bars.
-The mushroom Agaricus bisporus could contain Vitamin B12. This can be seen on some nutrition sites. Some sources say it is a form that is not usable as a Vitamin B12 source.
-Legumes have root nodules that contain Rhizobia. These bacteria can create Vitamin B12. It may not be a source of Vitamin B12 for nutrition purposes.
-Salt rising bread contains Clostridium perfringens which is known to create Vitamin B12. It may not be available as nutrition.

Caution, side effects, contraindication.
Vitamin B12 supplements in theory should be avoided in people sensitive or allergic to cobalamin, cobalt, or any other product ingredients. However, direct allergy to a vitamin or nutrient is extremely rare, and if reported, other causes should be sought.
• Dermatologic: Itching, rash, transitory exanthema, and urticaria have been reported. Vitamin B12 (20 micrograms/day) and pyridoxine (80 mg/day) has been associated with cases of rosacea fulminans, characterized by intense erythema with nodules, papules, and pustules. Symptoms may persist for up to 4 months after the supplement is stopped, and may require treatment with systemic corticosteroids and topical therapy.
• Gastrointestinal: Diarrhea has been reported.
• Hematologic: Peripheral vascular thrombosis has been reported. Treatment of vitamin B12 deficiency can unmask polycythemia vera, which is characterized by an increase in blood volume and the number of red blood cells. The correction of megaloblastic anemia with vitamin B12 can result in fatal hypokalemia and gout in susceptible individuals, and it can obscure folate deficiency in megaloblastic anemia. Caution is warranted.
• Leber’s disease: Vitamin B12 in the form of cyanocobalamin is contraindicated in early Leber’s disease, which is hereditary optic nerve atrophy. Cyanocobalamin can cause severe and swift optic atrophy, but other forms of vitamin B12 are available. However, the sources of this statement are not clear, while an opposing view concludes: “The clinical picture of optic neuropathy associated with vitamin B12 deficiency shows similarity to that of Leber’s disease optic neuropathy. Both involve the nerve fibres of the papillomacular bundle. The present case reports suggest that optic neuropathy in patients carrying a primary LHON mtDNA mutation may be precipitated by vitamin B12 deficiency. Therefore, known carriers should take care to have an adequate dietary intake of vitamin B12 and malabsorption syndromes like those occurring in familial pernicious anaemia or after gastric surgery should be excluded.”

Some interactions with drugs, herbs and dietary supplements
– Alcohol (ethanol): Excessive alcohol intake lasting longer than two weeks can decrease vitamin B12 absorption from the gastrointestinal tract.
– Antibiotics: An increased bacterial load can bind significant amounts of vitamin B12 in the gut, preventing its absorption. In people with bacterial overgrowth of the small bowel, antibiotics such as metronidazole (Flagyl) can actually improve vitamin B12 status. The effects of most antibiotics on gastrointestinal bacteria are unlikely to have clinically significant effects on vitamin B12 levels.
– Cobalt irradiation: Cobalt irradiation of the small bowel can decrease gastrointestinal (GI) absorption of vitamin B12.
– Metformin (Glucophage): Metformin may reduce serum folic acid and vitamin B12 levels. There are also rare reports of megaloblastic anemia in people who have taken metformin for 5 years or more. Reduced serum levels of vitamin B12 occur in up to 30% of people taking metformin chronically. However, clinically significant deficiency is not likely to develop if dietary intake of vitamin B12 is adequate. Deficiency can be corrected with vitamin B12 supplements even if metformin is continued. The metformin-induced malabsorption of vitamin B12 is reversible by oral calcium supplementation. The general clinical significance of metformin upon B12 levels is as yet unknown.
– Neomycin: Absorption of vitamin B12 can be reduced by neomycin, but prolonged use of large doses is needed to induce pernicious anemia. Supplements are not usually needed with normal doses.
– Nicotine: Nicotine can reduce serum vitamin B12 levels. The need for vitamin B12 supplementation in smokers has not been adequately studied.

– Folic acid: Folic acid, particularly in large doses, can mask vitamin B12 deficiency by completely correcting hematological abnormalities. In vitamin B12 deficiency, folic acid can produce complete resolution of the characteristic megaloblastic anemia, while allowing potentially irreversible neurological damage (from continued inactivity of methylmalonyl mutase) to progress. Thus, vitamin B12 status should be determined before folic acid is given as monotherapy.

– Potassium: Potassium supplements can reduce absorption of vitamin B12 in some people. This effect has been reported with potassium chloride and, to a lesser extent, with potassium citrate. Potassium might contribute to vitamin B12 deficiency in some people with other risk factors, but routine supplements are not necessary.

The following Metametrix Profiles can indicate B12 and folate insufficiencies;

– Organic Acid Test/ CMP Test where a confirmatory tests shows methylmalonate and FIGLU levels are high
– Amino Acids Tests Profile where levels of homocysteine and phosphoethanolamine are high.
– GIfx shows significant findings of dysbiosis and/or malabsorption; elevated leves of antigliadin antibodies