What is Vitamin B12 for?
Great Tasting Liquid
Cherry Charge or Tropical flavors
No problem on the stomach
The Energy Vitamin
What is Vitamin B12 for ?
Vitamin B12, the energy vitamin, is a high-potency natural energy source.
Formation of red blood cells
B-12 is found naturally in meat, eggs and milk; therefore, supplementation can by very important for vegans as well as those predisposed to anemia. Sixteen percent of older adults are B-12 deficient, most often related to an inability to absorb vitamin B-12 found in food.* “The Institute of Medicine recommends adults over 50 get most of their B-12 from supplements and fortified food because of impaired B-12 absorption.”*
1st STEP For Energy High Potency B-12: A great tasting supplement you will enjoy taking day after day. Regular, consistent supplementation provides the maximum benefits possible. As always with 1st STEP, there is no reflux or upset stomach, and 1st STEP is priced competitively to make it a part of your daily supplementation regimen.
*The physicians desk reference
How to Use: 1STEP is very easy to use. Simply loosen
or remove the cap from the chamber side, squeeze the
liquid up into the chamber and drink.
Usage:Take 1/2 ounce in the morning to
begin your day or
Storage: Refrigerate after opening.
Shelf life: 2 years
B12 Study Findings: Vitamin B12 deficiency symptoms
Supplement recommendations for chronic fatigue syndrome
BERKELEY, CALIFORNIA. Dr. Melvyn Werbach, MD of the UCLA School of Medicine has just published a thorough review of nutritional deficiencies involved in chronic fatigue syndrome (CFS). These include deficiencies In vitamin C, coenzyme Q10, magnesium, zinc, sodium, l-tryptophan, l-carnitine, essential fatty acids, and various B vitamins. He points out that there is some evidence that the deficiencies are caused by the disease itself, rather than by an inadequate diet. He suggests that the deficiencies not only contribute to the symptoms of CFS but also impair the healing process. Although the results of supplementation trials involving CFS patients have been inconclusive so far Dr. Werbach nevertheless recommends that CFS patients be given large doses of certain supplements for at least a trial period to see if their symptoms improve. His recommendations are:
• Folic acid: 1-19 mg/day for 3 months
• Vitamin B12: 6-70 mg (intramuscular injection) per week for 3 weeks
• Vitamin C: 10-15 grams/day
• Magnesium: 600 mg/day + 2400 mg/day of malic acid for 8 weeks
• Zinc: 135 mg/day for 15 days
• 5-hydroxytryptophan: 100 mg three times daily for 3 months (lf fibromyalgia is present)
• L-carnitine: 1-2 grams three times daily for 3 months
• Coenzyme Q10: 100 mg/day for 3 months
• Essential fatty acids: 280 mg GLA and 135 mg EPA daily for 3 months
The supplements should be administered with medical supervision and accompanied by a high-potency vitamin/mineral supplement for the duration of the trial. [95 references]
Werbach, Melvyn R. Nutritionaf strategies for treating chronic fatigue syndrome. Alternative Medicine Review, Vol. 5, NO.2 Apri/2000, pp. 93-108
Vitamin B-12 -Is oral supplementation effective?
CAMBRIDGE, UNITED KINGDOM. It is common medical dogma that patients suffering from pernicious anaemia are unable to absorb sufficient vitamin B-12 from their diet and therefore require intramuscular injections of the vitamin on a regular basis. Recent research is questioning this assumption. In a commentary in The Lancet Dr. M. Elia of the Dunn Clinical Nutrition Centre persuasively outlines the reasons why oral supplementation is at least as effective as intramuscular injections. Dr. Elia points out that vitamin B-12 is absorbed from the intestine via two different routes. One involves intrinsic factor and is estimated to lead to absorption of about 60 per cent of the amount of vitamin B-12 ingested in the diet. The other does not need intrinsic factor (which is absent in pernicious anaemia patients} and only leads to absorption of about 1 per cent of the ingested amount. The body needs about 1-2.5 micrograms/day so oral supplementation with 100-200 micrograms/day should be adequate. However, Dr. Elia suggests a daily intake of 1000 micrograms/day is needed to ensure successful long-term results in patients with pernicious anaemia. A recent study showed that oral supplementation with 2000 micrograms/day was three times as effective as intramuscular injections in increasing vitamin B-12 levels in pernicious anaemia patients. Dr. Elia also questions whether the current RDA (Recommended Dietary Allowance) of 1-2.5 micrograms/day is adequate for older people. He points out that mild vitamin B12 deficiency, which can lead to abnormalities in cognitive function and increased risk of cardiovascular disease, affects 12-15 per cent of all elderly people in the United States where the average daily vitamin B-12 intake is about six micrograms - well above the RDA.
Bia, M. Oral or parenteral therapy for B12 deficiency. The Lancet, Vol. 352, November 28, 1998, pp. 1721-22 (commentary)
Oral vitamin B12 and pernicious anaemia
Vitamin B12 deficiency symptoms
MINNEAPOLIS, MINNESOTA Pernicious anaemia can be treated with intramuscular injections of cobalamin (vitamin B12). These injections can be painful and expensive, but are still widely used despite the fact that research done 30 years ago clearly established that oral doses of one mg/day of vitamin B12 are effective in treating pernicious anaemia and other cobalamin deficiency disorders. The problem. according to Dr. Frank Lederle. MD of the Minneapolis Veterans Affairs Medical Center, is that physicians are unaware that oral cobalamin works. Dr. Lederle performed a survey among Minneapolis internists in 1989 and again in 1996. In 1989 none of tile 245 respondents used oral cobalamin in the treatment of pernicious anaemia. In 1991 a review of the use of oral cobalamin was published in the Journal of the American Medical Association. A subsequent survey in 1996 showed that 19 per cent of the 223 internists responding were now using oral cobalamin. However, even in 1996, 71 per cent of the internists still held the incorrect view that sufficient quantities of cobalamin cannot be absorbed from oral supplements (91 per cent of the internists held this view in 1989). Dr.Lederle concludes that the majority of Minneapolis interns are still unaware of the oral treatment option.
Lederle, Frank A. Oral cobalamin for pernicious anemia; back from the verge of extinction. Journal of the American Geriatrics Society, Vol. 46, September 1998, pp. 1125-27
Oral administration of vitamin B-12 is effective
BRUSSELS, BELGIUM. Older people are often found to have a vitamin B-12 deficiency even though they do not suffer from pernicious anaemia. The body's ability to absorb vitamin B-12 from food decreases markedly with age probably because of a lack of stomach acid. The conventional way of correcting a vitamin B-12 deficiency has been through intramuscular injection of the vitamin. Now researchers at the Universities of Brussels and Antwerp report that oral administration of free vitamin B· 12 is effective in normalizing low vitamin B-12 levels. Their experiment involved 94 patients without pernicious anaemia with a mean age of 84 years who through repeated tests had been found to have an average vitamin B-12 level (in serum) of 146.5 ng/L. The patients were treated for one month With 100 micrograms/day of vitamin B-12 taken as an oral solution of the vitamin in water (10 ml of a solution containing 1 mg vitamin B-12 in 100 ml water). After 10 days 69 per cent of the patients had normal Vitamin B-12 levels (271.5 ng/L average) and after 30 days 88 per cent had achieved normal levels (371.2 ng/L average). The researchers conclude that older patients with a vitamin B-12 deficiency unrelated to pernicious anaemia can be successfully treated with orally administered vitamin B-12.
Verhaeverbeke, L., et al. Normalization of low vitamin B-12 serum levels in older people by oral treatment. Journal of the American Geriatrics Society, Vol. 45, NO.1, January 1997, p. 124 (letter to the editor)
Vitamin E protects vitamin B-12
UTILE ROCK, ARKANSAS. Adenosylcobalamin is an important coenzyme, which is involved in the metabolism of branched-chain amino acids, cholesterol. methionine. and odd-chain fatty acids. It is synthesized in the cell nucleus from vitamin B-12 (cyanocobalamin). Now researchers at the University of Arkansas have found that the synthesis of adenosylcobalamin is impaired if the cell membranes have been subjected to peroxidative (free radical) attack. They also found, through experiments with cell cultures, that vitamin E effectively prevents the peroxidation and thereby allows the enzyme synthesis to proceed unhindered.
Turley, Charfes P. and Brewster, Marge A. Alpha-tocopherol protects against a reduction in adenosylcobalamin in oxidatively stressed human cells. Journal of Nutrition, Vol. 123, July 1993, pp. 1305-12
Vitamin B12 and Alzheimer's Disease
Vitamin B12 deficiency symptoms
Antibiotic combats Alzheimer's disease
BOSTON, MASSACHUSETTS. Two years ago researchers at the Massachusetts General Hospital reported that the antibiotic clioquinol inhibited and even reduced the build-up of amyloid plaques in the brain of mice engineered to developed Alzheimer-like deposits. Now researchers at the Harvard Medical School and the University of Melbourne are about to release the results of a phase II trial involving the use of clioquinol in human Alzheimer's patients. So far the findings are extremely promising. Clioquinol treatment slowed down the disease and significantly reduced the accumulation of beta-amyloid plaques, a cardinal feature of Alzheimer's.
Dr. Ashley Bush of the Harvard Medical School believes that Alzheimer's disease begins when iron, copper and zinc accumulates in the brain and turns beta-amyloid into a rogue enzyme that catalyses the production of hydrogen peroxide which then attacks and destroys brain cells. In the process beta.amyloid forms into the long chain of insoluble plaque so characteristic of Alzheimer's. Dr. Bush believes that c1ioquinol works by removing (chelating?) the metals from the brain. This, in turn, stops the formation of hydrogen peroxide and thus the destruction of brain cells and also prevents the beta-amyloid particles from clumping together. There is some concem that clioquinol depletes vitamin-B12 in the body so vitamin B12 supplementation is a must when taking clioquinol.
Helmuth, Laura. An antibiotic to treat Alzheimer's? Science, Vol. 290, November 17, 2000, pp. 1273- 74 Westphal, Sylvia Pagan. You must remember this... New Scientist, August 3,2002, p. 14
Vitamin B12 deficiency and Alzheimer's disease
Vitamin B12 deficiency symptoms
SACRAMENTO, CALIFORNIA. Vitamin B12 deficiency is associated with the development of megaloblastic anemia, mental dysfunction, and dementia resembling Alzheimer's disease. Vitamin-B12 (cobalamin) is a very important cofactor in several biochemical reactions including the conversion of homocysteine to methionine and the synthesis of SAMe (S-adenosylmethionine). These reactions are believed to be crucial in maintaining neurological health.
Researchers at the University of Milan now report that a vitamin B12 deficiency is associated with higher levels of the inflammatory cytokine, tumour necrosis factor-alpha (TNF-alpha) and reduced levels of epidermal growth factor (EGF). It is believed that high levels of TNF-alpha speed up the progression of Alzheimer's disease thus explaining the association between low vitamin B12 levels and Alzheimer's. The researchers point out that the increase in TNF-alpha and the decrease in EGF can both be reversed by vitamin B12 supplementation. TNF-alpha is also implicated in the progression of H IV to AIDS and vitamin B12 has been found to slow this progression. Editor's Note: Vitamin B12 deficiency is widespread among older people. Taking a 1 mg sublingual B12 could prevent a lot of future health problems.
Miller, Joshua W. Vitamin B12 deficiency, tumor necrosis factor-alpha and epidermal growth factor: a novel function of vitamin B12? Nutrition Reviews, Vol60. May 2002, pp.142-51
Vitamin deficiency implicated in Alzheimer's disease
Vitamin B12 deficiency symptoms
STOCKHOLM. SWEDEN. Some studies have found a correlation between low vitamin B121evels and the development of Alzheimer's disease (AD) and dementia; other studies have found no such correlation. Researchers at the Karolinska Institute now provide convincing evidence that a deficiency of either vitamin B12 or folic acid (folate) is associated with an increased risk of AD and dementia.
Their study involved 370 non-demented people aged 75 years and older who were not supplementing with vitamin B12 or folate. The participants were tested at baseline to determine mental status and had blood samples drawn for analysis of vitamin B12 and folate levels, Only 5ubjects who showed no signs of dementia was included in the follow-up group. Three years tater 77 of the participants had developed dementia; of these 59 were diagnosed with AD. Compared with participants with normal levels of vitamin B12 and folate the participants with low levels of at least one of the vitamins had a 2.3 times higher risk of AD and a 1.7 times risk of any kind of dementia. These risk estimates were obtained after adjusting for other risk factors such as age, sex. and educational attainment. The researchers speculate that homocysteine. a known neurotoxin, may be involved in the development of AD and that vitamin B12 and folic acid help prevent this effect by reducing homocysteine levels in the body.
Wang, H-X, et al. Vitamin B12 and folate in relation to the development of Alzheimers disease. Neurology, Vol. 56. NO.9, May 8, 2001, pp. 1188-94 .
Vitamin B12 deficiency implicated in Alzheimer's disease
Vitamin B12 deficiency symptoms
CLWYD, NORTH WALES. Suspicion has been growing that a lack of vitamin B12 is somehow implicated in the development of Alzheimer's disease. Now researchers in the United Kingdom have confirmed this suspicion. They evaluated members of a family with a genetic predisposition towards Alzheimer's disease. They found that four out of six (67 per cent) of family members with confirmed Alzheimer's disease had abnormally low vitamin B12 levels in their blood. This compares to only one out of 12 (8 per cent) among the family members who were at equal genetic risk for developing Alzheimer's disease but did not. The researchers speculate that a vitamin B12 deficiency could result in impaired methylation reactions in the central nervous system - a characteristic feature in Alzheimer's disease. They also consider the possibility that the genetic predisposition to Alzheimer's disease may actually be related to a genetic impairment in the ability to absorb vitamin 612. Vitamin B12 deficiency in itself often causes disorientation and confusion and thus mimics some of the prominent symptoms of Alzheimer's disease.
McCaddon, A. and Kelly, C.L. Familial Alzheimer's disease and vitamin B12 deficiency. Age and Ageing. Vol. 23, July 1994, pp. 334-37
Vitamin B12 and Homocysteine
Grain fortification with vitamin B12?
DUBLIN IRELAND. Since 1998 it has been mandatory to fortify grain-based foods with folic acid in the United States. Recent reports indicate that this measure has resulted in a 19 per cent decrease in the incidence of neural tube defects. A similar fortification program is being considered in the UK. Irish researchers now suggest that the fortification protocol should include not only folic acid, but also vitamin B12. They point out that folic acid supplementation also lowers the level of homocysteine, a potent risk factor for heart and vascular disease . However, a recent trial carried out by the Dublin researchers clearly showed that as blood levels of folic acid increased through supplementation, blood levels of vitamin-B12 became the limiting factor. In other words, additional folic acid as well as additional vitamin B12 is required in order to attain the maximum reduction in homocysteine levels. Four to five hundred micrograms per day of folic acid were found to increase folic acid levels by 80 to 180 per cent and lower homocysteine levels by about 30 per cent in both men and women, Both folate and homocysteine levels tended to revert to their pre-supplementation levels after 10 weeks of no supplementation; this shows that continuous supplementation is necessary in order to keep homocysteine levels under control.
Quinlivan, E, P., et af. Importance of both folic acid and vitamin B 12 in reduction of risk of vascular disease. The Lancet, Vol. 359, January 19, 2002, pp. 227-28 (research letter)
B vitamins and atherosclerosis
Vitamin B12 deficiency symptoms
TAIPEI, TAIWAN. High blood levels of the amino acid homocysteine have been associated with an increased risk of atherosclerosis. Homocysteine is formed in the body from methionine (an amino acid found in proteins) in a process that can be blocked by folic acid and vitamins B6 and B12, High homocysteine levels can induce endothelial dysfunction (a narrowing of the arteries), which in turn is believed to be a precursor of atherosclerosis. Researchers at the National Taiwan University Hospital now report that homocysteine-induced endothelial dysfunction can be avoided or very significantly ameliorated by supplementing with folic acid and vitamins B6 and B12. The study involved two men and fourteen women between the ages of 41 and 55 years. At the start of the study all participants had their blood levels of homocysteine and their blood flow through the brachial artery measured after a 10-14 hour overnight fast. They were then given an oral methionine-loading test to simulate the intake of a high protein meal. Four hours later their average homocysteine level had increased from 7 micromol/L to 22.7 mlcromol/L and the blood flow (f1ow·mediated vasod/latation) had decreased by 40 per cent. The experiment was repeated, but this time 5 mg of folic acid was given together with the methionine; the results were similar to those obtained in the first experiment indicating that folic acid does not act immediately as an "antidote" to a high intake of methionine. The participants were then given 5 mg of folic acid, 100 mg of vitamin B6, and 0.5 mg of vitamin B12 daily for five weeks. At the end of the five weeks their average homocysteine level had decreased to 5.2 micromol/L. The methionine-loading test was repeated. Four hours later the average homocysteine level among the participants had increased to 17 micromol/L, but there was no statistically significant difference in blood flow before and after the methionine-loading test. The researchers conclude that short-term (five weeks) administration of folic acid and vitamins B6 and B12 will reduce post-meihionine load homocysteine levels and eliminate or ameliorate endothelial dysfunction (an early manifestation of atherosclerosis).
Chao, Chia-Lun, et a/. Effect of short-term vitamin (folic acid, vitamins B6 and B12) administration on endothelial dysfunction induced by post-methionine load hyperhomocysteinemia. American Journal ofCardi%gy. Vol. 84, December 1, 1999, pp. 1359-61