EDTA Featured Product

Unlike other water-soluble nutrients, vitamin B12 is stored in the liver, kidney, and other body tissues. As a result, signs and symptoms of vitamin B12 deficiency may not show themselves until 5 to 6 years of poor dietary intake or inadequate secretion of intrinsic factor. The classic deficiency symptom of vitamin B12 deficiency is pernicious anemia. However, a deficiency of vitamin B12 actually affects the brain and nervous system first.

A vitamin B12 deficiency results in impaired nerve function, which can cause numbness, pins-and-needles sensations, or a burning feeling. It can also cause impaired mental function that, in the elderly, mimics Alzheimer's disease. Vitamin B12 deficiency is thought to be quite common in the elderly and is a major cause of depression in this age group.

In addition to anemia and nervous system symptoms, a vitamin B12 deficiency can also result in a smooth, beefy red tongue and diarrhea. This occurs because rapidly reproducing cells such as those that line the mouth and entire gastrointestinal tract cannot replicate without vitamin B12.

Measuring the level in the blood (serum cobalamin) or the level of methylmalonic acid in the urine is the best method to determine vitamin B12 deficiency. In addition, measuring the level of plasma homocysteine is emerging as a method to determine the status of both vitamin B12 and folate. Another test, the Schilling test, is used determine whether there is sufficient output of intrinsic factor. The test involves oral administration of radioactive vitamin B12 and then measuring the level excreted in the urine. Below-normal urinary excretion of the vitamin suggests impaired absorption because of lack of intrinsic factor.

Several investigators have found the level of vitamin B12 declines with age and that vitamin B12 deficiency is found in most persons aged 65 and over. Physicians should attempt to diagnose cobalamin deficiency early in the elderly because it is easily treatable and, if left untreated can lead to impaired neurological and cognitive function.

Researchers recently studied 100 consecutive geriatric outpatients who were seen in office-based settings for various acute and chronic medical illnesses; none of these outpatients presented symptoms of vitamin B12 deficiency-related diseases like pernicious anemia. In this group, 11 patients had serum cobalamin levels at 148 pmol/L (picomole per liter) or below, 30 patients had levels between 148 and 295 pmol/L, and 59 patients had levels above 296 pmol/L. After the initial cobalamin determination, the subjects were followed for up to 3 years. The patients with cobalamin levels below 148 pmol/L were treated and were not included in the analysis of declining cobalamin levels. The average annual serum cobalamin level decline was 18 pmol/L for patients who had higher initial serum cobalamin levels (actual range, from 224 to 292 pmol/L. For patients with lower initial cobalamin levels, the average annual serum cobalamin decline was much higher at 28 pmol/L.

These results indicate that in the elderly the following screen tests for vitamin B12 have a high cost-to-benefit ratio.

• Level of vitamin B12 in the blood (serum cobalamin)
• Urinary excretion of methylmalonic acid
• Level of homocysteine

Of these three tests, the urinary methylmalonic acid assay is perhaps the best test because it is sensitive, noninvasive, and relatively convenient for the patient. Correction of an underlying vitamin B12 deficiency improves mental function and quality of life in these patients quite significantly.

Vitamin B12 like folic acid, functions as a "methyl donor." A methyl donor is a compound that carries and donates methyl groups (a molecule of one carbon and three hydrogen molecules) to other molecules, including cell membrane components and neurotransmitters. As a methyl donor, vitamin B12 is involved in homocysteine metabolism and plays a critical role in proper energy metabolism, immune function, and nerve function.

Homocysteine is a factor in the progression of both atherosclerosis and osteoporosis. In fact, elevations in homocysteine are an independent risk factor for having a heart attack. Approximately 20 to 40 percent of patients with heart disease exhibit elevations in homocysteine. In addition to vitamin B12 and folic acid, vitamin B6 is also necessary in metabolizing homocysteine to nondamaging forms. Although research has focused much of its attention on folic acid supplementation as a mechanism to lower homocysteine levels, the prevalence of suboptimal levels of these nutrients in men with elevated homocysteine levels was 56.8 percent for B12 , 59.1 percent for folic acid, and 25 percent for B6, indicating that folic acid supplementation alone would not lower homocysteine levels in many cases. Folic acid supplementation lowers homocysteine levels only if there are adequate levels of vitamin B12 and B6. Because of the interconnectedness of these three B vitamins, it is best to supplement with all three. Folic acid and vitamin B12 supplementation lowers homocysteine levels even in individuals with normal vitamin B12, folic acid, and homocysteine levels.