Search

In cross-sectional studies, elevated plasma homocysteine levels have been associated with poor cognition and dementia. Studies of newly diagnosed dementia are required in order to establish whether the elevated homocysteine levels precede the onset of dementia or result from dementia-related nutritional and vitamin deficiencies.A total of 1092 subjects without dementia (667 women and 425 men; mean age, 76 years) from the Framingham Study constituted our study sample. We examined the relation of the plasma total homocysteine level measured at base line and that measured eight years earlier to the risk of newly diagnosed dementia on follow-up. We used multivariable proportional-hazards regression to adjust for age, sex, apolipoprotein E genotype, vascular risk factors other than homocysteine, and plasma levels of folate and vitamins B12 and B6.Over a median follow-up period of eight years, dementia developed in 111 subjects, including 83 given a diagnosis of Alzheimer's disease. The multivariable-adjusted relative risk of dementia was 1.4 (95 percent confidence interval, 1.1 to 1.9) for each increase of 1 SD in the log-transformed homocysteine value either at base line or eight years earlier. The relative risk of Alzheimer's disease was 1.8 (95 percent confidence interval, 1.3 to 2.5) per increase of 1 SD at base line and 1.6 (95 percent confidence interval, 1.2 to 2.1) per increase of 1 SD eight years before base line. With a plasma homocysteine level greater than 14 micromol per liter, the risk of Alzheimer's disease nearly doubled.An increased plasma homocysteine level is a strong, independent risk factor for the development of dementia and Alzheimer's disease.

Epidemiologic studies have identified hyperhomocysteinemia as a possible risk factor for atherosclerosis. We determined the risk of carotid-artery atherosclerosis in relation to both plasma homocysteine concentrations and nutritional determinants of hyperhomocysteinemia.We performed a cross-sectional study of 1041 elderly subjects (418 men and 623 women; age range, 67 to 96 years) from the Framingham Heart Study. We examined the relation between the maximal degree of stenosis of the extracranial carotid arteries (as assessed by ultrasonography) and plasma homocysteine concentrations, as well as plasma concentrations and intakes of vitamins involved in homocysteine metabolism, including folate, vitamin B12, and vitamin B6. The subjects were classified into two categories according to the findings in the more diseased of the two carotid vessels: stenosis of 0 to 24 percent and stenosis of 25 to 100 percent.The prevalence of carotid stenosis ofor = 25 percent was 43 percent in the men and 34 percent in the women. The odds ratio for stenosis ofor = 25 percent was 2.0 (95 percent confidence interval, 1.4 to 2.9) for subjects with the highest plasma homocysteine concentrations (or = 14.4 mumol per liter) as compared with those with the lowest concentrations (or = 9.1 mumol per liter), after adjustment for sex, age, plasma high-density lipoprotein cholesterol concentration, systolic blood pressure, and smoking status (P0.001 for trend). Plasma concentrations of folate and pyridoxal-5'-phosphate (the coenzyme form of vitamin B6) and the level of folate intake were inversely associated with carotid-artery stenosis after adjustment for age, sex, and other risk factors.High plasma homocysteine concentrations and low concentrations of folate and vitamin B6, through their role in homocysteine metabolism, are associated with an increased risk of extracranial carotid-artery stenosis in the elderly.

IN this issue of the Journal, Czeizel and Dudas1 report from Hungary that vitamin supplements can prevent the occurrence of neural-tube defects (spina bifida and anencephaly). This report is a land...

In the Book of Genesis, fish appeared in the waters on the fifth day of creation, after dry land and water separated. This may be the first reference to a functional, indeed lifesaving, food for humans. In the 19th century, New England ships harvested marine oil not for food but to light lamps. Fast forward to the 20th century and the identification of the “Eskimo paradox,” which refers to the extremely low rates of death from cardiovascular disease among the Inuit, as compared with their northern European counterparts, despite similarly high intakes of fat — about 40 percent of calories. . . .

FOLATE deficiency, probably the most common vitamin deficiency in this country, often occurs as a complication of gastrointestinal disease or of therapy with certain drugs. Like several other vitamins, folate exists in a variety of natural forms, and the study of folic acid represents a fascinating chapter in medical history. After its basic structure was described in 1945,1 more than a dozen previously identified and seemingly unrelated growth principles or antianemia factors, including Wills's "new hematopoietic principle," observed in 1931, factors R and S and vitamins M, Bc, B10 and B11, were recognized as free . . .

A rise in the serum level of free folate in man follows the ingestion of conjugated folate purified from yeast. Everted sacs of rat intestine release folate from conjugate, and homogenates of intestinal mucosa of man and rat contain enzyme (or enzymes) capable of releasing free folate from conjugated folate. We suggest that these enzymes of the intestinal mucosa participate in the absorption of folate from the peptide conjugates that predominate in the human diet.