Latest Evidence Fails to Link Homosysteine to Cardiovasular Disease

In 1969 K.S. McCully, M.D. published a report of his autopsy findings concerning 2 young victims of the somewhat rare metabolic disease known as homocystinuria (homocysteine in the urine); which is caused by a genetic condition now known as cystathionine beta-synthase (CBS) deficiency and is thought to affect at least 1 in 200,000 to 335,000 people worldwide.  McCully noted that the extent of atherosclerotic disease (hardening of the arteries) present in both victims was much more extensive than he would have expected to find in someone who had died from other causes, which led him to postulate that perhaps the high homocysteine levels present in the blood was somehow related to the extensive atherosclerosis.





Over the next 30 years higher blood levels homocysteine were cited as either the direct cause or as a significant contributor in a number of diseases such as Alzheimer’s disease, hardening of the arteries, osteoporosis, and arthritis.  Despite the enthusiasm and high expectations generated by these initial studies, there has been only one drawback:  therapies that were known to lower homocysteine levels (such as B-complex dietary supplementation) had no demonstrable effect on the course of the diseases that were supposedly caused by homocystine.  But why was this happening?




The original studies (those that uncovered the higher levels of homocysteine) were epidemiologic studies.  In this type of research large numbers of people with the same clinical diagnosis are evaluated to determine which, if any, factors can be found in the study population that seem to be associated with a particular disease or condition.  Once a tentative association is identified, the next step is to determine if changes in the suspected causative or contributing factor (such as vitamins that are known to lower homocysteine levels in the bloodstream) will result in changes in the number of subjects subsequently diagnosed with the disease under investigation.