A study at the National Institute on Aging found that homocysteine does more than just damage the arterial wall. As a major consequence of folic acid deficiency – a particular problem with the elderly – elevated homocysteine impairs DNA repair.
There is at the time of writing no universally agreed standard for defining "low", "optimal", "normal", "elevated" and "high" levels when it comes to homocysteine. The upper level for "normal" is generally taken to be 10-11µmol/L, although some go as high as 15 or even 17. Wikipedia, for example, states that "elevated" is defined as over 10.4µmol/L for women and 11.4µmol/L for men, and that the "therapeutic target" (or ideal level) is below 6.3µmol/L.
Many doctors believe that what some consider to be "normal" levels are in fact quite dangerous. Studies have shown that stroke risk starts to rise rapidly as homocysteine levels exceed 7µmol/L, with the risk of stroke being 70-80% higher in individuals with levels exceeding 11µmol/L.
S-Adenosylhomocysteine, which is the precursor of homocysteme, appears to be a more sensitive marker for differentiating cardiovascular patients from control subjects than homocysteine. [Am J Clin Nutr, 2001;74: pp.723-9]
People with elevated levels of homocysteine have nearly double the risk of developing Alzheimer's disease, according to a report from researchers at Boston University. The findings, which come from the long-running Framingham Study, are the first to tie homocysteine levels measured several years before with later diagnosis of Alzheimer's and other dementias. The report, which appeared in the New England Journal of Medicine, provides some of the most compelling evidence yet of an association between high plasma homocysteine and eventual significant memory loss.
Multiple studies indicate that 15-30% percent of patients with premature occlusive vascular disease have moderately elevated total plasma homocysteine concentrations. [ JAMA 1992; 268: pp.877-81]
Nutrients which lower elevated homocysteine levels, including the B-vitamins, are related to depression in several ways [Am J Psy 1997;154: pp.426-428]. The methyl group provided by normal homocysteine metabolism is necessary for the production of depression-relieving neurotransmitters such as serotonin and dopamine. The B-vitamins are also crucial in the direct synthesis of the brain neurotransmitters. [J Affect Disord. 1986;10: pp.9-13; Psychosomatics. 1980;21: pp.926-929]
Several studies have found that patients suffering from inflammatory bowel disease (IBD) such as ulcerative colitis and Crohn's disease are more likely to have elevated blood homocysteine levels (hyperhomocysteinemia).
Those suffering from IBD have a much higher risk of both thromboses and osteoporosis. Because elevated blood homocysteine levels are associated with an increased risk of atherosclerosis and thrombosis, a team of researchers from McGill University in Montreal explored the idea that homocysteine excess may play an important role in IBD.
To test this hypothesis, they measured homocysteine levels in the plasma of 65 patients with IBD and in 127 healthy controls. Their results revealed a striking difference: The patients with IBD had nearly a six-fold increased incidence of hyperhomocysteinemia (homocysteine levels above the normal range) compared to controls.
About one in every seven patients in the IBD group had hyperhomocysteinemia. As expected, those with vitamin B12 deficiency tended to have higher homocysteine levels. Yet researchers were also surprised to find that 80% of the IBD patients with hyperhomocysteinemia had normal blood levels of vitamins.
This suggests that homocysteine imbalances could be an early warning sign of B-vitamin deficiency inside cells – one that occurs well before vitamin levels actually decline in serum. It is still too early to tell if treating high homocysteine could actually reduce IBD symptoms in patients.
Importantly, as homocysteine levels rose in the patients with IBD, so did the clinical ratings of IBD disease severity, including its length of duration and the use of steroid medications to treat it. [Am J Gastroenterol. 2001 96(7): pp.2143-9]
Homocysteine levels are often increased in patients with Crohn's disease. [Am J Gastroenterol. 2000 Dec;95(12): pp.3498-502]
Homocysteine levels in patients suffering from chronic renal failure are significantly elevated at an early stage. The kidney plays a very significant role in homocysteine metabolism but this does not occur during chronic renal failure. In addition, there is a decreased extra-renal catabolism, which contributes to the hyperhomocysteinemia state. [Hyperhomocysteinemia: A Role in The Accelerated Atherogenesis of Chronic Renal Failure?, Netherlands Journal of Medicine, 1995;46: pp.244-251]
Homocysteine imbalances could be an early sign of B-vitamin deficiency inside cells, one that occurs well before vitamin levels actually decline in serum. "Homocysteine may, in fact, be a more sensitive marker of vitamin B12, B6 or folate deficiency and... may precede deficiency of circulating vitamins." [Am J Gastroenterol. 2001 96(7): pp.2143-9]
A recent large-scale prospective study of 4700 Norwegian men and women between the ages of 65 and 67 revealed that higher levels of homocysteine in plasma were associated with a significantly increased risk of mortality. For each 5 mmol/L increase in plasma homocysteine levels, the number of deaths from all causes in this "youthful" senior population jumped by 49%. This included:
These dramatic results may indicate a need for more routine screening in the elderly population. [Am J Clin Nutr 2001;74: pp.130-6]
Elevated homocysteine levels are believed to exacerbate oxidative injury to blood vessels and increase pro-clotting mechanisms linked to stroke and heart attack.
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