Nutrition now and in the future is about understanding biological proceses and how the constituents of food may affect these processes. An obvious statement.
A very interesting article in the Lancet ( Spyridopoulos and Dimmeler 2007 , 369, 81-2
Can telomere length predict cardiovascular risk ? )

Telomeres—TTAGGG DNA are the repeats at the ends of chromosomes—and are widely regarded to be the internal biological clock of a living organism as they shorten with every cell division.1 Telomeres in human blood cells contain about 10000-20000 nucleotides at birth. This length decreases by about 50 bp a year, thereby being reduced to a few thousand bp in elderly individuals.’ Critically short telomeres are assumed to have functional implications, such as the induction of cellular senescence, which is characterised by the expression of specific markers of ageing and the inability of the cell to divide further.1 Although age is an important independent predictor for the development of cardiovascular disease, shortening of age-corrected telomere length in leucocytes exposes individuals to an additional substantial risk of mortality from cardiovascular and infectious complications.’1
In the Lancet, Scott Brouilette and colleagues ( Lancer 2007, 369, 107-114 ) report the correlation between telomere length and risk of developing coronary heart disease/ Telomere length was measured in white blood cell DNA from a subgroup of more than 1500 patients in the West of Scotland Primary Prevention Study (WOSCOPSJ, in which the use of pravastatin was tested in men with raised concentrations of LDL cholesterol to prevent cardiovascular events. This substudy shows that individuals with shorter telomere length have about a two-fold increased risk of developing coronary artery disease in the 5 years from the start of treatment. Interestingly, pravastatin completely attenuated this telomere-attributed risk. The randomised case-control design of the study is better than to all previous studies on the association of telomere length and cardiovascular risk.
Several aspects of Brouilette and colleagues’ study merit special attention. The first is the potential mechanism behind the correlation between mean telomere length and coronary heart disease. One might speculate that shorter telomeres could indicate functional changes within cell populations—eg, senescent lymphocytes that produce higher amounts of inflammatory cytokines. Furthermore, telomere shortening in stem or progenitor cells could limit the repair capacity of the vessel wall. Telomere shortening associated with a dysfunction of circulating endothelial progenitor cells, which contribute to endothelial repair and seem to be atheroprotective, could aggravate atherosclerotic disease progression.
Interestingly also smoking and obesity accelerate this shortening process.
What a rich field for nutritional studies. –

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Martin Eastwood

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