Mammalian research suggests that long-term calorie reduction is associated with life extension. The telomere is the repetitive nucleotide sequence at the end of a chromatid that protects the chromosomes from fusion during replication. As mammals age, this telomere shortens, with length being proportional to the attrition of the telomere since birth. Telomere length can therefore be considered a biomarker of biological age. Oxidative stress and inflammation are associated with ageing and both accelerate telomere shortening. Because diet can also increase systemic oxidative stress and inflammation, the quality of the nutrition may have an effect on the rate of telomere attrition. Short telomere length is associated with cardiovascular disease, increased mortality risk and diminished longevity. In the 1930s seminal work showed that life span in rodents could be increased through energy restriction. This effect was enhanced by application of energy restriction at a young age.
Energy restriction may therefore increase life span by decreasing the rate of attrition in the telomeres. Based on early animal experiments, researchers have investigated the effects of energy restriction on telomere length in humans. For example, in one study1, diet was assessed in 405 men and 204 women by use of a frequent food questionnaire and related to telomere length which was assessed by use of a Southern blot. The results showed that baseline energy intake (mean age 30.1 years) was inversely associated with follow-up (mean aged 43.2 years) telomere length in men, but not in women. For men, the difference in telomere length between the highest and the lowest quintile for energy intake was 244 base pairs, and the difference in energy intake between the highest and lowest quintiles for telomere length was 440 kcal. These results suggests that energy restriction is inversely associated with telomere length in humans.
Interestingly, the researchers found an inverse association for all macronutrients, but the association was particularly strong for unsaturated fatty acids. Polyunsaturated fatty acids are increasingly being linked to cardiovascular disease and cancer because they are able to increase oxidative stress if consumed in high amounts. The increase in oxidative stress and inflammation associated with polyunsaturated fatty acid consumption may therefore accelerate the attrition of the telomere. The strong association between unsaturated fatty acids and telomere length could be related to a recent increase in the n-6 to n-3 fatty acid ratio in developed nations. Increased consumption of the n-6 fatty acid linoleic acid (LA, C18:2 (n-6)) in the presence of deficient intake on n-3 fatty acids can cause inflammation and oxidative stress by increased production of pro-inflammatory eicosanoids. Restoring the natural n-6 to n-3 ratio decreases inflammatory eicosanoid formation and therefore may be beneficial to longevity.
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