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What about exercise? We can't always change our station in life, but we can always go out for a walk. Researchers studied 2400 twins, and those that exercised more pumped up their telomeres along with their muscles.These were mostly folks in their 40s, does it still work in your 50s? Yes. These "habitual" exercisers were working out three hours a week, better than the younger group. The "heavy" exercise group was only averaging about a half-hour a day. What happens if you study hard-core athletes?Here's the telomere lengths of young healthy regular folks at around age 20, and then age 50, which is what we'd expect, our telomeres get eaten away as we age.But what about the athletes? They start out in the same boat, nice long young healthy telomeres capping all their chromosomes. And then at age 50? They appear to still have the chromosomes of a 20 year old. But these were marathon runners, triathletes running 50 miles a week for, oh, 35 years. That's worse than the meditation retreat!That doesn't help us with the original question, What was it about the Ornish intervention that so powerfully protected telomeres after just three months? We saw that just stress management seems to help, but what about the diet versus exercise. Was it the plant-based diet, was it the walking 30 minutes a day—or, was it just because of the weight loss? In those three months, participants lost about 20 pounds. Maybe your telomeres are happy if you lose 20 pounds using any method, you know, starting a cocaine habit, getting tuberculosis, whatever.To answer this critical question—was it the plant-based diet specifically, the exercise, or the weight loss—ideally you'd do a study where you randomized people into at least three groups, a control group that did nothing, sedentary with a typical diet, a group that just exercised, and a group that lost weight eating pretty much the same diet, but just in smaller portions. And I'm happy to report in 2013 just such a study was published.They took about 400 women and randomized them up into four groups: a portion-controlled diet group, and exercise group, and a portion controlled diet and exercise group for a full year.And here they are. This is how long their telomeres were at baseline. After a year of doing nothing, there was essentially no change in the control group, which is what we'd expect.The exercise group was no whimpy Ornish 30 minute stroll, but 45 minutes of moderate-to-vigorous exercise like jogging. After a year of that, how did they do? They did no better. What about just weight loss? Nothin'. And exercise and weight loss? No significant change either.So as long as you're eating the same diet, it doesn't appear to matter how small your portions are, or how much weight you lose, or how hard you exercise, after a year, they saw no benefit. Whereas the Ornish group on the plant-based diet, lost the same amount of weight after just three months, exercising less than half as hard and saw significant telomere protection.So it wasn't the weight loss, wasn't the exercise, it was the food.What about a plant-based diet is so protective? Higher consumption of vegetables, less butter, and more fruit. From the latest review, foods high in fiber and vitamins, but the key may be avoiding saturated fat. Swapping just 1% of saturated fat calories in our diet for anything else can add nearly a whole year of aging's worth of length onto our telomeres. Researchers have calculated how much of our telomeres we may shave off per serving of foods like ham or hot dogs, bologna, salami, or other lunch meats. Fish consumption was also significantly associated with shortened telomeres.Saturated fats like palmitic acid, the primary saturated fat in salmon, and found in meat, eggs, and dairy in general can actually be toxic to cells. This has been demonstrated in heart cells, bone marrow cells, pancreatic cells and brain cells. And the toxic effects on cell death rates happen right around what you'd see in the blood stream of people who eat a lot of animal products. It may not be the saturated fat itself, though saturated fat may just be a marker for the increased oxidative stress and inflammation associated with those foods.With this link to saturated fat, no wonder lifelong low cholesterol levels have been related to longer telomeres and a smaller proportion of short telomeres—in other words markers of slower biological aging.In fact there's a rare congenital birth defect called progeria syndrome, where children essential age 8-10 times faster than normal. It seems associated with a particular inability to handle animal fats. They started trying lower her cholesterol levels starting at age 2, but sadly, she died shortly after this picture was taken at age 10.The good news is that even if you've been beating up on your telomeres, despite past accumulated injury leading to shorter telomere lengths, current healthy behaviors might help to decrease a person’s risk of some of the potential consequences, like heart disease. Eating more fruit and vegetables and less meat, and having more support from friends and family to attenuate the association between shorter telomeres and the ravages of aging.To summarize, here's a schematic of this constant battle. Inflammation, oxidation, damage and dysfunction are constantly hacking away at our telomeres, at the same time our antioxidant defenses, a healthy diet and exercise, stress reduction are constantly rebuilding them.Telomere length shortens with age. Progressive shortening of our telomeres leads to cell death or transformation into cancer, affecting the health and lifespan of an individual. But the rate of telomere shortening can be either increased or decreased by specific lifestyle factors. Better choice of diet and activities has great potential to reduce the rate of telomere shortening or at least prevent excessive telomere shrinkage, leading to delayed onset of age-associated diseases and increased lifespan.

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INTRODUCTION: Endothelial dysfunction is known to occur in patients with coronary artery disease. Flow-mediated dilation of the brachial artery using Doppler ultrasound is a non-invasive technique for the assessment of endothelial function. The objective of the study was to use the above method to evaluate the pathophysiology of high-fat (HF) intake on endothelial function in a local population. A popular local dish "nasi-lemak", a source of high saturated fat content from coconut milk, was chosen to represent a local high-fat meal (LHF).

CONCLUSION The results suggest that in a local population, impairment of endothelial function is a possible mechanism in the pathophysiology of atherosclerosis from HF intake, beyond just affecting lipid levels. This effect is observed after both a LHF and a WHF meal intake. This technique to study endothelial function may be a useful non-invasive screening tool in the study of other HF diet choices and provides further information for the education of the influence of dietary choices on atherosclerosis.