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New York / Heidelberg, 4 March 2013

Obesity, age and your heart – is it too late to go on a diet?

Study finds that the protective cardiac effects of calorie restriction benefit the young but not the old in mice

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Two major risk factors for heart disease are obesity and age, with increases in both being detrimental to the heart. Recent studies in humans have found that restricting calorie intake can have profound heart benefits in obese adults with improvements seen in both heart structure and function. However, the exact mechanisms involved and the relationships between the effects of obesity and aging are not clear.
A new study published in Springer’s Journal of Cardiovascular Translational Research helps to clarify some of these issues. Majd AlGhatrif from the Johns Hopkins University School of Medicine in Baltimore and his colleagues looked at whether the protective effects of caloric restriction would still apply in leptin-deficient obese mice and further whether these effects were similar in different age groups. Leptin is a hormone produced by the fat cells that triggers the sense of feeling full. Deficiency of this hormone causes overeating and obesity.
The researchers studied the effects of caloric restriction in two-month-old versus six- to seven-month-old leptin-deficient obese mice. Both young and old mice lost a similar amount of weight on the restricted diet. In the younger mice, restricting calories was found to have several positive effects on the heart. As well as restoring normal heart stiffness (diastolic function), it helped reverse the amount of fat deposited in the heart cells and helped normalize cellular processes in the heart. None of these benefits were seen in the older mice.
However, the team discovered that although fat deposition in the hearts of the older mice did not change, caloric restriction reduced the negative effects of this fat on the heart tissue. Thus, the mice should have been better able to repair the free radical cellular damage inflicted by the fat deposits. Surprisingly, this did not lead to an improvement in heart function in older mice, indicating that the oxidative damage had reached a point where it had become irreversible. Exactly when this point is reached is not currently known.
AlGhatrif and his colleagues conclude that “discovering the exact mechanism of reversibility and determining what ultimately can reduce the persistent oxidative damage and diastolic dysfunction will greatly enhance our understanding of the physiology of cardiovascular aging.” They add that many aspects of their research warrant further study in order to fully elucidate exactly when oxidative damage gets to the stage where caloric restriction will no longer be able to normalize heart function.
Reference
AlGhatrif M et al. (2013) Beneficial cardiac effects of caloric restriction are lost with age in a murine model of obesity. Journal of Cardiovascular Translational Research. DOI 10.1007/s12265-013-9453-4
The full-text article is available to journalists on request.

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