Life Extension Update
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Calorie restriction prevents some age-related brain changes
Calorie restriction involves reducing the consumption of calories without restricting the nutritional substances essential to good health. The practice has been shown to extend lifespan in most species in whom it has been tested, and to delay some age-related diseases. A study of humans who voluntarily practiced calorie restriction found among them a lower risk for atherosclerosis, including less inflammation. Readers of Life Extension Update may also recall the August 16 2002 issue which described the findings of a study in which older individuals who consumed fewer calories experienced a lower risk of Alzheimer’s disease. One of the principle theories explaining how the technique works is that it reduces free radical damage.
In the current study, researchers from Washington University School of Medicine in St. Louis fed young and old mice normal diets and compared them to old mice given 35 percent less calories starting at one year of age (equivalent to age 40 in humans). They found that old mice given normal diets had significantly greater amounts of the radical superoxide in several areas of their brains than the younger mice and the old mice provided with the restricted diet. The presence of superoxide was particularly noted in the substantia nigra, an area involved in Parkinson’s disease.
When tested for behavioral tasks, the older calorie restricted animals were found to have maintained grip strength, coordination and flexibility at levels comparable to young mice, whereas old mice on normal diets did not. But when cognitive function was tested, both old groups performed more poorly than the young, non-restricted group.
Lead researcher and associate professor of neurology, of medicine and of anatomy and neurobiology at Washington University Laura L. Dugan, MD stated, “Our findings help us understand the processes underlying both normal aging and calorie restriction benefits. If some aspects of aging are influenced by free radical damage, we may be able to prevent or reverse these impairments.
For the last 20 years there have been studies that suggest free radicals, particularly superoxide, are involved in cumulative damage with aging and that the nervous system may be one of the most vulnerable targets... We believe sensitive signaling pathways that are particularly important in the brain are disrupted by high levels of free radicals and that these disruptions may explain why, under normal circumstances, brain function declines over time. Fortunately, it would be much easier to reverse a misregulation in signaling than it would to reverse cell damage."
In other research, the team is testing antioxidants on older mice to see if they can also help prevent some of the effects of aging.
Fasting and calorie restriction
The concept of restricting calories to improve health was first introduced in the early 1900s, but the theory was advanced (1930s) when it was found that calorie-restricted rats lived longer than those allowed to eat ad libitum. Although decades have passed since these initial findings, the mechanisms whereby dietary restriction retards aging and extends life span are not fully understood. Data suggests that calorie-restricted rodents lived longer and aged more slowly because they were more resistant to stress and their cells were protected against damaging agents (Van Remmen et al. 2001).
Accumulating evidence strongly suggests that oxidative stress underlies the aging process. Senescence can be forestalled by calorie restriction that may work through an antioxidative mechanism. An imbalance in reduction-oxidation reactions (redox) occurring during the aging process may be minimized through the anti-oxidative action of calorie restriction (Cho et al. 2003). Animals chronically calorie-restricted had limited oxidative stress as evidenced by the rapid recovery in glutathione levels in previously hypoxic heart muscle. The kappa-B-responsive cytokines (interleukin-1-B and tumor necrosis factor-a) were transiently expressed in the calorie-restricted group, but persisted in the control group. The expression of manganese superoxide dismutase, a key antioxidant enzyme, was delayed in the group receiving unlimited calories. These data indicate that calorie restriction significantly reduces myocardial oxidative stress and the post-ischemic inflammatory responses (Chandrasekar et al. 2001; Sreekumar et al. 2002).
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