Studies on calorie restriction have been going on for years. Scientists are eagerly investigating to find how eating less food can increase our lifespan.
Laboratory studies have shown that life can be extended. Calorie restriction has been tried on species ranging from spiders to monkeys. The result has been the same; a diet can boost up health and slow the aging process. However, the whole mechanism of how eating less actually affects our physiology and metabolism, in a positive way avoiding tissue and cell degeneration, has remained unknown.
It was reported by a team of scientists and colleagues coming from the University of Wisconsin-Madison how a particular molecular pathway affects the whole anti-aging process behind calorie restriction. The research does both explain the unfolding events causing aging and the potential ways to intervene through medicine to delay aging. The study itself can help to sustain health until old age. This study was recently published in the Journal Cell, (18th of November 2010).
Tomas A. Prolla, an UW-Madison professor of genetics as well as a senior author of the new Cell study says that hey are slowly grasping “good understanding of how caloric restriction works,” . This study is the first of its kind to identify the fundamental anti-aging effects derived from calorie restriction.
The team at Wisconsin emphasis their study on an enzyme called Sirt3. It is an enzyme that is grouped in the family of sirtuins. This family of enzymes has been involved in several longevity studies ranging from programmed cell death, gene transcription as well as stress resistance related to calorie restrictions. For instance, mammals as well as humans have seven sirtuins that are highly linked to cell fate as well as physiology.
However, sirt3 has been slightly under-examined compared to other enzymes of the sirtuin family. John M. Denu who is a professor of biomolecular chemistry in the UW School of Medicine and Public Health of Wisconsin Institute for Discovery as well as the author of the report says that this study does provide solid evidence that sirtuins produces anti-aging effects for mammals.
Denu describes how Sirt3 enzyme affects the mitochondria; where energy is produced in cells, which are commonly responsible for the production of free radicals (highly reactive forms of oxygen). The reactive oxygen produced while generating energy for cells do usually cause damage to cell structures and therefore, hastens aging. The study revealed that calorie-restrictions actually increased the presence of Sirt3. This changed the metabolism and did equally decrease the volume of free radicals generated by mitochondria.
Prolla has been studying calorie restriction for more than 10 years. He says that the study shows a clear link between calorie restrictions and healthy mitochondria. He claims that Sirt3 has a vital role in the reprogramming mitochondria when calorie restriction changes mammals’ metabolic state.
The postdoctoral fellows Wei Yu of UW-Madison and Shinichi Someya from UW-Madison as well as the University of Tokyo were the lead author of this research. The experiment used to understand the calorie restriction benefit on aging was investigated through a mouse model.
A mouse model was used in the experiment. Mice had experienced an age-related hearing loss, which was linked to damages caused to cell through free radicals. For instance, hearing loss occurs when cells of the cochlea are damaged; the inner part of the ear which actually change sound vibrations into nerve impulses for the brain to recognise. Moreover, age-related hearing loss is equally frequent for humans. This has been proven through the use of ultrasonic cell phone ring tones which only young children can hear, as the highest hearing frequencies that can be heard are the first cell structures to be damaged.
Prolla, says that hearing loss is linked to the damage of various cell types present in the cochlea. There is a clear link between cell deaths and age-related hearing loss. Interestingly, hearing loss can be hampered by simply eating fewer calories.
In the Cell report, the team of scientists found that a higher volume of Sirt3, increased the cell’s protection against stress and risk of death from free radicals.
Denu claims that Sirt3 provides enough protection to safeguard cells from oxidative damage.
It should be noted that sirtuins have been considered to play a fundamental role in aging. There have been a dozen of studies suggesting this particular relation. However, the Wisconsin study is the first one to demonstrate how the enzymes are actually associated to the aging process of mammals.
Denu, says that the comprehension of the role of sirtuin enzymes in the mechanism of aging can promote the development of medications that can directly slow down the speed of aging. Drugs that either triggers the pathway of Sirt3 or other anti-aging enzymes could be released. This would therefore, mimic the benefit of calorie restriction and delay aging.
Source: Physorg and University of Wisconsin-Madison
Sun, Dec 5, 2010
Anti Aging, Health And Aging