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Biomedical subjects

Michael Fossel

Publications and source records attributed to Michael Fossel.

4 recordsLinked to original sources
PubMed2002

Is there an antiaging medicine?

In spite of considerable hype to the contrary, there is no convincing evidence that currently existing so-called "antiaging" remedies promoted by a variety of companies and other organizations can slow aging or increase longevity in humans. Nevertheless, a variety of experiments with laboratory animals indicate that aging rates and life expectancy can be altered. Research going back to the 1930s has shown that caloric restriction (also called dietary restriction) extends life expectancy by 30-40% in experimental animals, presumably at least partially by delaying the occurrence of age-dependent diseases. Mutations that decrease production of insulin growth factor I in laboratory mammals, and those that decrease insulin-like signaling in nematodes and fruit flies, have increased life expectancy as well. Other general strategies that appear promising include interventions that reduce oxidative stress and/or increase resistance to stress; hormone and cell replacement therapies may also have value in dealing with specific age-related pathologies. This article reports the findings of a consensus workshop that discussed what is known about existing and future interventions to slow, stop, or reverse aging in animals, and how these might be applied to humans through future research.

Aging↗
PubMed2002

Cell senescence in human aging and disease.

The most common causes of death and suffering, even in most underdeveloped nations, are age-related diseases. These diseases share fundamental and often unappreciated pathology at the cellular and genetic levels, through cell senescence. In cancer, enforcing cell senescence permits us to kill cancer cells without significantly harming normal cells. In other age-related diseases, cell senescence plays a direct role, and we may be able to prevent and reverse much of the pathology. While aging is attributed to "wear and tear," genetic studies show that these effects are avoidable (as is the case in germ cell lines) and occur only when cells down-regulate active (and sufficient) repair mechanisms, permitting degradation to occur. Aging occurs when cells permit accumulative damage by wear and tear, by altering their gene expression rather than vice versa. Using telomerase in laboratory settings, we can currently reset this pattern and its consequences both within cells and between cells. Doing so resets not only cell behavior but the pathological consequences within tissues comprising such cells. We can currently grow histologically young, reconstituted human skin using old human skin cells (keratinocytes and fibroblasts). Technically we could now test this approach in joints, vessels, the immune system, and other tissues. This model is consistent with all available laboratory data and known aging pathology. Within the next decade, we will be able to treat age-related diseases more effectively than ever before.

Age Factors↗