A new analysis suggests that an acne medication that was tried as a possible skin cancer preventative in a 1998 clinical trial probably did not cause the deaths of several veterans participating in that research.

The earlier study was halted six months early, when a increased risk of death was seen in those using retinoid tretinoin cream when compared to those taking a placebo.

However, a closer look at the data from that trial did not uncover a definitive link between the treatment and an increased risk of death.

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Retin A (generically known as tretinoin) is a Vitamin A analogue that is a popular acne medication. It is also used “off label” to prevent skin cancers, treat wrinkles and prevent skin aging. Renova, which is also a form of tretinoin, is FDA-approved to reduce the signs of wrinkles.

These products have been used safely and effectively for many years. However, a recent study by Weinstock, published in the reputable journal Archives of Dermatology, was very disturbing. It showed that patients treated in a VA hospital with 0.1% tretinoin topically to prevent skin cancer had a higher risk of death than those not using tretinoin. The veterans in this study were predominately elderly men.

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Cigarette smoke causes the same cellular defect seen in people with Werner’s syndrome — a rare genetic disease that makes people age very fast.

Smoking speeds the aging process, causing smokers to die about 10 years before their time. Now researchers may have found a clue to this process, giving them unexpected new paths to treatment.

The clue comes from the observation that smokers aren’t the only people who age too fast. In their 20s, people with a rare genetic disorder called Werner’s syndrome get gray hair, thin skin, and hoarse voices.

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An interesting paper from the owner of senescence.info and collegues: “Numerous microarray studies of aging have been conducted, yet given the noisy nature of gene expression changes with age, elucidating the transcriptional features of aging and how these relate to physiological, biochemical, and pathological changes remains a critical problem. … We performed a meta-analysis of age-related gene expression profiles using 27 datasets from mice, rats, and humans. Our results reveal several common signatures of aging, including 56 genes consistently overexpressed with age, the most significant of which was APOD, and 17 genes underexpressed with age. We characterized the biological processes associated with these signatures and found that age-related gene expression changes most notably involve an overexpression of inflammation and immune response genes and of genes associated with the lysosome. An underexpression of collagen genes and of genes associated with energy metabolism, particularly mitochondrial genes, as well as alterations in the expression of genes related to apoptosis, cell cycle, and cellular senescence biomarkers, were also observed. … We suggest these molecular signatures reflect a combination of degenerative processes but also transcriptional responses to the process of aging.” Supplementary data are available over at senescence.info.

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Researchers have unraveled crucial details of how aging causes broken bones to heal slowly, or not at all, according to study results published in the Journal of Bone and Mineral Research. The research team also successfully conducted preclinical tests on a potential new class of treatments designed to “rescue” healing capability lost to aging.

In the worst cases, an age-related delay in healing keeps the two sides of a fractured bone from ever rejoining (non-union), leaving many confined to wheelchairs, unable to walk or to live independently.

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