Aging is exactly an accumulation of biochemical damage and the resulting disarray caused by that damage. We all know that smoking is bad for you, but it seems that smoking causes some of the same effects as one of the genetic conditions that causes accelerated aging: “Smoking can accelerate the aging process and shorten the lifespan by an average of more than 10 years. We focused on what happens within the lungs because of the similar aging effects, including atherosclerotic diseases and cancer, seen in people with Werner’s syndrome and people who smoke … Werner’s syndrome involves a genetic mutation that causes a deficiency in what’s known as Werner’s syndrome protein. The protein normally helps repair DNA damage. Smoking does not appear to cause the same mutation, but our study showed that it does decrease Werner’s syndrome protein … The team also applied cigarette smoke extract to cultured lung fibroblasts taken from nonsmokers. They saw that Werner’s syndrome protein expression was decreased, and the cells had lost their ability to repair wounds. In contrast, when the team caused the lung fibroblasts in petri dishes to overexpress Werner’s syndrome protein, it had a protective effect and helped resist the damaging effects of cigarette smoke.”

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Your mother’s wrinkles - or lack there of, may not be the best predictor of how you’ll age. In fact, a new study claims just the opposite. The study, involving identical twins, suggests that despite genetic make-up, certain environmental factors can add years to a person’s perceived age. Results just published on the web-based version of Plastic and Reconstructive Surgery®, the official medical journal of the American Society of Plastic Surgeons (ASPS), reveal that factors like divorce or the use of antidepressants are the real culprits that can wreak havoc on one’s face.

“A person’s heritage may initially dictate how they age - but if you introduce certain factors into your life, you will certainly age faster. Likewise, if you avoid those factors you can slow down the hands of time,” said ASPS Member Surgeon and study author Bahaman Guyuron, MD, professor and chairman, department of plastic surgery, University Hospitals Case Medical Center.

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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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Another longevity mutation is shown to work by reducing the all-important emmission of free radicals from the mitochondria: “first discovered in 2000 [a] mutation in the Indy (’I'm Not Dead Yet’) gene [extends] the life span of fruit flies .. Subsequent studies of the Indy flies have led to the new finding that a mechanism in those genetically altered fruit flies appears to reduce significantly the production of free radicals, a cellular byproduct that can contribute to the aging process. This intervention takes place with few or no side effects on the quality of life for the fruit fly. The discovery could lead to the development of new anti-aging treatments. … There are very few, if any, interventions that are known to dramatically extend healthy lifespan. Understanding how [the] Indy mutation alters the metabolic state of the fruit fly would allow someone to come up with pharmacological interventions that could mimic it and give you the benefit of genetic manipulation without having to do genetics.”

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As reported in the journal, Cell Stem Cell, researchers from Imperial College London have identified critical molecular pathways that may boost the quantity of stem cells released from bone marrow, potentially helping heal heart or bone damage faster and more completely. Initial studies found that the bone marrow of treated mice released 100 times as many stem cells – the key to regenerating tissue.

“We hope that by releasing extra stem cells, as we were able to do in mice in our study, we could potentially call up extra numbers of whichever stem cells the body needs in order to boost its ability to mend itself and accelerate the repair process,” notes Imperial College London Researcher, Dr. Sara Rankin.

Scientists have already developed techniques to increase the production of stem cells from bone marrow. However, this study concentrated on two other types of cells: endothelial and mesenchymal. The mice were given a “growth factor” drug, which occurs naturally in bone marrow, followed by a second drug called Mozobil. The researchers found that both endothelial and mesenchymal cells were released at a much faster rate. Determining if the extra stem cells have a practical application – for example, being able to quickly and fully repair damage caused by a heart attack – is the next step. Human trials may be able to begin within 10 years.
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