Main Category: Smoking / Quit Smoking
Also Included In: Heart Disease;  Cardiovascular / Cardiology
Article Date: 24 Feb 2012 – 4:00 PST

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Cigarette smoke has long been considered the main risk factor for heart disease. But new research from Brown University in Providence, R.I., shows that nicotine itself, a component of cigarette smoke, can contribute to the disease process by changing cell structure in a way that promotes migration and invasion of the smooth muscle cells that line blood vessels. In particular, invading cells can remodel structures called podosomes, and this leads to further degradation of vessel integrity.

Ultimately, this cellular migration and invasion process gives rise to the formation of vessel-clogging fatty deposits known as plaque – the hallmark of heart and blood vessel disease. The results on the nicotine-podosome link will be presented at the 56th Annual Meeting of the Biophysical Society (BPS), held Feb. 25-29 in San Diego, Calif.

If confirmed in further studies, the finding that nicotine itself promotes vessel damage by changing podosomes appears to question the health benefits of helping people quit smoking through smokeless nicotine delivery agents such as gum or patches.

“The finding that nicotine is as effective as cigarette smoke in enhancing cellular structural changes, and breakdown of scaffold proteins by vascular smooth muscle cells, suggests that replacing cigarette smoking by nicotine treatment may have limited beneficial effects on atherosclerosis,” notes lead researcher Chi-Ming Hai, professor of medical science in the department of molecular pharmacology, physiology, and biotechnology at Brown University.

Hai’s research illuminates the multistep process of plaque formation, and suggests that a new powerful player, nicotine, may be involved. The plaque formation process begins as a response to cellular injury, and progresses to destructive and chronic inflammation of the vessel walls that attracts mobs of white blood cells, further inflaming the vessels. This damage-causing inflammation can be triggered by chemical insults from high blood sugar, modified low-density lipoproteins (LDL, the “bad cholesterol“), physical stress from high blood pressure, or chemical insult from tobacco smoke. Now nicotine itself appears to remodel key structures in a way that primes and enhances the invasion of smooth muscle lining the vessel wall.

Identifying a possible nicotine-posodome link in the invasion step of plaque formation process suggests a new means of intervening in the process: targeting the cell structures that are changed by nicotine and that promote invasion of the smooth muscle lining the vessel wall. If a therapy could prevent, slow, or reverse that step, it would likely interrupt the plaque-production cycle.

Fatty deposits accumulate in blood vessels beginning as young as age 10 and progress over a person’s lifetime. Heart disease results if the deposits continue to build and harden into vessel-clogging plaque. When plaque ruptures, it can block blood flow, starving the heart or brain of oxygen and leading to a heart attack or stroke.

MLA

Main Category: Genetics
Also Included In: Cardiovascular / Cardiology;  Smoking / Quit Smoking;  Obesity / Weight Loss / Fitness
Article Date: 18 Feb 2012 – 0:00 PST

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Every cell in the body has chromosomes with so-called telomeres, which are shortened over time and also through lifestyle choices such as smoking and obesity. Researchers have long speculated that the shortening of telomeres increases the risk of heart attack and early death. Now a large-scale population study in Denmark involving nearly 20,000 people shows that there is in fact a direct link, and has also given physicians a future way to test the actual cellular health of a person.

In an ongoing study of almost 20,000 Danes, a team of researchers from the University of Copenhagen have isolated each individual’s DNA to analyse their specific telomere length – a measurement of cellular aging.

“The risk of heart attack or early death is present whether your telomeres are shortened due to lifestyle or due to high age,” says Clinical Professor of Genetic Epidemiology Borge Nordestgaard from the Faculty of Health and Medical Sciences at the University of Copenhagen. Professor Nordestgaard is also a chief physician at Copenhagen University Hospital, where he and colleagues conduct large scale studies of groups of tens of thousands of Danes over several decades.

Lifestyle can affect cellular aging

The recent “Copenhagen General Population Study” involved almost 20,000 people, some of which were followed during almost 19 years, and the conclusion was clear: If the telomere length was short, the risk of heart attack and early death was increased by 50 and 25 per cent, respectively.

“That smoking and obesity increases the risk of heart disease has been known for a while. We have now shown, as has been speculated, that the increased risk is directly related to the shortening of the protective telomeres – so you can say that smoking and obesity ages the body on a cellular level, just as surely as the passing of time,” says Borge Nordestgaard.

One in four Danes has short telomeres

The study also revealed that one in four Danes has telomeres with such short length that not only will they statistically die before their time, but their risk of heart attack is also increased by almost 50 per cent.

“Future studies will have to reveal the actual molecular mechanism by which the short telomere length causes heart attacks,” says Borge Nordestgaard, and asks, “Does one cause the other or is the telomere length and the coronary event both indicative of a third – yet unknown – mechanism?”

Another possible prospect of the study is that general practitioners could conduct simple blood tests to reveal a person’s telomere length and thereby the cellular wear and age.

MLA