Brain Injury Stops Smokers Cold

In a research development that the director of the National Institute on Drug Abuse (NIDA) calls nothing short of “ming-boggling,” stroke victims lost all desire for cigarettes after suffering damage to a tiny structure in the forebrain. The stroke victims who smoked were seemingly freed from nicotine addiction by damage to the insula, a part of the brain that has not previously been a primary target of addiction research.

Along with the nucleus accumbens, the amygdala, and other structures in the limbic system, certain regions of the cerebral cortex are also implicated in active addiction. Now, said NIDA’s Dr. Nora Volkow, “Everybody’s going to be looking at the insula.”

Researchers at the University of Iowa and the University of Southern California collaborated on the brain injury study, published in the January 26 issue of Science. Neuroscientist Antoine Bechara of USC had learned of a stroke patient known only as N.

A heavy smoker from the age of 14, N. quit cold after a stroke at age 28, telling doctors: “My body forgot the urge to smoke.” A striking percentage of smokers with similar damage to the insula had apparently quit smoking after the injury just as effortlessly as had Patient N.

The role of the insula in brain activity is not well understood, but neurologists believe that the structure may help integrate subcortical inputs into coherent emotions and conscious urges.

No one is suggesting brain surgery for nicotine addiction, but researchers hope to discover ways of interfering with the operation of the insula, perhaps by means of a targeted drug. However, it is not yet clear what other functions the insula may perform, and whether the damage that seemingly eliminates the cigarette urge might also eliminate more positive urges and emotions as well.

Sources:

--Naqvi. N.H., et. al. “Damage to the insula disrupts addiction to cigarette smoking.” Science 315 531-534. Jan 26, 2007.

--Brownlee, Christen. “Addiction Subtraction: Brain damage curbs cigarette urge.” Science News 171 51. Jan 27, 2007.

--Carey, Benedict. “In Clue to Addiction, Brain Injury Halts Smoking.” New York Times. January 26, 2007.

Snail Toxin and Nicotine

This post courtesy of Biology-blog.com

http://www.biology-blog.com/

A New Tool Against Brain Disease

University of Utah scientists isolated an unusual nerve toxin in an ocean-dwelling snail, and say its ability to glom onto the brain's nicotine receptors may be useful for designing new drugs to treat a variety of psychiatric and brain diseases.

"We discovered a new toxin from a venomous cone snail that may enable researchers to more effectively develop medications for a wide range of nervous system disorders including Parkinson's disease, Alzheimer's disease, depression, nicotine addiction and perhaps even schizophrenia," says J. Michael McIntosh.

McIntosh is the same University of Utah researcher who as an incoming freshman student in 1979 discovered another "conotoxin" that was developed into Prialt, a drug injected into fluid surrounding the spinal cord to treat severe pain due to cancer, AIDS, injury, failed back surgery and certain nervous system disorders. Prialt was approved in late 2004 in the United States and was introduced in Europe last month.

Prialt, sold by Ireland's Elan Pharmaceuticals, took roughly 25 years to reach market after its discovery in venom from the fish-eating cone snail Conus magus or magician's cone. McIntosh says he expects it will take 10 to 20 years to develop new medications based on what is learned from the new toxin named alpha conotoxin OmIA (oh-em-one-ay) isolated from a cone snail species named Conus omaria, which lives in the Pacific and Indian oceans and eats other snails. It ranges from 1 to 3 inches long....

Diseases that Might Benefit from the New Snail Toxin

McIntosh says the OmIA toxin will be useful in designing new medicines because it fits like a key into certain lock-like "nicotinic acetylcholine receptors" found on nerve cells in the brain and the rest of the nervous system.

"Those are the same types of receptors you activate if you smoke a cigarette," he says, explaining that nicotine in cigarette smoke "binds" to the receptor to trigger the release of a neurotransmitter, which is a chemical that carries a nerve impulse from one nerve cell to another, allowing nerve cells to communicate....

A medicine that could block certain nicotinic receptors could be used to help people stop smoking cigarettes, and the same method might work for alcoholism because nicotinic receptors may be involved in alcohol addiction, McIntosh says.

Other nicotinic receptors trigger the release of neurotransmitters involved in memory, so activating the right receptors might lessen Alzheimer's memory loss.

"One reason people smoke is they feel their thinking may be a little better, with increased attention and focus," McIntosh says, noting that pharmaceutical companies "would like to mimic that positive benefit without all the downsides of cigarette smoke".

Other nicotinic receptors influence "the release of serotonin and norepinephrine, two neurotransmitters strongly implicated in mood disorders" such as depression, so a drug to activate those receptors might treat depression, he adds.

Schizophrenics tend to smoke heavily because something in cigarette smoke "seems to help them filter out irrelevant stimuli. They can focus better," McIntosh says. So a drug aimed at certain nicotinic receptors might treat schizophrenia.

New Neurotoxin is a Key for Designing New Medicines

McIntosh says the new toxin itself is unlikely to become a drug because it blocks rather than stimulates nicotinic receptors. But because it can act on some types of nicotinic receptors and not others like a key that opens some locks but not others it has great potential as a tool for precisely identifying the shape and structure of the receptor "locks," thus making it easier to design new medicines or "keys" to fit those receptors and trigger them to release desired neurotransmitters....


Posted by: Kelly Source: http://www.unews.utah.edu/

New Drug For Smokers

First there was Wellbutrin, an antidepressant which helped cut down on the cravings and nicotine withdrawal symptoms for many addicted smokers when it was marketed as the smoking cessation aid Zyban. In May, the Food and Drug Administration (FDA) okayed a second medication for the treatment of nicotine addiction. Chantix, the trade name for varenicline tartrate, works on the dopamine system to reduce withdrawal and craving symptoms, like Zyban. In randomized, placebo-controlled clinical studies involving more than 3,500 smokers, Chantix outperformed both placebos and Zyban. Common side effects included nausea, headache and vomiting. Two studies published in the Journal of the American Medical Association (JAMA) showed that about 22 per cent of smokers on Chantix were abstinent at the one-year mark, compared to 15 per cent for Zyban, and 9 per cent for placebos.

Zyban and Chantix are frequently used by doctors in combination with nicotine replacement therapy, such as gum or patches. Zyban was the first major success story in the burgeoning field of pharmacological treatments for addiction--fighting fire with fire.

According to the Centers of Disease Control and Prevention (CDC), more than 44 million American adults continue to smoke cigarettes, a fifth of whom suffer from smoking-related illnesses.

See more on anti-craving drugs at http://dirkhanson.org

Sources:

--”FDA Approves Novel Medication for Smoking Cessation.” U.S. Food and Drug Administration. www.fda.gov/bbs/topics/NEWS/2006/NEW1370.html. May 11, 2006.

Kotulak, Ronald. “New Drug Shows Promise in Helping Smokers Quit.” Chicago Tribune July 5 2006.

Smokers Drink More

It’s no secret that smoking and drinking go together like salt and pepper. No comes further evidence that smoking helps drinkers hold more liquor. Put simply, “Cigarette smoking appears to promote the consumption of alcohol,” says Wei-Jeun Chen of the Texas A&M Health Science Center.

Nicotine seems to slow the movement of alcohol through the intestines, leaving more alcohol molecules backed up and metabolised before reaching the bloodstream by means of intestinal absorption. In animal studies, in which rats were given stomache injections of alcohol and nicotine, clinicians found that “smoking” rats exhibited lower blood-alcohol levels than rats given the same amount of alcohol without the addiction of nicotine.

Dr. David Ball of the Institute of Psychiatry in London, told BBC news: This is a really interesting study. I’m surprised nobody has done it before.”

Chen, an associate professor of neuroscience and experimental therapeutics at Texas A&M College of Medicine, stressed that the results of such “cross tolerance” between alcohol and nicotine could be to “encourage drinkers to drink more to achieve the pleasurable or expected effect.”*

Susan Maier, a spokesperson for the National Institutes of Health (NIH), which sponsored the research, pointed to the potential for harm among young binge drinkers who choose to smoke, and who could “develop chronic alcohol-related diseases earlier in life because of it.”

Conceivably, other drugs might interact with alcohol in a similar fashion. Scientists are beginning to take a look at popular gastric upset products like Pepcid and Tagamet. “Individuals who abuse alcohol are likely to use other drugs,” Chen said. “The potential interactive effects of alcohol and other drugs needs to be considered. For example, the co-use of alcohol and cocaine will result in the formation of cocaethylene, which is highly toxic and has led to a higher mortality rate in animal studies.”

*Coffee and cigarettes go very naturally together as well. This is probably true for as many different reasons as there are coffee drinkers and cigarette smokers, but as we previously noted in the case of alcohol and tobacco, there is a metabolic synergism at work. The two drugs really do seem to have been made for each other. Rats on caffeine will self-administer nicotine faster and more steadily than decaffeinated control rats. This is because nicotine causes caffeine to clear the body at twice the normal rate, thereby allowing coffee or tea drinkers to imbibe larger amounts than usual, whether consciously aware of it or not. In turn, caffeine has an equivalent reinforcing effect on nicotine. The more you smoke, the more coffee you can drink, and vice versa. At the chemical level, smokers may be drinking caffeine in order to more finely balance the mood-altering effects of nicotine. A moment’s reflection brings us to the coffee house, an ancient establishment wherein tobacco and coffee are combined to maximum effect. Coffee and cigarettes, to be sure, are the least psychoactive of the psychoactive drugs—more proof that the sheer intensity of the drug high is not the primary determinant of addiction.

--excerpted from The Chemical Carousel: What Science Tells Us About Beating Addiction © Dirk Hanson 2008, 2009.

Sources:

--Scott E Parnell, James R West, Wei-Jung A Chen. “Nicotine Decreases Blood Alcohol Concentrations in Adult Rats: A Phenomenon Potentially Related to Gastric Function” Alcoholism: Clinical and Experimental Research 30 (8), 2006 1408–1413.

--”Smoking ‘reduces alcohol effect.’” BBC News, July 24, 2006. http://news.bbc.co.uk/go/pr/fr/-/2/hi/5209990.stm.