Tag Archives: genetics and smoking

Nicotine Dependency Linked to Bitter Tastes

University research suggests individuals with greater sensitivity to bitter tastes are less likely to develop a dependence on nicotine than those with a lower sensitivity to such tastes.

“If a person is a [sensitive] taster, then that person is less likely to become a smoker,” said lead investigator Ming Li, professor of psychiatry and neurobehavioral sciences. “In other words, [being a] taster is kind of protective and [being a] non-taster is kind of like a risk factor.”

Li explained that the research project consisted of two components, the first of which was published in the Journal of Medical Genetics and the second of which was published in the American Journal of Human Genetics. The first component of the research focused on genetic analysis of DNA samples taken from more than 2,200 human subjects over a period of nearly 10 years, Li said. The individuals taking part in the study were classified as tasters, non-tasters or intermediate, Li said. If a person was classified as a non-taster, he or she was more likely to become a smoker.

The second component of the research introduced a mathematically based methodology that provided a novel method of detecting gene-gene interaction for other human genetic researchers, Li said, and was used to analyze genetic data on two taste receptor genes, known as TAS2R16 and TAS2R38. The researchers found that these two genes interact with each other in the development of smoking dependence. This component of the research extended the finding of the first report, and together the research offers a “complete story,” Li said.

Jamie Mangold, a former research assistant in Li’s lab who was primarily involved in the first component of the study, commented that the development of the research between the two publications focused on the role of the taste receptor genes.

There was evidence in earlier research, Mangold said, indicating that people who are more sensitive to bitter substances are less likely to be smokers and drinkers. Mangold said she looked through the literature and thought that taste could be a major factor.

“With publication of the first paper, we kind of decided that the TAS2R16 gene was not a primary player … but after the second paper we realized that the TAS2R16 gene may also be important through its interaction with TAS2R38,” Mangold said.

Li explained that older methodologies could only handle either binary traits, such as whether a person did or did not have a disease, or continuous traits, such as height. Moreover, Li said, these methods could not account for all the variables that may affect an individual’s characteristics, such as age, gender and ethnicity.

“With our method, you can correct [the algorithm] for all [factors] that you think may affect this disease,” Li said.

Xiang-Yang Lou, assistant professor of psychiatry and neurobehavioral sciences and first author of the second paper, said his portion of the study showed a relatively small, but still noticeable, relation between the two interacting genes and nicotine dependency. Lou explained that this is likely because smoking is a complex, multivariable behavior; however, he emphasized that the findings in his report were noteworthy because they had a low level of statistical error for the relatively small quantities with which they dealt.

“This new method is better than [the previously] existing method and able to detect even a relatively small difference,” Lou said. “Genetic researchers are very interested in finding these kinds of interactions these days.”

While the two components of the project were largely independent efforts within the research group, Lou noted, the second paper referred to data that had been examined in the first.

In contrast to the size and longevity of the sample for the first project, Lou said he used data from more than 600 families in a simulation of the algorithm to validate the new method and data from about 400 families in the final nicotine dependence study.

Ultimately, Mangold explained, the new findings may prove valuable for future medical use.

Bitter Taste from Cigarettes “This in particular would be a useful way to screen out for those who would be more susceptible,” Mangold said. “So early on before smoking behavior begins, if one is screened for this genotype, we may actually be able to predict who may become dependent and then actually target more preventive programs toward them.”

Source:  Prateek Vasireddy,  Cavalier Daily

Critical Genetic Link Found Between Human Taste Differences and Nicotine Dependence

University of Virginia Health System researchers found that two interacting genes related to bitter taste sensitivity play an important role in a person’s development of nicotine dependence and smoking behavior.

People with higher taste sensitivity aren’t as likely to become dependent on nicotine as people with decreased taste sensitivity, the researchers discovered.

Newswise — Could an aversion to bitter substances or an overall heightened sense of taste help protect some people from becoming addicted to nicotine? That’s what researchers at UVA have found using an innovative new method they’ve developed to analyze the interactions of multiple genetic and environmental factors. Their findings one day may be key in identifying people at risk for nicotine dependence.

In a study published in the October 10, 2008 issue of The American Journal of Human Genetics, University of Virginia Health System researchers report that two interacting genes related to bitter taste sensitivity, TAS2R16 and TAS2R38, play an important role in a person’s development of nicotine dependence and smoking behavior.

Researchers found that people with higher taste sensitivity aren’t as likely to become dependent on nicotine as people with decreased taste sensitivity.

“This new knowledge is an important tool in predicting whether a person is likely to become a smoker or not,” says lead investigator Ming Li, Ph.D., professor of psychiatry and behavioral neurosciences who specializes in addiction and genetics research.

It’s long been known that a person’s ability to taste bitter substances plays a crucial role in the rejection of potentially toxic foods, but taste sensitivity varies widely among individuals and between ethnic groups.

Previous studies have suggested a link between so-called taster status and nicotine dependence, but genetic evidence underlying such a link has been lacking.

“Until now, the method for analyzing gene to gene or gene to environment interactions could only handle one type of trait without correcting for other important covariants, such as age or gender, but we’ve developed a novel algorithm and corresponding computer program that can handle all types of genetic data and correct for any number of variants – gender, age, race, and so on,” explains Dr. Li, who with his team studied genetic data of more than 2,000 participants from more than 600 families of African American or European American origin.

“This new approach significantly expands our ability to study gene-gene or gene-environmental interactions. It provides a far better analytical tool for every scientist out there doing genetics work,” says Dr. Li.

Taste Buds on the Tongue“We’re laying an important foundation for addressing nicotine dependence. First we need to establish a comprehensive understanding of how all associated genes work together to affect smoking behaviors and addiction; that’s what we’re doing now. Once we have that base of knowledge, we can move on to develop effective prevention and treatment for nicotine dependence.”

Source:  University of Virginia Health System

Genetic Achilles Heel May Support Nicotine Addiction

Do genes play a role in tobacco addiction?

Recent studies suggest they may, particularly the CHRNA5 gene.

A University of Michigan press release notes a genetic variation suggests a finding that may help explain the path that leads from that first cigarette to lifelong smoking.

In the press release studies smokers and non-smokers to find if you have the less common rs16969968 form of the CHRNA5 gene and you smoke a cigarette you are more likely to get hooked.

Yet another reduction in the possible scope for free will.

Study on Genetics, Genes and Smoking

In a paper published in the September Issue of the journal Addiction, a multi-university collaborative team of researchers specializing in statistical genetics, gene analysis, and trait analysis reports an association between a variant in the CHRNA5 nicotine receptor gene, initial smoking experiences, and current smoking patterns.

The genetic and smoking data come from 435 volunteers. Those who never smoked had tried at least one cigarette but no more than 100 cigarettes in their lives, and never formed a smoking habit. The regular smokers had smoked at least five cigarettes a day for at least the past five years.

The regular smokers in the study were far more likely than the never-smokers to have the less common rs16969968 form of the CHRNA5 gene, in which just one base-pair in the gene sequence was different from the more common form. This kind of genetic variation is called a single nucleotide polymorphism or SNP.

Smokers were also eight times as likely to report that their first cigarettes gave them a pleasurable buzz.

“It appears that for people who have a certain genetic makeup, the initial physical reaction to smoking can play a significant role in determining what happens next,” says senior author and project leader, Ovide Pomerleau, a professor of psychiatry at the University of Michigan Medical School and founder of the U-M Nicotine Research Laboratory.

“If cigarette smoking is sustained, nicotine addiction can occur in a few days to a few months,” he adds. “The finding of a genetic association with pleasurable early smoking experiences may help explain how people get addicted — and, of course, once addicted, many will keep smoking for the rest of their lives.”Among those who ever try smoking this gene explains only part of the difference between those who become addicted and those who do not. Expect more discoveries of genes that contribute to the odds of getting addicted.

Achilles HeelWe are witnessing an acceleration of the rate of discovery of genetic factors that influence behavior. This acceleration in the rate of discovery will accelerate as DNA testing costs continue to drop. So expect to see many more reports of genes that influence behavior.

Source: Randall Parker, FuturePundit

Could Genetics Play a Role in Degrees of Addiction?

As a practicing hypochondriac it was of particular interest to me to learn about a research company in, of all places, Iceland, which is making what could be historic advances in medicine through the study of human genetics.

This company, deCODE genetics, is exploiting a most unusual data base: that of the total population of Iceland where excellent records have been kept since Norwegian and Celtic (Scottish and Irish) settlers arrived there about ten centuries ago. Today there are only slightly more than 300 000 Icelanders, of whom 94 percent are descended from the original settlers. For gene searchers this is, apparently, like a gift from heaven.

It is akin to having a vast private laboratory, enabling research on thousands of volunteers uniquely related in a manner which renders the search for genetic clues to future health problems. For example, more than 50,000 Icelanders, that is one-sixth of the population, participated in research into the disposition to smoking and, for smokers, the inherent risks of contracting diseases linked to nicotine.

Now deCODE is coming up with suggestions that, through the study of human genetic makeup, or our DNA, it can be predicted with accuracy that one will be predisposed to a particular kind of illness or even, as in the case of cigarette smoking, particular types of addiction.

The company’s scientists have established “a clear link between a single-letter variant of the human genome (SNP) and susceptibility to nicotine dependence.”

Such addiction can lead, for example, to lung cancer and peripheral arterial disease (PAD), a common and debilitating constriction of the arteries to the legs.

The odds of this happening to a given individual can be calculated using these genetic techniques.

The research, which also studied smokers in New Zealand, Austria, Sweden, Italy, the Netherlands and Spain, revealed that there is correspondence not only between genetic makeup and the likelihood of addiction but also to the approximate number of cigarettes an addict is likely to smoke daily.

DeCODE has also isolated key genes “contributing to major public health challenges from cardiovascular disease to cancer, genes that are providing us with drug targets rooted in the basic biology of disease”.

smoking cigarettesGiven the incidence in South Africa of dermatological problems such as the deadly cutaneous melanoma (CM) and basal cell carcinoma (BCC) it is interesting to learn that it is not only very fair skin, blue or green eyes, freckles, red hair and exposure to ultraviolet light (obviously prevalent in South Africa) that can expose one to CM and BCC.

Scientists at deCODE have discovered that “a novel, tightly-linked pair of single-letter variants” near a certain gene on chromosome 20 and another on chromosome 11 specifically increases our susceptibility to sunburn and hence to its dangers.

All this should be of enormous future use to the medical profession, although one suspects that our health minister, Manto Tshabalala-Msimang, would probably prefer some quackery or other for guidance rather than the research of serious Icelandic scientists.

Interestingly, the company offers a personal, on-line service for those wishing to explore their genome tree or whatever geneticists call these things. Just log on to www.decodeme.com – although I haven’t done this, so I cannot advise you what to expect.

By the way, this little cutting edge company is listed on the Nasdaq in New York and the stock quote is DCGN. This writer holds no shares.

Source: Stephen Mulholland, Dispatch Online

Quitting Smoking is a Pack Behavior

Smokers tend to quit in groups, according to a new study.

One person who quits can have ripple effects across his or her entire social network, prompting others to kick the habit.

The New York Times offers this delightfully evocative explanation of how the process works:

As the investigators watched the smokers and their social networks, they saw what they said was a striking effect — smokers had formed little social clusters and, as the years went by, entire clusters of smokers were stopping en masse. So were clusters of clusters that were only loosely connected.

Dogs in a FieldStudy co-author Dr. Nicholas Christakis described watching the vanishing clusters as like lying on your back in a field, looking up at stars that were burning out. “It’s not like one little star turning off at a time,” he said. “Whole constellations are blinking off at once.”

Continue Reading About the Stop Smoking Ripple Effect

Researchers Identify Genetic Variant Linked To Nicotine Addiction

NIDA Researchers Identify Genetic Variant Linked To Nicotine Addiction And Lung Cancer – Variant Also Increases Risk For Cardiovascular Disease

Scientists have identified a genetic variant that not only makes smokers more susceptible to nicotine addiction but also increases their risk of developing two smoking-related diseases, lung cancer and peripheral arterial disease.

The research was supported by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health (NIH).

The study, published in the April 3 issue of the journal Nature, “highlights the advances that are being made in genetics research, which can now identify gene variants that increase the risk of complex bio-behavioral disorders,” says NIH Director Dr. Elias Zerhouni. “This finding will help us in our efforts to further reduce the scope and devastating consequences of cigarette smoking.”

“These results suggest for the first time that a single genetic variant not only can predispose to nicotine addiction but may also increase sensitivity to extremely serious smoking-related diseases,” explains NIDA Director Dr. Nora Volkow. “Additionally, it points to potential targets for new smoking-cessation medications that may be more effective at helping smokers to quit.”

The variant is closely linked to two of the known subunits of nicotine receptors, the sites on the surface of many cells in the brain and body that can be bound by nicotine. When nicotine attaches to these receptors in the brain, there are changes in cell activity that results in its addictive effects.Carriers of this genetic variant are more likely than noncarriers to be heavy smokers, dependent on nicotine, and less likely to quit smoking. “The variant does not increase the likelihood that a person will start smoking, but for people who do smoke it increases the likelihood of addiction,” says Dr. Kári Stefánsson, the study’s principal investigator and chief executive officer of deCODE Genetics, a biopharmaceutical company based in Reykjavik, Iceland.

The variant was identified through a technique known as genome-wide association, in which DNA samples (from more than 10,000 Icelandic smokers) were analyzed for the presence of more than 300,000 genetic markers. Subsequent investigation showed that carriers of the variant strongly associated with nicotine dependence were also at increased risk for two smoking-related diseases, peripheral arterial disease and lung cancer. The findings were replicated in populations from five European countries and New Zealand. The researchers estimate that the variant explains 18 percent of cases of lung cancer and 10 percent of cases of peripheral arterial disease in smokers.

Nicotine addictionThe same variant was identified as one that increased risk for lung cancer in two other articles appearing in the April 3rd, 2008, issues of Nature and Nature Genetics, partially funded by two other NIH institutes–the National Cancer Institute and the National Human Genome Research Institute.

For more information on Smoking/Nicotine: http://www.drugabuse.gov/DrugPages/Nicotine.html

The National Institute on Drug Abuse

The National Institute on Drug Abuse is a component of the National Institutes of Health, U.S. Department of Health and Human Services. NIDA supports most of the world’s research on the health aspects of drug abuse and addiction.

The Institute carries out a large variety of programs to inform policy and improve practice. Fact sheets on the health effects of drugs of abuse and information on NIDA research and other activities can be found on the NIDA web site at http://www.drugabuse.gov.

The National Institutes of Health

(NIH) – The Nation’s Medical Research Agency – includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services.

It is the primary Federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

Smoking’s Effects on Genes May Play a Role in Lung Cancer Development and Survival

Smoking plays a role in lung cancer development, and now scientists have shown that smoking also affects the way genes are expressed, leading to alterations in cell division and regulation of immune response.

Notably, some of the changes in gene expression persisted in people who had quit smoking many years earlier.

These findings by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health, appeared in the Feb. 20, 2008, issue of PLoS ONE.

“Smoking, we are well aware, is the leading cause of lung cancer worldwide,” said NCI Director John E. Niederhuber, M.D. “Yet, a mechanistic understanding of the effects of smoking on the cells of the lung remains incomplete. This study demonstrates an important piece of this complicated puzzle. Greater understanding of the genetic alterations that occur with smoking should provide greater insight into the development of cellular targets for treating, and possibly preventing, lung cancer.”

“We were able to look at actual lung tissue, tumor and non-tumor, taking into account the differences by gender, verifying the smoking status by measuring levels of cotinine, a metabolite of nicotine, in participants’ plasma, and confirming results in independent samples,” said Maria Teresa Landi, M.D., Ph.D., in NCI’s Division of Cancer Epidemiology and Genetics, the first author of the study report.

To investigate the effects of smoking on gene activity in lung tissue, the researchers examined the gene expression profiles — patterns of gene activity — in early-stage lung tumors and non-tumor lung tissue of smokers, former smokers, and people who had never smoked cigarettes. Gene expression was measured in 58 fresh-frozen tumor and 49 fresh-frozen non-tumor samples from 74 participants of the Environment And Genetics in Lung cancer Etiology (EAGLE) study, a large lung cancer study that was conducted in the Lombardy region of Italy.

Adenocarcinoma tumor samples were evaluated in this study because adenocarcinoma is the most common type of lung cancer, and it occurs in both smokers and people with no history of smoking. The participants were 44 to 79 years of age, and 28 were current smokers, 26 were former smokers, and 20 had never smoked. The researchers also obtained detailed medical information about the participants (for example, whether individuals had previous lung diseases or chemotherapy) and biochemically confirmed participants’ smoking status.

Using microarray techniques, which allow researchers to look at the activity of thousands of genes simultaneously, they identified 135 genes that were differently expressed in tumors of smokers vs. people who had never smoked. Among these genes, 81 showed decreased expression and 54 showed increased expression in tumor tissue.

Most of the genes showing significantly increased expression, e.g., TTK, NEK2, and PRC1, are involved in cell cycle regulation and mitosis. The cell cycle is a step-wise sequence of events in which a cell grows and ultimately divides to produce two progeny, or daughter, cells. During the cell cycle, the chromosomes of the parent cell are duplicated and then, in a step called mitosis, divided equally between the daughter cells, ensuring that each daughter cell inherits a complete set of chromosomes. The cell apparatus responsible for the proper division of chromosomes is called the mitotic spindle.

Picture of Lungs“Our results indicate that smoking causes changes in genes that control mitotic spindle formation,” said Jin Jen, Ph.D., in NCI’s Center for Cancer Research, a senior author of the study report. “Irregular division of chromosomes and chromosome instability are two common abnormalities that occur in cancer cells when the chromosomes do not separate equally between the daughter cells. Therefore, changes in the mitotic process are very relevant in the development of cancer.” Several of the identified genes have been suggested in the past as potential targets for cancer treatment.

The researchers also found similar expression of many genes among current smokers and former smokers in tumor tissue. Several of these genes, such as STOM, SSX2IP, and APLP2, remained altered in participants who had quit smoking more than 20 years before the study. Therefore, smoking seems to cause long-lasting changes in gene expression, which can contribute to lung cancer development long after cessation.

Looking at non-tumor lung tissues, the team found decreased activity for 73 genes and increased activity for 25 genes in current smokers. The genes most affected by smoking play a role in immune response-related processes, possibly as a lung defense mechanism against the acute toxic effects of smoking. However, non-tumor tissues seem to be able to recover from the effects of smoking. The researchers did not identify significant changes in the immune response-related genes in former smokers.

To gain a better understanding of the impact of smoking-related changes in gene expression on lung cancer survival, the researchers compared the overall gene expression smoking profile in lung tumor and non-tumor tissues with survival. They found that the altered expression of the cell cycle-related genes NEK2 and TTK in non-tumor tissues was associated with a three-fold increased risk of lung cancer mortality in smokers.

“Our data provide clues on how cigarette smoking affects the development of lung cancer, indicating that the very same mitotic genes known to be involved in cancer development are altered by smoking and affect survival. More studies are needed to confirm that the gene expression changes are due to smoking and affect tumor development or progression,” said Landi. “If confirmed, these genes could become important targets for preventing and treating lung cancer.”

About 90 percent of lung cancer deaths among men and almost 80 percent of lung cancer deaths among women can be attributed to smoking. In 2006, approximately 20.8 percent of U.S. adults were cigarette smokers. Cigarette smoking remains the leading preventable cause of death in the United States, causing an estimated 438,000 deaths, or about one out of every five deaths each year.

For more information on research in Dr. Landi’s group, please go to http://dceg.cancer.gov/about/staff-bios/landi-maria.

For more information about the EAGLE study, please go to http://dceg.cancer.gov/eagle.

For more information about cancer, please visit the NCI website at http://www.cancer.gov/, or call NCI’s Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

The National Institutes of Health (NIH) — The Nation’s Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.


Reference:
Landi MT, Dracheva T, Rotunno M, Figueroa, JD, Liu H, Dasgupta A, Mann FE, Fukuoka J, Hames M, Bergen AW, Murphy SE, Yang P, Pesatori AC, Consonni D, Bertazzi PA, Wacholder S, Shih JH, Caporaso NE, and Jen J. February 2008. Gene Expression Signature of Cigarette Smoking and Its Role in Lung Adenocarcinoma Development and Survival. PLoS ONE. Vol. 3, No. 2.

Crazy Cravings May Be Genetic

Individual brain chemistry and genes could be the key to understanding why some people become addicted to nicotine, University of Colorado at Boulder researchers say.

The depth of a person’s addiction to nicotine appears to depend on his or her unique internal chemistry and genetic make-up,  said lead author Jerry Stitzel, an assistant professor in CU-Boulder’s department of integrative physiology and researcher with CU-Boulder’s Institute for Behavioral Genetics.

It’s also why the chemical compound’s effects appear to diminish at night, said Stitzel, who presented his team’s findings in San Diego last week during the Neuroscience 2007, an annual scientific meeting.

Stitzel and his team set out to evaluate the effects of nicotine over the course of a day by examining mice that could make and “recognize” melatonin, a powerful hormone, and others that could not.

Scientists believe that melatonin, which is produced by darkness, tells our bodies when to sleep. The CU researchers found that the reduced effects of nicotine at night were dependent on the mice’s genetic make-up, and whether their brains and bodies were able to recognize melatonin.

Crave ImageThey also found that the daytime effects of nicotine were greatest when levels of the stress hormone corticosterone were high.

The second finding could explain why many smokers report that the first cigarette of the day is the most satisfying.

Cortisol, the human equivalent of corticosterone, is at peak levels in the early morning, Stitzel said.

“The negative health consequences of smoking have become well known, and a large majority of smokers say that they would like to quit,” Stitzel said. “As such, we need to understand the interaction between smoking, genes and internal chemistry so we can target new therapies to those who have a hard time quitting.”

While the team’s research could shed light on why people smoke, Stitzel says more research is needed to determine the role that melatonin plays in altering the effects of nicotine, and whether the correlation between higher corticosterone levels and nicotine sensitivity is a coincidence.

Researchers from Yale, Florida State, the University of Minnesota and the Baylor College of Medicine also presented findings based on research into the effects of smoking and nicotine.

Source: Colorado Daily

Corticosterone, Genetics And The Addiction Of Nicotine

Individual brain chemistry and genes could be key to understanding why some people become addicted to nicotine and why the chemical compound’s effects appear to diminish at night, University of Colorado at Boulder researchers say.

“The depth of a person’s addiction to nicotine appears to depend on his or her unique internal chemistry and genetic make-up,” said lead author Jerry Stitzel, an assistant professor in CU-Boulder’s department of integrative physiology and researcher with CU-Boulder’s Institute for Behavioral Genetics.

He and his team set out to evaluate the effects of nicotine over the course of a day by examining mice that could make and “recognize” melatonin, a powerful hormone and antioxidant, and others that could not. Scientists believe that melatonin, which is produced by darkness, tells our bodies when to sleep.

The CU researchers found that the reduced effects of nicotine at night were dependent on the mice’s genetic make-up and whether their brains and bodies were able to recognize melatonin. They also found that the daytime effects of nicotine were greatest when levels of the stress hormone corticosterone were high.

The second finding could explain why many smokers report that the first cigarette of the day is the most satisfying. Cortisol, the human equivalent of corticosterone, is at peak levels in the early morning, Stitzel said.

“The negative health consequences of smoking have become well known, and a large majority of smokers say that they would like to quit,” Stitzel said. “As such, we need to understand the interaction between smoking, genes and internal chemistry so we can target new therapies to those who have a hard time quitting.”

While the team’s research could shed light on why people smoke and how nicotine affects them, Stitzel says more research is needed to determine the role that melatonin plays in altering the effects of nicotine, and whether the correlation between higher corticosterone levels and nicotine sensitivity is a coincidence.

The CU-Boulder study was funded by the National Institute on Drug Abuse, a part of the National Institutes of Health.

CorticosteroneResearchers from Yale, Florida State, the University of Minnesota and the Baylor College of Medicine also presented findings based on research into the effects of smoking and nicotine.

Among their conclusions: Smoking may predispose adolescents to mental disorders in adolescence and adulthood; a network of neurons, or cells in the nervous system, may regulate the body’s craving response; and smoking may affect decision-making.

– University of Colorado at Boulder

*Thanks goes to Cuckoo from AS3 for submission to CF.

Gene Links Alcoholism, Tobacco Addiction, Stress

A team of Quebec researchers has uncovered a series of genes linking the response to stress and high blood pressure with alcoholism and tobacco dependence.

If a person has that series of genes, he or she will be more prone to drink or smoke in order to cope with stress and high blood pressure, according to researchers.

“What that tells us is that it’s not only bad education or family behaviour that matters,” explained Dr. Pavel Hamet, who is leading the study of 120 families in the Saguenay Lac-St.-Jean region.

“The fight against alcohol and tobacco should not only be moralistic, but also give people ways to manage stress,” he said, adding that one in five persons has the predisposition.

He gave his findings at the Canadian Cardiovascular Congress in Quebec City yesterday.

Alcohol and TobaccoHamet believes this discovery could explain why men are more prone to alcohol abuse than women.

His team found that the genes that govern alcohol intake appear on chromosome X. Men only have one chromosome X, while women have two.

“A man can only get his chromosome X from his mother, so he is more at risk than the woman who gets one from her mother and one from her father,” said Hamet, director of research at the University of Montreal Hospital Centre.

Hamet believes this study could be helpful to help high-risk people reduce stress and blood pressure, often leading to heart diseases and higher risks of getting a stroke.

Source: The Vancouver Province