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A Developmental Twin Study of Church Attendance and Alcohol and Nicotine Consumption: A Model for Analyzing the Changing Impact of Genes and Environment  

Conclusions: As individuals mature, they increasingly shape their own social environment in large part as a result of their genetically influenced temperament. When individuals are younger and living at home, frequent church attendance reflects a range of familial and social-environmental influences that reduce levels of substance use. In adulthood, by contrast, high levels of church attendance largely index genetically influenced temperamental factors that are protective against substance use. Using genetically informative designs such as twin studies, it is possible to show that the causes of the relationship between social risk factors and substance use can change dramatically over development.

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Genes may explain why churchgoers are teetotalers 

Churchgoers have been found to have lower rates of drinking and smoking than those who spend their Sundays elsewhere. Now a new study suggests that for adults, it may not be church attendance itself that explains much of the phenomenon. It might be genes.

The study, which included nearly 1,800 adult male twins, found that in adolescence, the relationship between church attendance and lower rates of drinking and smoking appeared largely a matter of "shared" environment -- those factors influencing both members of a twin pair.

That is, teenagers who attended church regularly were more likely to want to follow their parents' wishes and conform to community expectations.

By adulthood, however, those environmental influences had faded, the researchers found. Instead, genes seemed to account for the relationship between church-going and lesser alcohol and nicotine use. . . .

SOURCE: American Journal of Psychiatry, October 2009.

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SRI International's Research on Nicotine Use and Dependence Featured in the National Cancer Institute's Tobacco Control Monograph Series 

SRI International, an independent nonprofit research and development institute, today announced that new research on nicotine dependence is featured in National Cancer Institute's Tobacco Control Monograph 20, Phenotypes and Endophenotypes: Foundations for Genetic Studies of Nicotine Use and Dependence. Gary E. Swan, Ph.D., director of SRI's Center for Health Sciences, was the senior scientific editor of the monograph.

"It was an honor to work with a broad range of experts to develop a greater understanding of behavioral genetics and how these findings can improve public health approaches to tobacco control," said Dr. Swan. "By understanding the role of genetics in the context of nicotine dependence, more effective treatment and prevention programs can be developed."

New studies by researchers from SRI's Center for Health Sciences are described in the monograph, including an analysis of subgroups among adolescent tobacco users. This research shows that the subgroup that started smoking at a younger age and maintained a high level of tobacco use is at high risk for adult nicotine dependence. The monograph also presents the first example of a metabolism ontology--a formal system to represent causal relationships between the administration of nicotine and its subsequent metabolism through the action of various genes. The monograph further summarizes work from the first-ever twin study of nicotine metabolism, work that was published previously and conducted by scientists working at SRI and elsewhere in the United States and Canada.

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Exposure to Tobacco Smoke Before Birth Affects DNA  

Women who smoke while pregnant increase their unborn child's long-term risk for health problems, including childhood asthma, cardiovascular disease and lower pulmonary function, and a new study may help experts understand why.

Researchers at the Keck School of Medicine of the University of Southern California (USC) found that maternal smoking actually changes the unborn child's DNA patterns.

The new study found that fetal exposure to maternal smoking was linked to differences in DNA methylation, an epigenetic mechanism.

Epigenetics is the study of how chemicals that attach to DNA can switch genes on and off, which leads to differences in gene expression without changing basic genetic information, according to background information in a USC news release about the study.

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Weight History, Smoking, Physical Activity and Breast Cancer Risk among French-Canadian Women Non-Carriers of More Frequent BRCA1/2 Mutations 

Our study showed that more than 9 pack-years of smoking had a significant positive association with breast cancer risk among both pre- and postmenopausal women; however, this result does not support our previous report of a reduced risk of breast cancer in carriers of BRCA gene mutations who had smoked more than 4 pack-years [28]. The weaker breast cancer risk in these subjects may have been associated with lower levels of circulating estrogens [29]. In contrast, a recent case-control study among Polish women indicated an increased risk of invasive breast cancer with the consumption of ≥10 cigarettes/d among both premenopausal (OR = 2.55; 95% CI: ) and postmenopausal (OR = 1.78; 95% CI: ) women [30]. Likewise, another recent study [31] suggested that BRCA mutation carriers who smoked had 2.3-fold (95% CI: ) and 2.6-fold (95% CI: ), respectively, greater risk of breast cancer. Cigarette smoke contains compounds that damage DNA, and the repair of such damage may be impaired in women with germline mutations. Some genotoxic carcinogens in tobacco smoke are mammary carcinogens in rodents [32]. The enzymatic machinery required for their metabolic activation is present in human mammary epithelial cells [33], and there is evidence of carcinogen-DNA adducts in human mammary tissue [34, 35], some of which may be smoking-related.

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Study finds changes in DNA patterns are linked to prenatal smoke exposure 

A new study by researchers at the Keck School of Medicine of the University of Southern California (USC) has found that the life-long effects of maternal smoking during pregnancy may occur through specific changes in DNA patterns.

The study found that children exposed in the womb to maternal smoking had differences in DNA methylation, an epigenetic mechanism in which small chemical compounds are added to DNA. The findings provide researchers with valuable insight into a biological process that is not well understood.

The study appears in the September issue of the American Journal of Respiratory and Critical Care Medicine and is now available online. . . .

"This study provides some of the first evidence that in utero environmental exposures such as tobacco smoke may be associated with epigenetic changes," says one of the lead authors Carrie Breton, Sc.D., assistant professor in the Department of Occupational and Environmental Health at the Keck School of Medicine of USC. "This could open up a new way for researchers to investigate biological mechanisms that might explain known health effects associated with maternal smoking."

Prenatal exposure to smoke is associated with a number of health problems, including childhood asthma, cardiovascular disease and lower pulmonary function later in life.

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Deciphering the Impact of Common Genetic Variation on Lung Cancer Risk: A Genome-Wide Association Study  

To explore the impact of common variation on the risk of developing lung cancer, we conducted a two-phase genome-wide association (GWA) study. . . .

These data indicate few common variants account for 1% of the excess familial risk underscoring the necessity of having additional large sample series for gene discovery.

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More evidence that genes increase a smokers' risk of lung cancer 

CANCER RESEARCH UK funded scientists have confirmed that inherited changes in certain regions of the genome can increase a smokers' risk of developing lung cancer lung cancer, and determine the type of lung cancer that develops. Their results were published in this week's edition of the journal Cancer Research*.

The researchers at The Institute of Cancer Research scanned the genomes of 1,900 lung cancer patients and compared them to 1,400 healthy individuals to identify specific changes in the DNA that were linked with an increased risk of lung cancer.

They then scanned the genes of a further 2,000 lung cancer patients for these changes and compared these to a similar number of healthy people.

This identified changes in three regions of the genome which were more common in lung cancer patients than healthy individuals. These regions sat on chromosomes 5, 6, and 15, implicating these regions in lung cancer.

Their work shows more complexity than originally thought for the chromosome 15 association.

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The Genotoxicity of Mainstream and Sidestream Marijuana and Tobacco Smoke Condensates  

While the prevalence of tobacco use has decreased in Canada over the past decade, that of marijuana use has increased, particularly among youth. However, the risks of adverse health effects from marijuana smoke exposure, specifically as compared to tobacco, are currently not well understood. The objectives of this study were to evaluate the relative ability of matched marijuana and tobacco condensates to induce (geno)toxic responses in three in vitro test systems. This study provides comparative data for matched sidestream and mainstream condensates, as well as condensates prepared under both a standard and an extreme smoking regime designed to mimic marijuana smoking habits. The results indicate that tobacco and marijuana smoke differ substantially in terms of their cytotoxicity, Salmonella mutagenicity, and ability to induce chromosomal damage (i.e., micronucleus formation). Specifically, the marijuana condensates were all found to be more cytotoxic and more mutagenic in the presence of S9 than the matched tobacco condensates. In contrast, the tobacco condensates appeared to induce cytogenetic damage in a concentration-dependent manner, whereas the matched marijuana condensates did not. In addition, when corrected for total particulate matter yield, little difference was observed in the mutagenic activity of samples smoked under the extreme vs the standard regime for both tobacco and marijuana condensates.

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ACS News Service Weekly PressPac: August 5, 2009: Growing evidence of marijuana smoke's potential dangers 

In a finding that challenges the increasingly popular belief that smoking marijuana is less harmful to health than smoking tobacco, researchers in Canada are reporting that smoking marijuana, like smoking tobacco, has toxic effects on cells. Their study is scheduled for the Aug. 17 issue of ACS' Chemical Research in Toxicology, a monthly journal.

Smoking marijuana causes more damage to cells and DNA than smoking tobacco, scientists say. Credit: Wikimedia Commons (High resolution version)

Rebecca Maertens and colleagues note that people often view marijuana as a “natural” product and less harmful than tobacco. As public attitudes toward marijuana change and legal restrictions ease in some countries, use of marijuana is increasing. Scientists know that marijuana smoke has adverse effects on the lungs. However, there is little knowledge about marijuana's potential to cause lung cancer due to the difficulty in identifying and studying people who have smoked only marijuana.

The new study begins to address that question by comparing marijuana smoke vs. tobacco smoke in terms of toxicity to cells and to DNA. Scientists exposed cultured animal cells and bacteria to condensed smoke samples from both marijuana and tobacco. There were distinct differences in the degree and type of toxicity elicited by marijuana and cigarette smoke. Marijuana smoke caused significantly more damage to cells and DNA than tobacco smoke, the researchers note. However, tobacco smoke caused chromosome damage while marijuana did not.

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Smoke exposure interacts with ADAM33 polymorphisms in the development of lung function and hyperresponsiveness  

Introduction: ADAM33 is the first identified asthma gene by positional cloning, especially asthma combined with bronchial hyperresponsiveness (BHR). Moreover, ADAM33 is associated with early-life lung function and decline of forced expiratory volume in 1 s (FEV1) in the general population. In utero and postnatal cigarette smoke exposure (CSE) are associated with reduced lung function, and development of BHR and asthma. We hypothesized that this may occur via interaction with ADAM33.

Aim: To replicate the role of ADAM33 in childhood lung function and development of BHR and asthma. Furthermore, we investigated gene–environment interaction of ADAM33 with in utero and postnatal CSE in the Dutch PIAMA cohort. . . .

Conclusions: We confirm associations between ADAM33 and the development of asthma (+BHR). This is the first study suggesting that interaction of in utero CSE with ADAM33 results in reduced lung function and the development of BHR, which needs further confirmation.

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ADAM33 genotype ‘interacts with in utero smoke exposure’ 

Variations in the so-called asthma gene, ADAM33, interact with exposure to cigarette smoke in utero to influence lung function in childhood, a study has found.

The research, if confirmed, underlines the importance of maternal cigarette smoking as an environmental risk factor for reduced lung function, acting in concert with genetic factors such as ADAM33.

The finding is reported in the journal Allergy by Dutch researchers, who analyzed data from a birth cohort study, the Prevention and Incidence of Mite Allergy. The study, which began in 1996, included 4146 children, 1327 of whom were considered at high risk based on a positive maternal history of atopy.

Dirkje Postma (University of Groningen) and fellow authors first sought to verify the previously reported association between ADAM33 genotype and asthma risk.

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The Genotoxicity of Mainstream and Sidestream Marijuana and Tobacco Smoke Condensates 

While the prevalence of tobacco use has decreased in Canada over the past decade, that of marijuana use has increased, particularly among youth. However, the risks of adverse health effects from marijuana smoke exposure, specifically as compared to tobacco, are currently not well understood. The objectives of this study were to evaluate the relative ability of matched marijuana and tobacco condensates to induce (geno)toxic responses in three in vitro test systems. This study provides comparative data for matched sidestream and mainstream condensates, as well as condensates prepared under both a standard and an extreme smoking regime designed to mimic marijuana smoking habits. The results indicate that tobacco and marijuana smoke differ substantially in terms of their cytotoxicity, Salmonella mutagenicity, and ability to induce chromosomal damage (i.e., micronucleus formation). Specifically, the marijuana condensates were all found to be more cytotoxic and more mutagenic in the presence of S9 than the matched tobacco condensates. In contrast, the tobacco condensates appeared to induce cytogenetic damage in a concentration-dependent manner, whereas the matched marijuana condensates did not. In addition, when corrected for total particulate matter yield, little difference was observed in the mutagenic activity of samples smoked under the extreme vs the standard regime for both tobacco and marijuana condensates.

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Growing Evidence Of Marijuana Smoke's Potential Dangers 

In a finding that challenges the increasingly popular belief that smoking marijuana is less harmful to health than smoking tobacco, researchers in Canada are reporting that smoking marijuana, like smoking tobacco, has toxic effects on cells. Their study is scheduled for the Aug. 17 issue of ACS' Chemical Research in Toxicology, a monthly journal. . . .

Scientists know that marijuana smoke has adverse effects on the lungs. However, there is little knowledge about marijuana's potential to cause lung cancer due to the difficulty in identifying and studying people who have smoked only marijuana.

The new study begins to address that question by comparing marijuana smoke vs. tobacco smoke in terms of toxicity to cells and to DNA. Scientists exposed cultured animal cells and bacteria to condensed smoke samples from both marijuana and tobacco. There were distinct differences in the degree and type of toxicity elicited by marijuana and cigarette smoke. Marijuana smoke caused significantly more damage to cells and DNA than tobacco smoke, the researchers note. However, tobacco smoke caused chromosome damage while marijuana did not.

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Possible Benefit From Online Genetic Testing For Lung Cancer 

As scientists continue to decode the human genome and the information becomes publicly available, private companies that offer online genetic testing are multiplying. Scientists at the National Institutes of Health were concerned that perhaps these tests posed a risk.

They evaluated responses to an online test among smokers who did or did not have a common genetic variant associated with risk for lung cancer. The results, published in a recent issue of Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research, raise a new set of questions, but also allay some of the early concerns.

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