REASONS TO STOP SMOKING

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Stop smoking! Quitting at any age reduces the risk of death after 70 sooner than those who did not smoke or stopped earlier.

Tobacco use continues to be a major cause of cancer and premature death. Most studies of cigarette smoking and mortality have focused on middle-aged populations, with fewer studies examining the impact of tobacco cessation on disease and mortality risk among the elderly. A new study published in the American Journal of Preventive Medicine, found that people aged 70 or older currently smoking were more than three times more likely to die than never-smokers, while former smokers were less likely to die the sooner they quit.

In the U.S., the number of individuals aged 70 years and older is expected to increase from 29.2 million (9.3% of the population) in 2012, to 63.6 million individuals (15.9%) in 2050. “U.S. adults aged 70 and older have a very high lifetime prevalence of cigarette smoking, so it’s important to examine the risks associated with smoking and the benefits of quitting at older ages among these individuals,” explained lead investigator Sarah H. Nash, PhD, who conducted the research as part of her postdoctoral training at the National Cancer Institute, NIH, Bethesda, MD.

Investigators reviewed data for more than 160,000 individuals aged 70 and over who participated in the NIH-AARP Diet and Health Study. They completed a questionnaire in 2004-2005 detailing their smoking use, and reported deaths were tracked until the end of 2011. Analyses conducted between 2014 and 2016 correlated age at death with self-reported age at smoking initiation and cessation and amount smoked after 70 years of age.

The 2004-2005 questionnaire assessed smoking intensity in cigarettes per day and smoking history through nine age periods. For this study, participants still smoking in their 70s were identified as current smokers, and former smokers were classified by the decade of life when quitting. For the follow-up, the National Death Index Plus was used to determine deaths, while ICD-9 and ICD-10 codes for smoking-related mortality were used to further identify outcomes. These included lung cancer; other smoking-related cancers, including bladder, colorectal, esophageal, head and neck, kidney and renal pelvis, liver, pancreatic and stomach cancers, and acute myeloid leukemia; heart disease; stroke; diabetes; and respiratory disease (e.g., pneumonia, influenza, chronic obstructive pulmonary disease, and allied conditions).

Data were adjusted for age, sex, level of education, and alcohol use. Since NIH-AARP participants are predominantly white, adjusting for race did not affect the results and was not included in the final models.

At the beginning of the study (2004-2005), the median age of participants was 75 years. Almost 56% were former smokers and 6% were current smokers. Males were less likely (31% vs 48% of females) to be never-smokers. Males smoked more than females (18.2 pack years vs 11.6 pack years), and males were more likely to have started smoking before 15 years (19% vs 9.5% of female smokers).

During an average follow-up of 6.4 years, almost 16% of the participants died. While 12.1% of the never smokers died, 16.2%, 19.7%, 23.9%, and 27.9% of former smokers who quit between ages 30-39, 40-49, 50-59, and 60-69 years died, respectively. Current smokers fared the worst, with 33.1% dying. Mortality rates for women were lower than men at each level of smoking use.

“These data show that age at smoking initiation and cessation, both key components of smoking duration, are important predictors of mortality in U.S. adults aged 70 years and older,” commented Dr. Nash. “In the NIH-AARP study population, younger age at initiation was associated with increased risk of mortality, highlighting the importance of youth and early-adult smoking on lifetime mortality risk, even among people who live to age 70 years. In addition, former smokers were at substantially reduced risk of mortality after age 70 years relative to current smokers, even those who quit in their 60s. These finding show that smoking cessation should be emphasized to all smokers, regardless of age.”


Journal Reference:

  1. Sarah H. Nash, Linda M. Liao, Tamara B. Harris, Neal D. Freedman. Cigarette Smoking and Mortality in Adults Aged 70 Years and Older: Results From the NIH-AARP Cohort. American Journal of Preventive Medicine, 2016; DOI: 10.1016/j.amepre.2016.09.036

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If Your First Cigarette Gave You A Buzz And You Now Smoke, A Gene May Be To Blame

 

The new study links a person’s initial experience with smoking, and their current smoking status, with variation in a gene that encode a nicotine receptor in the brain.
Credit: Image courtesy of University of Michigan Health System

Anyone who has ever tried smoking probably remembers that first cigarette vividly. For some, it brought a wave of nausea or a nasty coughing fit. For others, those first puffs also came with a rush of pleasure or “buzz.”

Now, a new study links those first experiences with smoking, and the likelihood that a person is currently a smoker, to a particular genetic variation. The finding may help explain the path that leads from that first cigarette to lifelong smoking.

The new finding also adds to growing suspicion surrounding the role of a particular nicotine-receptor gene in smoking-related behaviors and in lung cancer. Other researchers have already linked variations in the same genetic region to smokers’ level of dependence on nicotine, to the number of cigarettes smoked per day and to a far higher risk of lung cancer — the ultimate outcome of a lifetime of smoking.

In a paper published online today in 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.”

The researchers point out that the genetic variant explains only a portion of human smoking behavior, and that a more complete explanation of why people smoke and why they can’t quit will require much more information about how genes interact with social influences and other environmental factors.

Pomerleau predicts that the ability to link behavioral patterns in smoking to individual genotypes will need extensive information concerning behavior, genes, and the environmental context — as well as bioinformatic tools to bring it all together. “Understanding the genetics of complex disorders such as nicotine addiction will require much more research on key traits,” he says.

The team notes that the CHRNA5 relationships appear to be strong and that practical applications from this research include new genetic tests for smoking risk and the development of medications that target smoking-risk genes.

Pomerleau states that the new paper builds on findings reported last year by fellow author Laura Bierut, in which a whole-genome study found that the same single nucleotide polymorphism, rs16969968, of the CHRNA5 gene was associated with smokers’ level of nicotine dependence.

He also notes that, this year, three papers published independently of one another demonstrated that variations in the same gene, and related genes, greatly increase the risk of lung cancer.

Taking into account its links to increased liking of initial smoking, stronger likelihood of getting addicted to nicotine, and greater probability of developing lung cancer, this genetic variant may well constitute a “triple whammy” for smoking-related disease, he says.

A mechanism for explaining increased disease risk, proposed by one of the cancer genetics researchers, is the possibility that certain chemicals, for instance N-nitrosonornicotine in tobacco smoke, act on nicotine receptors in the lung to produce cancer-causing changes – a process known as tumorigenesis.

The new findings linking first smoking experiences, smoking habits, and genetic variation build on previous research by Ovide Pomerleau and Cynthia Pomerleau, Ph.D., at U-M. In studies conducted over a 10-year span, they documented a link between nicotine-dependent smoking and positive first smoking experiences.

Ovide Pomerleau also credits earlier animal research by his colleagues Allan Collins and Jerry Stitzel at the University of Colorado, for providing the impetus for the idea that initial reactivity to nicotine might set the stage for the development of nicotine dependence — and that nicotine receptor genetic variations underlie this process.

Ovide Pomerleau and Laura Bierut serve on advisory boards for nicotine treatment pharmaceuticals for Pfizer, Inc. Laura Bierut and John Rice at Washington University hold a patent on the CHRNA5 SNP that has been licensed by Perlegen Sciences.


Story Source:

Materials provided by University of Michigan Health System. Note: Content may be edited for style and length.

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Smoking a pack a day for a year causes 150 mutations in lung cells

Genetic damage caused by smoking measured in different organs of the body

Date:
November 3, 2016
Source:
Welcome Trust Sanger Institute
Summary:
Scientists have measured the catastrophic genetic damage caused by smoking in different organs of the body and identified several different mechanisms by which tobacco smoking causes mutations in DNA. Researchers found smokers accumulated an average of 150 extra mutations in every lung cell for each year of smoking one packet of cigarettes a day.

 

Cigarettes (stock image).
 
 Scientists have measured the catastrophic genetic damage caused by smoking in different organs of the body and identified several different mechanisms by which tobacco smoking causes mutations in DNA. Researchers at the Wellcome Trust Sanger Institute, the Los Alamos National Laboratory and their collaborators found smokers accumulated an average of 150 extra mutations in every lung cell for each year of smoking one packet of cigarettes a day.

Reported in the Journal Science, the study provides a direct link between the number of cigarettes smoked in a lifetime and the number of mutations in the tumour DNA. The highest mutation rates were seen in the lung cancers but tumours in other parts of the body also contained these smoking-associated mutations, explaining how smoking causes many types of human cancer.

Tobacco smoking claims the lives of at least six million people every year and, if current trends continue, the World Health Organization predicts more than 1 billion tobacco-related deaths in this century. Smoking has been epidemiologically associated with at least 17 types of human cancer, but until now no-one has seen the mechanisms by which smoking causes many of these cancer types.

Cancer is caused by mutations in the DNA of a cell. In the first comprehensive analysis of the DNA of cancers linked to smoking, researchers studied over 5,000 tumors, comparing cancers from smokers with cancers from people who had never smoked. They found particular molecular fingerprints of DNA damage — called mutational signatures — in the smokers’ DNA, and counted how many of these particular mutations were found in the different tumors.

The authors found that, on average, smoking a pack of cigarettes a day led to 150 mutations in each lung cell every year. These mutations represent individual potential start points for a cascade of genetic damage that can eventually lead to cancer. The numbers of mutations within any cancer cell will vary between individuals, but this study shows the additional mutational load caused by tobacco.

Dr Ludmil Alexandrov, first author from Los Alamos National Laboratory, said: “Before now, we had a large body of epidemiological evidence linking smoking with cancer, but now we can actually observe and quantify the molecular changes in the DNA due to cigarette smoking. With this study, we have found that people who smoke a pack a day develop an average of 150 extra mutations in their lungs every year, which explains why smokers have such a higher risk of developing lung cancer.”

Other organs were also affected, with the study showing that a pack a day led to an estimated average 97 mutations in each cell in the larynx, 39 mutations for the pharynx, 23 mutations for mouth, 18 mutations for bladder, and 6 mutations in every cell of the liver each year.

Until now, it has not been fully understood how smoking increases the risk of developing cancer in parts of the body that don’t come into direct contact with smoke. However, the study revealed different mechanisms by which tobacco smoking causes these mutations, depending on the area of the body affected.

Prof David Phillips, an author on the paper and Professor of Environmental Carcinogenesis at King’s College London, said: “The results are a mixture of the expected and unexpected, and reveal a picture of direct and indirect effects. Mutations caused by direct DNA damage from carcinogens in tobacco were seen mainly in organs that come into direct contact with inhaled smoke. In contrast, other cells of the body suffered only indirect damage, as tobacco smoking seems to affect key mechanisms in these cells that in turn mutate DNA.”

The study revealed at least five distinct processes of DNA damage due to cigarette smoking. The most widespread of these is a mutational signature already found in all cancers. In this case, tobacco smoking seems to accelerate the speed of a cellular clock that mutates DNA prematurely.

Professor Sir Mike Stratton, joint lead author from the Wellcome Trust Sanger Institute, said: “The genome of every cancer provides a kind of “archaeological record,” written in the DNA code itself, of the exposures that caused the mutations that lead to the cancer. Our research indicates that the way tobacco smoking causes cancer is more complex than we thought. Indeed, we do not fully understand the underlying causes of many types of cancer and there are other known causes, such as obesity, about which we understand little of the underlying mechanism. This study of smoking tells us that looking in the DNA of cancers can provide provocative new clues to how cancers develop and thus, potentially, how they can be prevented.”


Story Source:

Materials provided by Welcome Trust Sanger Institute. Note: Content may be edited for style and length.


Journal Reference:

  1. Ludmil Alexandrov et al. Mutational signatures associated with tobacco smoking in human cancer. Science, November 2016 DOI: 10.1126/science.aag0299

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No one has to tell anyone that smokes , the dangers the unnatural act of smoking. But I hope this information has helped you decide to seek help in quitting smoking.  HERE”S TO YOUR HEALTH.