Women smokers who quit before 40 gain nine years in lifespan

Women can add nine years to their lives by quitting smoking before the age of 40 but still face a 20-percent higher death rate than those who never smoked, a study said Saturday.

30 oct 2012--Published in The Lancet, a survey of nearly 1.2 million women in Britain showed that smoking throughout adulthood chopped on average 11 years off lifespan.

These results echoed the findings of earlier research conducted on men.

Among women who kicked the habit before the age of 40, the researchers measured an average lifespan gain of more than nine years compared with those who never stopped.

For those who quit before 30 the gains were even bigger—about 10 years.

"Whether they are men or women, smokers who stop before reaching middle age will on average gain about an extra 10 years of life," study co-author Richard Peto of the University of Oxford said.

But the paper warned this did not mean that it was safe to continue smoking until 40 before quitting.

"Women who do so have throughout the next few decades [of their lives] a mortality rate 1.2 times that of never-smokers. This is a substantial excess risk, causing one in six of the deaths among these ex-smokers."

In Europe and the United States, the popularity of smoking reached its peak among women in the 1960s, decades later than for men.

The Lancet study is one of the most extensive probes into the impacts of smoking on this generation of women, the first likely to have smoked substantially throughout their adult lives.

The research is part of a vast survey that enrolled 1.2 million women in the UK between 1996 and 2001. The volunteers were asked to detail their smoking history, and were followed for an average of 12 years.

The women were on average 55 years old when they signed up. Twenty percent of them were smokers, 28 percent ex-smokers, while 52 percent had never smoked.

The researchers found that the group of women who continued smoking had three times the overall mortality rate of never-smokers.

While the risks increased with the amount smoked, "Even those smoking fewer than 10 cigarettes per day... had double the overall mortality rate than never-smokers," warned the study.

It also cautioned against so-called "light" cigarettes, smoked by most of the women in the study.

"Low-tar cigarettes are not low-risk cigarettes and... more than half of those who smoke them will eventually be killed by them," the authors warned.

The key causes of death among smokers were chronic lung disease, lung cancer, stroke and heart disease.

Smoking takes 10 years off life expectancy in Japan, not 4 as previously thought, experts warn

Smoking reduces life expectancy by ten years in Japan, but much of the risk can be avoided by giving up smoking, a paper published on bmj.com today shows.

27 oct 2012--Previous studies in Japan suggested smoking reduced life expectancy by only a few years compared with about ten years in Britain and the USA. This new report, from researchers in Oxford and Japan, investigates the impact of smoking on mortality in a large group of Japanese people who were living in Hiroshima or Nagasaki in 1950. The findings are, however, nothing to do with radiation exposure from the bombs.

The Life Span Study (LSS) was initiated in 1950 to investigate the effects of radiation, tracking over 100,000 people. However, most received minimal radiation exposure, and can therefore provide useful information about other risk factors. Surveys carried out later obtained smoking information for 68,000 men and women, who have now been followed for an average of 23 years to relate smoking habits to survival.

The younger a person was when they started smoking the higher the risk in later life. Older generations did not usually start to smoke until well into adult life, and usually smoked only a few cigarettes per day. In contrast, Japanese born more recently (1920-45) usually started to smoke in early adult life, much as smokers in Britain and the USA.

These differences in smoking habits are reflected in the mortality patterns. Smokers born before 1920 lost just a few years. In contrast, men born later (1920-45) who started to smoke before age 20 lost nearly a decade of life expectancy, and had more than double the death rate of lifelong non-smokers, suggesting that more than half of these smokers will eventually die from their habit. Results on the few women who had smoked since before age 20 were similar.

Previous studies of the effects of smoking in Japan had been mainly of individuals born in the first few decades of the twentieth century who probably didn't start to smoke until well into adult life and smoked only a few cigarettes per day. This explains why the risks of smoking seemed low. Nowadays, however, young Japanese smokers tend to smoke more cigarettes per day and to start at a younger age, so their risks will be higher.

In addition to studying the risk of smoking, the researchers were able to examine the benefits of stopping. As elsewhere, those who stopped smoking before age 35 avoided almost all the excess risk among continuing smokers, and even those who stopped around age 40 avoided most of it.

The researchers conclude that the future health risks to young smokers are likely to be just as big in Japan as in other countries although much of the risk can be avoided by stopping.

Provided by British Medical Journal

Smoking may lead to cataracts in aging population

Cigarette smoking is a well-known risk factor for a wide-range of diseases. Now, scientists have evidence that smoking may also increase the risk of age-related cataract, the leading cause of blindness and vision loss in the world.

13 oct 2012--Reported in Investigative Ophthalmology & Visual Science (Smoking and Risk of Age-related Cataract: A Meta-analysis), the new findings are the result of a meta-analysis conducted by a team of researchers from China.

"Although cataracts can be removed surgically to restore sight, many people remain blind from cataracts due to inadequate surgical services and high surgery expenses," said author Juan Ye, MD, PhD, of the Institute of Ophthalmology, Zhejiang University in China. "Identifying modifiable risk factors for cataracts may help establish preventive measures and reduce the financial as well as clinical burden caused by the disease."

The team performed the analysis using 12 cohorts and eight case-control studies from Africa, Asia, Australia, Europe and North America, to compare the prevalence of age-related cataract in individuals who ever smoked cigarettes to those who have never smoked. Further subgroup analyses were performed based on the subjects' status as a past or current smoker and the three subtypes of age-related cataract.

The results showed that every individual that ever smoked cigarettes was associated with an increased risk of age-related cataract, with a higher risk of incidence in current smokers. In the subgroup analysis, former and current smokers showed a positive association with two of the subtypes: nuclear cataract, when the clouding is in the central nucleus of the eye, and subscapular cataract, when the clouding is in the rear of the lens capsule. The analysis found no association between smoking and cortical cataract, in which the cloudiness affects the cortex of the lens.

While the overall analysis suggests that smoking cigarettes may increase the risk of age-related cataracts, the researchers point out that further effort should be made to clarify the underlying mechanisms.

"We think our analysis may inspire more high-quality epidemiological studies" said Ye. "Our analysis shows that association between smoking and the risk of age-related cataract differ by subtypes, suggesting that pathophysiologic processes may differ in the different cataract types."

Provided by Association for Research in Vision and Ophthalmology

Genetic alteration may represent early stage of smoking-induced cardiovascular damage

A new study uncovers a previously unrecognized link between tobacco smoking and a gene known to influence the cardiovascular system, possibly identifying an early stage of smoking-associated cardiovascular pathology. The research, published by Cell Press in the April issue of The American Journal of Human Genetics, may serve to guide future research strategies aimed at identifying and counteracting mechanisms of smoking-induced pathology.

01 april 2011--Tobacco smoking is powerfully addictive and damages the pulmonary and cardiovascular systems, leading to malignancy and premature death. "Although the promotion of smoking cessation clearly remains imperative, a better understanding of the pathophysiological processes linking tobacco smoking and its sequelae could yield opportunities to positively influence disease risk in the large population of continuing smokers," explains lead study author Dr. Lutz P. Breitling, from the German Cancer Research Center in Heidelberg, Germany.

One possible mechanism that has the potential for mediating the harmful effects of tobacco smoking is DNA methylation. DNA methylation, the attachment of methyl groups to specific sites within a section of DNA, is recognized as an important mechanism for regulating gene function and may play a significant role in diseases with a complex phenotype. Although previous studies have linked nicotine and smoking with altered methylation of several genes, comparison of methylation status between heavy smokers who do not have cancer and individuals who have never smoked has not been fully examined.

Dr. Breitling and colleagues used a recently developed genetic screening technique to conduct a genome-wide search for differential methylation correlated with tobacco smoking in 177 current, former, and never smokers. The researchers discovered a single section of DNA that exhibited lower methylation in smokers. The site was located within a gene called coagulation factor II receptor-like 3 (F2RL3). F2RL3 has been linked with the process of blood clotting and with other cardiovascular functions. Interestingly, the protein coded by this gene has never been mentioned in the smoking literature.

"Our results show that the gene coding for a potential drug target of cardiovascular importance features altered methylation patterns in smokers," concludes Dr. Breitling. "Intriguing perspectives lie in the possibility that this gene could be causally involved at a very initial stage of smoking-related cardiovascular pathology. A better understanding of its role might open up avenues for preventing the development of associated disease in subjects unable to quit smoking."

Provided by Cell Press

'A stark warning:' Smoking causes genetic damage within minutes after inhaling

In research described as "a stark warning" to those tempted to start smoking, scientists are reporting that cigarette smoke begins to cause genetic damage within minutes -- not years -- after inhalation into the lungs.

17 jan 2011--Their report, the first human study to detail the way certain substances in tobacco cause DNA damage linked to cancer, appears in Chemical Research in Toxicology, one of 38 peer-reviewed scientific journals published by the American Chemical Society.

Stephen S. Hecht, Ph.D., and colleagues point out in the report that lung cancer claims a global toll of 3,000 lives each day, largely as a result of cigarette smoking. Smoking also is linked to at least 18 other types of cancer. Evidence indicates that harmful substances in tobacco smoke termed polycyclic aromatic hydrocarbons, or PAHs, are one of the culprits in causing lung cancer. Until now, however, scientists had not detailed the specific way in which the PAHs in cigarette smoke cause DNA damage in humans.

The scientists added a labeled PAH, phenanthrene, to cigarettes and tracked its fate in 12 volunteers who smoked the cigarettes. They found that phenanthrene quickly forms a toxic substance in the blood known to trash DNA, causing mutations that can cause cancer. The smokers developed maximum levels of the substance in a time frame that surprised even the researchers: Just 15-30 minutes after the volunteers finished smoking. Researchers said the effect is so fast that it's equivalent to injecting the substance directly into the bloodstream.

"This study is unique," writes Hecht, an internationally recognized expert on cancer-causing substances found in cigarette smoke and smokeless tobacco. "It is the first to investigate human metabolism of a PAH specifically delivered by inhalation in cigarette smoke, without interference by other sources of exposure such as air pollution or the diet. The results reported here should serve as a stark warning to those who are considering starting to smoke cigarettes," the article notes.

Provided by American Chemical Society

Heavy Smoking Linked to Alzheimer's in Study

26 oct 2010-- Heavy smoking in middle age seems to increase the risk for developing Alzheimer's disease or another dementia, a large new study suggests.

"We found that people who reported heavy smoking in midlife had more than a 100 percent increase in risk of Alzheimer's disease and vascular dementia," said lead researcher Rachel A. Whitmer, a research scientist in Kaiser Permanente's Division of Research in Oakland, Calif.

"We have known that smoking is a risk factor for cancer, stroke and cardiovascular disease," she said. "This adds to the evidence that what is bad for the heart is bad for the brain."

The report is published in the Oct. 25 online edition of the Archives of Internal Medicine.

For the study, Whitmer's group collected data on 21,123 ethnically diverse people in the Kaiser Permanente health care system who were surveyed between 1978 and 1985, when they were 50 to 60 years old.

During an average follow-up of 23 years, the researchers found that 25.4 percent were diagnosed with dementia, including Alzheimer's (1,136 people) or vascular dementia (416 people), which is the second most common form of dementia after Alzheimer's disease. Vascular dementia is caused by damage to the arteries in the brain.

Compared with non-smokers, those who smoked more than two packs of cigarettes a day in midlife had a "dramatic increase" in the incidence of dementia -- more than a 157 percent increased risk of developing Alzheimer's disease and a 172 percent increased risk of developing vascular dementia, Whitmer's team found.

Former smokers and people who smoked less than half a pack a day did not appear to be at increased risk of Alzheimer's or vascular dementia, the researchers note.

The associations between smoking and dementia did not change even after adjusting for race or gender, high blood pressure, high cholesterol or heart attack, stroke or weight, they add.

A link between Alzheimer's and smoking has been shown before, but this new study pinpoints the specific risk for middle-age smokers for developing both Alzheimer's and vascular dementia, the researchers say.

Smoking, an established risk factor for stroke, may contribute to the likelihood of vascular dementia by causing small clots in the brain. Smoking also contributes to oxidative stress and inflammation, which may be linked to the risk of developing Alzheimer's disease, the researchers say.

"The brain is not immune to long-term damage from smoking," Whitmer said.

Two smaller studies of predominantly white participants also suggested that mid-life smoking raised the risk of developing Alzheimer's, researchers noted.

Commenting on the new study, William Thies, chief medical and scientific officer at the Alzheimer's Association, said "this is a sound confirmation of something that's been known for a while."

Another expert, Dr. Samuel E. Gandy, the Mount Sinai Professor of Alzheimer's Disease Research at Mount Sinai School of Medicine in New York City, said the findings are promising.

"Environmental factors in Alzheimer's disease have been long sought, and, until now, only head injury has emerged," Gandy said. "Unlike head injury, a tobacco smoking association is especially important because that is a risk that can be modified."

Men who never smoke live longer, better lives than heavy smokers

Other studies in Archives of Internal Medicine focus on smoking cessation strategies

14 oct 2008--Health-related quality of life appears to deteriorate as the number of cigarettes smoked per day increases, even in individuals who subsequently quit smoking, according to a report in the October 13 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Smoking has been shown to shorten men's lives between seven and 10 years, according to background information in the article. It also has been linked to factors that may reduce quality of life, including poor nutrition and lower socioeconomic status.
Arto Y. Strandberg, M.D., of the University of Helsinki, and colleagues followed 1,658 white men born between 1919 and 1934 who were healthy at their first assessment, conducted in 1974. Participants were mailed follow-up questionnaires in 2000 that assessed their current smoking status, health and quality of life. Deaths were tracked through Finnish national registers.
During the 26-year follow-up period, 372 (22.4 percent) of the men died. Those who had never smoked lived an average of 10 years longer than heavy smokers (more than 20 cigarettes per day). Non-smokers also had the best scores on all health-related quality of life measures, especially those associated with physical functioning. Physical health deteriorated at an increasing rate as the number of cigarettes smoked per day increased, with heavy smokers experiencing a decline equivalent to 10 years of aging.
"Although many smokers had quit smoking between the baseline investigation in 1974 and the follow-up examination in 2000, the effect of baseline smoking status on mortality and the quality of life in old age remained strong," the authors write. "In all, the results presented here are troubling for those who were smoking more than 20 cigarettes daily 26 years earlier; in spite of the 68.9 percent cessation rate during follow-up, 44.1 percent of the originally heavy smokers had died, and those who survived to the mean [average] age of 73 years had a significantly lower physical health-related quality of life than never-smokers."
The findings may add to the view of smoking as a burden on society and might also encourage individual smokers to quit, the authors note. "The argument of better quality of life may be especially meaningful for the aging smoker but, as our results show, for the best health-related quality of life, the habit should not be started at all," they write. "The highly addictive nature of nicotine is revealed by the persistence of the smoking habit in spite of the declining health-related quality of life among older heavy smokers. For those not able to quit smoking, reduction may also be beneficial because mortality [death] and health-related quality of life showed a dose-dependent trend according to the number of cigarettes smoked daily."
Additional papers related to smoking in the October 13 issue found that:
Offering smoking cessation counseling to hospitalized smokers appears to be effective as long as supportive contacts are offered for more than one month after discharge. Nancy A. Rigotti, M.D., of Massachusetts General Hospital and Harvard Medical School, Boston, and colleagues reviewed 33 trials of smoking cessation interventions that began during hospitalizations. Programs that offered telephone or in-person support lasting longer than one month improved smoking cessation rates six to 12 months after discharge. "Adding nicotine replacement therapy to counseling may further increase smoking cessation rates and should be offered when clinically indicated, especially to hospitalized smokers with nicotine withdrawal symptoms," the authors write.
Hospital-based smoking cessation programs, along with referrals to cardiac rehabilitation, also appear to be associated with increased rates of quitting smoking following heart attack. Nazeera Dawood, M.D., M.P.H., at Emory University School of Medicine, Atlanta, and colleagues studied 639 patients who smoked at the time of their hospitalization for myocardial infarction (heart attack). Six months later, 297 (46 percent) had quit smoking. The odds of quitting were greater among patients who received discharge recommendations for cardiac rehabilitation and those who were treated at a facility offering an inpatient smoking cessation program; however, individual counseling was not associated with quit rates.
A pay-for-performance program may increase referrals to tobacco quitline services, particularly among clinics who have not previously participated in quality improvement activities. Lawrence C. An, M.D., of the University of Minnesota, Minneapolis, and colleagues randomly assigned 24 primary care clinics to participate in a program offering $5,000 for 50 quitline referrals. Between Sept. 1, 2005, and June 31, 2006, these clinics referred 11.4 percent of eligible smokers, compared with 4.2 percent among 25 clinics offering usual care. "Quitlines are widely available, and application of pay-for-performance strategies to encourage health care provider referral should be strongly considered by health care organizations seeking to reduce the health and economic burden of tobacco-related disease," the authors write.
"Smoking remains the largest avoidable cause of death and disability in the United States, but it is a problem against which we are making steady albeit far too slow progress," writes David M. Burns, M.D., Del Mar, Calif., in an accompanying editorial. "Smoking cessation is one of the most important changes needed to achieve the goal so often articulated by Dr. Ernst Wynder, one of the founders of the field of preventive medicine: die young as late in life as possible."
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(Arch Intern Med. 2008; 168[18]:1968-1974, 1950-1960, 1961-1967, 1993-1999, 1946-1947. Available pre-embargo to the media at www.jamamedia.org.)

Pleasure from Smoking -- and Addiction to It -- Is a Genetic Thing

By Charles Bankhead
ANN ARBOR, Mich., 09 aug 2008-- The nicotine "buzz" that leads to addiction in some people arises from a genetic mutation that enhances pleasurable responses, investigators here reported. The mutation in a subunit of the neuronal acetylcholine receptor (CHRNA5) increased the odds of nicotine dependence by 50%, and Caucasians with the mutation were 60% more likely to feel a pleasurable rush or "buzz" when they smoked their first cigarette, Ovide Pomerleau, Ph.D., of the University of Michigan, and colleagues reported in the August issue of Addiction. "The findings suggest that phenotypes related to subjective experiences upon smoking experimentation may mediate the development of nicotine dependence," the authors said.
Many studies have underscored the genetic influence on smoking habits, including initiation, persistence, and addiction, and recently, several common variants have been shown to be associated with nicotine dependence in Caucasians, the authors said.
The variants, or single nucleotide polymorphisms (SNPs), had several effects with functional significance, including effects on nicotine metabolism, they continued. Additional research showed that an SNP in exon 4 of CHRNA5 altered the nicotine receptor.
Subsequently, a highly correlated CHRNA5/CHRNA3 haplotype was found to have a strong influence on smoking behavior, specifically the number of cigarettes smoked per day, the authors said.
In an attempt to expand on the previous work, Dr. Pomerleau and colleagues focused on phenotype associations for the top 25 SNPs associated with nicotine dependence. They began with the SNP previously shown to alter the nicotine receptor (rs16969968) and then examined the other 24.
Their case-control study involved 203 smokers and 232 controls between ages 25 and 65 and included 72 African Americans among the 435 total participants. The smokers had at least a five-year history of smoking five or more cigarettes a day, including six months at their current level. Cases had smoked as many as 100 cigarettes in their lifetime but never regularly.
The study participants retrospectively rated pleasurable and unpleasurable sensations they felt when they smoked a cigarette for the very first time.
Of the 25 SNPs evaluated, only the rs16969968 variant demonstrated a significant association with smoking behavior (OR 1.48, 95% CI 1.08 to 2.03).
Caucasians accounted entirely for the significant effect (OR 1.51 versus OR 0.68 for African Americans).
The variant significantly predicted smoking behavior in the combined analysis and the analysis by race (P=0.01).
Minor alleles at rs16969968 were significantly associated with a pleasurable rush or buzz during early smoking in Caucasians (OR 1.61, P=0.01).
The sensations correlated strongly with current smoking (OR 8.2, P<0.0001), a correlation that persisted in a combined analysis of both races (OR 6.2, P<0.0001).
"No other initial smoking experience was associated significantly with the rs16969968 genotype," the authors said.
"The gene-association analysis in the present study indicates that minor alleles at rs16969968 may have contributed to smoking by enhancing the reinforcing effects of nicotine in nicotine-naive individuals who went on to become regular smokers," they added.
The findings, combined with those of previous studies, "implicate initial sensitivity as a key variable in smoking development," they concluded.
They pointed out that the study of relationships in the African-American sample was inconclusive because of the small number of participants available.
They also indicated that the data suggested that African Americans may be more reactive to initial cigarettes than Caucasians but it is unlikely that this particular polymorphism is involved in the differences observed.
The study was supported by the National Institutes of Health.
Dr. Pomerleau and two co-authors have served as consultants to Pfizer. Two co-authors invented a patented process used to evaluate SNPs in diagnosis and treatment of addiction.
Primary source: AddictionSource reference:Sherva R, et al "Association of a single nucleotide polymorphism inneuronal acetylcholine receptor subunit alpha 5 (CHRNA5) with smoking status and with 'pleasurable buzz' during early experimentation with smoking" Addiction 2008; 103: 1544-1552.

WHO urges countries to adopt smoking bans

1 july 2008--Smoking bans are an effective way of preventing heart disease, getting cigarette users to quit and protecting children from second-hand smoke, a World Health Organization (WHO) report issued on Monday said.
The report by scientists at the WHO's International Agency for Cancer Research urged more countries to adopt smoking bans in public and at the workplace, saying there was enough evidence to prove they work, without hurting businesses such as restaurants and bars.
"Implementation of such policies can have a broader population effect of increasing smoke-free environments," the researchers wrote in the Lancet Oncology special report.
"Not only do these policies achieve their aim of protecting the health of non-smokers by decreasing exposure to second-hand smoke, they also have many effects on smoking behavior, which compound the health benefits."
Many local and national governments, mainly in Western nations, have enacted varying types of smoking bans in recent years to protect people from second-hand smoke.
A separate report issued by Cancer Research UK on Monday found England's ban adopted a year ago has spurred more smokers than ever to kick the habit, and predicted the restrictions would prevent 40,000 deaths over the next 10 years.
The researchers involved in the WHO report -- who included John Pierce of the University of California, San Diego, and Maria Leon at the International Agency for Cancer Research --- reviewed more than 900 studies and government reports looking at the impact of smoking bans across the world.
They cited studies that suggest smoke-free workplaces have lead to a 10 to 20 percent decrease in hospital admissions for heart disease a year after a smoking ban.
The WHO says smoking kills about four million people each year, causing a quarter of deaths related to heart disease.
(Reporting by Michael Kahn; Editing by Caroline Drees)

Smoking Linked to Increased Risk for Type 2 Diabetes

December 11, 2007 — Smoking is associated with an increased risk for type 2 diabetes, according to the results of a meta-analysis reported in the December 12 issue of the Journal of the American Medical Association.
"Observational studies have suggested an association between active smoking and the incidence of type 2 diabetes," write Carole Willi, MD, from the University of Lausanne in Switzerland, and colleagues. "Active smoking could be independently associated with glucose intolerance, impaired fasting glucose, and type 2 diabetes; smoking may therefore be a modifiable risk factor for type 2 diabetes. . . . We therefore conducted a systematic review and meta-analysis of prospective cohort studies describing the association between active smoking and the incidence of diabetes or other glucose metabolism irregularities."
The investigators searched MEDLINE from 1966 to May 2007 and EMBASE from 1980 to May 2007, as well as bibliographies of key retrieved articles and abstracts from scientific meetings, and they also contacted experts. Studies were included in the meta-analysis if they had a cohort design; a reported risk for impaired fasting glucose, impaired glucose tolerance, or type 2 diabetes in relationship to baseline smoking status; and excluded persons with diabetes at baseline.
Two of the study authors independently extracted data from these studies, which included baseline status regarding active smoking, diabetes risk, methods used for diagnosis of diabetes, and criteria for methodologic study quality. A random-effects model was used to pool relative risks (RRs), and associations were tested in subgroups representing different patient characteristics and methodologic quality criteria.
Among 25 prospective cohort studies identified and meeting inclusion criteria, a total of 1.2 million participants were enrolled. During a study follow-up period ranging from 5 to 30 years, 45,844 incident cases of diabetes were reported.
The pooled adjusted RR was 1.44 (95% confidence interval [CI], 1.31 - 1.58), and 24 of the 25 studies reported adjusted RRs greater than 1 (range, 0.82 - 3.74). The findings were consistent and statistically significant for all subgroups. Heavy smokers (≥ 20 cigarettes/day) had a greater risk for diabetes (RR, 1.61; 95% CI, 1.43 - 1.80) vs lighter smokers (RR, 1.29; 95% CI, 1.13 - 1.48). Former smokers also had a lower risk for diabetes (RR, 1.23; 95% CI, 1.14 - 1.33) vs active smokers, suggesting a dose-response effect.
"Active smoking is associated with an increased risk of type 2 diabetes," the study authors write. "Future research should attempt to establish whether this association is causal and to clarify its mechanisms."
Limitations of the study include inability of observational studies to prove causality, limited controlling for possible confounding factors, less than optimal quality of individual studies, conversion of ORs to RRs could have underestimated the variance of the RRs derived from ORs, and possible publication bias.
"Considering the consistent finding of increased diabetes incidence associated with active cigarette smoking across a large number of studies, we believe that there is no need for further cohort studies to test this hypothesis," the study authors conclude. "However, there is a need for studies that include detailed measurement and adjustment for potential confounding factors such as socioeconomic status, education, and exercise with a goal of establishing whether the association with smoking is causal. We recommend that future studies focus on plausible causal mechanisms or mediating factors such as obesity, lack of physical activity, dietary habits, and stress levels."
The Alberta Heritage Foundation for Medical Research and Canada Health Services Research helped support one of the study authors. Another study author has also obtained funding. The remaining study authors have disclosed no relevant financial relationships.
In an accompanying editorial, Eric L. Ding, ScD, and Frank B. Hu, MD, PhD, from Brigham and Women's Hospital and Harvard Medical School in Boston, Massachusetts, note that the adverse effect of smoking on type 2 diabetes has been generally under-recognized. They point out that these study findings are likely a conservative underestimate of the true association between smoking and type 2 diabetes.
"While obesity prevalence continues to increase, the decline in smoking rates in the United States has stalled in the past several years," Drs. Ding and Hu write. "Therefore, further focus on public health and clinical interventions is needed to prevent tobacco use and promote smoking cessation. As jointly recognized and highlighted by the American Diabetes Association, the American Heart Association, and the American Cancer Society, prevention of diabetes, cardiovascular disease, and cancer share many common agendas — a central focus of which is the avoidance of cigarette smoking."
Dr. Ding is supported by a fellowship award from the American Diabetes Association. Dr. Hu has disclosed no relevant financial relationships.
JAMA. 2007;298:2654-2664, 2675-2676.

More Hollywood Studios Say ‘No Smoking’

By MICHAEL CIEPLY
LOS ANGELES, Sept. 30 — In the movie musical “Dreamgirls” last year, James “Thunder” Early, Eddie Murphy’s soul-singing, chain-smoking character, was so infuriated by a fumbled food order that he mashed his cigarette into a chicken sandwich that was supposed to have no mayonnaise.
That portrayal and scene could still fly these days at DreamWorks, which made the movie. But if Universal Pictures were to produce the movie today, Mr. Murphy might consider having his character switch to chewing gum.
The biggest studios are usually like-minded when it comes to what is fit to portray on screen. But they have become divided lately in confronting one of the entertainment industry’s touchiest issues: smoking in movies that reach the young.
Under pressure from an antismoking lobby unsatisfied by a promise that the industry’s trade group made in May to consider tobacco use as a factor in film ratings, the six largest studio owners have been patching together individual responses to those who want cigarettes out of films rated G, PG or PG-13.
Smoking opponents view the result as surprising progress toward a virtual ban on tobacco images in all but films with R or NC-17 ratings.
Yet Hollywood is also waking to the realization that a committed band of advocates is rapidly changing what is permissible in the movies. And that precedent could embolden other groups campaigning to rid movies of portrayals of gun use, transfat consumption or other behavior that can be proved harmful to the public.
“It’s a chilling idea,” said Bill Condon, who wrote and directed “Dreamgirls” for the DreamWorks and Paramount Pictures units of Viacom.
General Electric, the corporate parent of Universal Pictures, decided last April that, with few exceptions, “no smoking incidents should appear in any youth-rated film” produced by the studio or its sister units, Focus, Rogue and Working Title Films.
“Movies are supposed to reflect reality,” Mr. Condon said. “You’re taking away a detail that is one of the more defining aspects of a lifestyle.”
The extent to which depictions of smoking actually spur the young to smoke remains a subject of debate. Widely cited research by Dr. James A. Sargent of the Dartmouth Medical School showed a connection between adolescent exposure to smoking in movies and addiction to tobacco. But Dr. Deborah Glik, director of the Health and Media Research Group at the University of California, Los Angeles, said the connection appeared strongest among those who were already predisposed by other factors to smoke.
In any case, corporate Hollywood is in a hurry to find the right side of the issue. The companies are being prodded by a network of antismoking campaigners, some of them flush from Big Tobacco’s settlement with various state attorneys general, and already successful in much of the country in banning smoking in bars, restaurants and other public places.
The Rev. Michael Crosby, who coordinates antismoking efforts for the Interfaith Center on Corporate Responsibility, compared the state of play to a horse-race game in a carnival, with each company leaping past the other in recent months. “G.E. is now ahead,” said Mr. Crosby, who has been pressing the studios on the issue via shareholder resolutions and executive meetings for the last decade.
Before G.E. moved with what is widely regarded as the toughest antismoking policy to date, Time Warner had said it “strongly discourages” smoking in youth films produced by its Warner Brothers and New Line units, and seeks to limit smoking depictions in films marketed to what it called mixed audiences.
In July, the Walt Disney Company said it would ban smoking in its Disney-branded movies, like the “Pirates of the Caribbean” series, while trying to discourage tobacco use in youth-rated movies from its Miramax and Touchstone units. A spokesman for the Sony Corporation’s Sony Pictures Entertainment said the studio — which showed tobacco use in all three of its PG-13 rated “Spider-Man” films — has a policy under which it tries to discourage the depiction of tobacco products in youth-oriented films.
Viacom is meanwhile scrambling to devise a smoking policy of its own, having been assured two weeks ago by Mr. Crosby and his allies that it was increasingly out of step with its studio brethren. That warning came about because antismoking groups had recently discovered that the News Corporation and its 20th Century Fox Film division were already on the bandwagon, thanks to a strict though intentionally unpublicized policy of rooting tobacco out of youth-friendly films for the last three years.
Since 2004, the studio’s production manual has mandated that no principal character can be seen to smoke in a film set in contemporary times and to be rated G, PG or PG-13 unless the studio’s president of production signs off on the scene. Tobacco ads and promotions are not supposed to be visible in Fox movies. Even antismoking messages on screen are not to have been provided by tobacco companies.
The reduction of on-screen smoking is a pet project of the studio’s co-chairman, Tom Rothman, according to both Mr. Crosby and industry executives who requested anonymity because they did not want to offend a competitor or were not authorized to discuss the policy.
Yet Mr. Rothman has been reluctant to make a public issue of the studio’s policy, for fear that it might open the door to demands from groups with other causes, or put the studio at a competitive disadvantage with filmmakers who see blanket restrictions on smoking as threatening the credibility of their work.
Indeed, James L. Brooks, one of the most powerful filmmakers in Hollywood, was not stopped by that policy last year. His Gracie Films delivered the animated PG-13 rated “Simpsons Movie,” featuring enough tobacco (even in the trailer) to earn a “black lung” rating from the scenesmoking.org Web site, which monitors smoking impressions in movies.
Mr. Brooks and Fox executives did not respond to queries about why the smoking portrayals were allowed despite the policy.
Even the most aggressive studios have built wiggle room into their policies. To date, no company has said that it would bar smoking in the many films that are produced independently and later acquired for distribution by a studio. Thus, the hard-bitten, soft-hearted table server played by Cheryl Hines in the PG-13 rated “Waitress,” picked up by Mr. Rothman’s Fox Searchlight at the last Sundance Film Festival, can still wield a cigarette near the pregnant character played by Keri Russell.
Neither has any studio figured out how to deal with directors who may rely on their contractual right of “final cut” to include such scenes. Sony’s guidelines allow for exceptions if the scenes are needed for historical authenticity or to deliver an antismoking message. And even at G.E. and Universal, the policy says the presumption against a smoking scene can be “rebutted” based on its importance to the film, the difficulty of removing it, and whether or not the picture will be marketed to adolescents.
Advocates are naturally suspicious that such loopholes will only delay what they see as progress. “In about five years, they’ll live up to promises they’re making now,” said Michael Passoff, associate director of As You Sow, a socially responsible investment group based in San Francisco that has pressed studio owners on the smoking issue.
Eventually, the approach of the industry’s trade group, the Motion Picture Association of America — which relies on the ratings system to reduce tobacco impressions reaching the young — may diminish the need for individual solutions.
“This is still a new policy, and it’s going to take time to develop,” said Seth Oster, the association’s executive vice president and chief communications officer. Mr. Oster said 22 films have had warnings about smoking attached to their ratings since the system went into effect. And at least one film, “Saving Sarah Cain,” released by the News Corporation’s FoxFaith unit, has had its rating bumped to PG from G because it depicted tobacco use.
Some opponents of smoking on film see a chaos of individual policies as the prelude to an inevitable broad agreement to banish tobacco from all but adult-rated films.
“I think success is going to come very suddenly,” said Stanton A. Glantz, director of the Center for Tobacco Research and Education at the University of California, San Francisco, and whose proposal would led to an R rating for virtually all tobacco use in movies. “It will take the monkey off the individual companies’ backs.”
Edward J. Markey, Democrat of Massachusetts who is chairman of the House subcommittee on telecommunications and the Internet, said he would prefer to see an industrywide antismoking initiative, perhaps like the agreement in 2000 to limit the marketing of violent films, though he did not expect that to happen without further hearings.
Should an industrywide policy happen, of course, some young viewers might turn to entertainment they find less pinched, and more authentic. Not incidentally, the pilot episode of “quarterlife,” a new series about recent college graduates planned for direct distribution on the Web, concludes with a soulful discussion between two friends on a cigarette break.
Or, as Mr. Condon pointed out, the push for tobacco prohibition in film for the young might simply add new cachet to what is forbidden. “If they succeed, they may well glamorize smoking again,” he said.

Genes Promoting Lung Cancer May Not Normalize When Smoking Stops

VANCOUVER, British Columbia, Aug. 29 -- For some genes involved in the development of lung cancer, smoking may be forever, according to researchers here.
Smoking irreversibly activates some lung genes and down-regulates others, offering a possible explanation for the elevated lung cancer risk of former smokers, reported Raj Chari, Ph.D., of the British Columbia Cancer Agency, and colleagues, online in BMC Genomics.
They studied lung biopsy specimens from current, former, and nonsmokers and found that smoking induces specific changes in gene activity, some of which are permanent.
DNA repair genes are irreversibly damaged by smoking, which also turns off genes that protect against lung cancer. Down-regulated genes that regain normal function with smoking cessation are involved in xenobiotic functions, nucleotide metabolism, and mucus secretion.
"Expression levels of some of the genes related to tobacco smoking return to levels similar to never-smokers upon cessation of smoking, while expression of others appears to be permanently altered despite prolonged smoking cessation," the authors concluded. "These irreversible changes may account for the persistent lung cancer risk despite smoking cessation."
Recent gene microarray studies revealed differences in gene expression among current, former, and nonsmokers. The studies linked smoking's genetic effects to specific functions and showed that some smoking-induced changes are not reversed by smoking cessation.
Despite the recent findings, relatively little is known about genes involved in smoking-induced airway remodeling.
Dr. Chari and colleagues used serial analysis of gene expression (SAGE) to examine gene expression profiles in lung tissue. SAGE determines expression profiles by analyzing the types and concentration of short sequence tags. The investigators compared bronchial epithelial transcriptomes of current, former, and never smokers.
The study involved eight current smokers, 12 former smokers, and four never-smokers. Analysis of bronchial specimens from the participants resulted in 3,111,471 SAGE tags, representing 110,000 potentially unique transcripts. The investigators also identified 1,733 constitutively expressed genes in the transcriptomes of current, former, and never-smokers.
Further analysis revealed 609 SAGE transcript tags that were differentially expressed between current and never smokers. Chari and colleagues subsequently found that the tags classified current, former, and never smokers.
Additional comparisons of current, former, and never-smokers separated the tags and their associated genes into categories of reversible, partly reversible, and irreversible. Examples included:
Completely reversible with smoking cessation-increased expression of TFF3, CABYR, and ENDPD8, which are involved in xenobiotic metabolism and airway mucosal response.
Partly reversible-increased expression of MUC5AC, also involved in airway mucosal response.
Irreversible-decreased expression of GSK3B, which regulates expression of cyclooxygenase-2.
These finding were validated using quantitative reverse transcriptase-polymerase chain reaction on a secondary cohort of nine current smokers, seven former smokers, and six never-smokers.
The identification of reversible changes in gene expression in response to smoking cessation may help guide future studies of polymorphisms, the authors stated. Genes and functions that do not revert to normal upon smoking cessation may provide insight into former smokers' ongoing risk of developing lung cancer.
The authors had no disclosures.Additional source: BMC GenomicsSource reference: Chari R et al. "Effect of active smoking on the human bronchial epithelium transcriptome." BMC Genomics 2007; 297: doi:10.1186/1471-2164-8-297

Smoking Hikes Risk of Age-Related Macular Degeneration

SIDNEY, Australia, Aug. 14 -- Age-related macular degeneration is four times more likely to affect current smokers than those who never smoked, found researchers here.
Current smokers had a nearly four-fold higher risk of the serious late, but not early, macular degeneration compared with those who had never smoked, the researchers said.
The risk also held for past smokers who were three times likelier to have geographic atrophy, Jie Jin Wang, M.Med., Ph.D., of the University of Sydney here, and colleagues, reported in the July issue of the Archives of Ophthalmology.
Late age-related macular degeneration, the more severe form of the eye disorder with the poorest prognosis, is thought to share risk factors with cardiovascular disease. Although there was a suggestion of a causal relationship between lipid levels and the eye disease, the interactions were not statistically significant, the researchers reported.
The findings emerged from a prospective study of 2,454 Australians, ages 49 and older at baseline (1992 through 1993), with a mean age of 64.4. Of the participants 57.6% were women.
Participants were examined five years or 10 years later, or both. Retinal photographs were used to assess macular degeneration, while smoking status was recorded at each interview. Body mass index and blood pressure were also measured.
After controlling for age, sex, and other factors, current smokers had a 3.9 times relative risk (95% confidence interval, 1.7-8.8), on average five years earlier than never smokers.
Past smokers had 3.4 relative risk of geographic atrophy (CI, 1.2-9.7), suggesting some benefit from smoking cessation and supporting a likely causal effect between smoking and macular degeneration, the researchers said.
The effect of past smoking was not evident at five years, the researchers said, but appeared after 10 years, with the risk persisting above that of never-smokers for a considerable time after quitting smoking.
Past smokers were divided above and below the median of 17 years for smoking cessation. The risk of late age-related macular degeneration was 1.9 (CI, 0.8-4.4) for those who quit fewer than 17 years earlier, and 1.2 (CI 0.6-2.7) for those with 17 or more years smoke-free.
Combined exposure to current smoking and the lowest level of HDLs, the highest ratio for total cholesterol to HDL cholesterol, or low fish consumption was associated with a higher risk of the eye disease than the effect of any risk factor alone. However, these interactions were not statistically significant, the researchers said.
Data from other studies have not shown a consistent association between lipid levels and age-related macular degeneration. The present findings, the investigators said, should therefore be interpreted with caution, as chance findings cannot be excluded.
A biological model involving atherosclerosis could explain the joint effects of smoking and lipid levels on risk. For example, it has been postulated that lipid accumulation in the sclera and the Bruch's membrane increases choroidal vascular resistance, causing leakage and deposition of proteins and lipids in the membrane.
Animal models support a role for cholesterol and the possibility of joint effects in the pathogenesis of macular degeneration, the researchers said.
Furthermore, they added, high levels of polyunsaturated fatty acids in the retina support the biological plausibility of a protective effect from fatty acids derived from fish intake.
The researchers wrote that this is only the second (after the Beaver Dam Eye Study) prospective population-based study to assess the long-term association between baseline smoking and age-related macular degeneration. A strength of the study, they wrote, included its long follow-up, and detailed side-by-side comparison of the eye-examination photographs.
An important source of bias in this study was the loss to follow-up of about 25% of the survivors. Those alive but lost to follow-up were more likely to be current smokers at baseline, leading to an underestimation of the relationship between current smoking and macular degeneration.
Alternatively, smokers diagnosed with macular degeneration may have been more likely to attend follow-up than smokers without vision problems, leading to an apparent association between smoking and the vision disorder when none was really present.
These findings add evidence to a possible causal relationship between smoking and the long-term risk of late, but not early, age-related macular degeneration, the researchers wrote.
In addition, these results suggest a possibly greater joint effect in persons with low HDLs, a high ratio of total cholesterol to HDLs, and low fish consumption.
"This supports speculation that macular degeneration is a condition with multiple etiologic factors, and such joint effects contributing to the pathogenesis of macular degeneration could mirror the pathogenesis of cardiovascular disease," Dr. Wang concluded.
No financial disclosures were reported. This study was supported in part by grants from the Australian National Health and Medical Research Council.Primary source: Archives of OphthalmologySource reference: Tan JSL, et al "Smoking and the Long-term Incidence of Age-Related Macular Degeneration" Arch Ophthalmol 2007; 125: 1089-1095.

Smoking may damage your sperm, study finds

Here's one more reason not to smoke -- smoking may damage sperm, passing along genetic damage to a man's children, Canadian researchers report.
A study in mice shows that cigarette smoke caused changes in the DNA of sperm cells, the researchers said in this week's issue of the journal Cancer Research. Such mutations, know as germline mutations, are known to be permanent.
"If inherited, these mutations persist as irreversible changes in the genetic composition of offspring," said Carole Yauk of Health Canada's Environmental and Occupational Toxicology Division, who led the study.
"We have known that mothers who smoke can harm their fetuses, and here we show evidence that fathers can potentially damage offspring long before they may even meet their future mate."
Yauk and colleagues studied the stem cells that produce sperm in mice exposed to cigarette smoke for either six or 12 weeks. All male mammals continuously produce sperm.
They found 1.7 times as many DNA mutations in the cells of the smoke-exposed mice as in those of the unexposed mice after 12 week, and 1.4 times as many mutations after six weeks.
"This suggests that damage is related to the duration of exposure, so the longer you smoke the more mutations accumulate and the more likely a potential effect may arise in the offspring," Yauk said.

NIDA study identifies genes that might help some people abstain from smoking

Findings move science closer to targeted, improved therapies
Scientists supported by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health, have for the first time identified genes that might increase a person’s ability to abstain from smoking. The breakthrough research was conducted by Dr. George Uhl at NIDA’s Intramural Research Program and a team led by Dr. Jed Rose at the Center for Nicotine and Smoking Cessation Research at Duke University Medical Center.
The study, published in the journal BMC Genetics, available on line April 2, brings researchers a step closer toward tailoring individualized drug therapy for addiction based on an individual’s unique genetic makeup.
“This research marks the first time we’ve been able to identify genes involved in the ability to quit smoking,” says NIDA Director Dr. Nora D. Volkow. “It marks a movement from identifying the genetics of addiction vulnerability to identifying the genetic basis of successful abstinence. This knowledge could impact the success rate of cessation programs by helping health care providers choose the most appropriate treatment based on individual differences.”
Dr. Uhl and his colleagues performed a genome-wide analysis on the DNA of two types of nicotine-dependent individuals, one that was able to successfully quit the cigarette- smoking behavior and one that was not.
“We identified 221 genes that distinguished successful quitters from those who were unsuccessful,” says Dr. Uhl. “We know the functions of about 187 of these genes, but 34 have functions that are unknown at present. We also found that at least 62 of the genes that we had previously identified as playing roles in dependence to other drugs also contribute to nicotine dependence.”

Smoking Damages Skin Where the Sun Doesn't Shine

ANN ARBOR, Mich., March 19 -- The entire body is subject to premature aging from cigarette smoking, irrespective of sun-exposure, researchers here found.
Smoking was second only to chronological age in predicting fine wrinkling of photo-protected skin, reported Yolanda R. Helfrich, M.D., of the University of Michigan, and colleagues in the March issue of Archives of Dermatology.
Controlling for age, years of hormone therapy for women, years of smoking, and hours of lifetime sun exposure, the "optimal model" for predicting inner upper arm wrinkling included only chronological age (P<0.001) and packs of cigarettes smoked per day (P=0.04).
"Cigarette smoking has long been investigated as a risk factor for premature skin aging," the researchers said. However, the focus on research has been primarily facial wrinkling with no scales available to measure photo-protected skin, they added.
So they took standardized photographs of the inner upper arm skin of 38 men and 44 women who were patients at a dermatology clinic. They then picked five illustrating varying degrees of fine wrinkling on which basis three blinded judges scored the rest of the photographs twice, one year apart.
http://www.medpagetoday.com/PrimaryCare/Smoking/tb1/5279