However bad you thought smoking was, it's even worse. The New York Times reports that this is according to a new study that adds as least five diseases and 60,000 deaths a year to the toll taken by tobacco in the US. Before the study, smoking was already blamed for nearly half a million deaths in the US from 21 diseases, including 12 types of cancer.
The new findings are based on health data from nearly a million people who were followed for 10 years. In addition to the well-known hazards of lung cancer, artery disease, heart attacks, chronic lung disease and stroke, the researchers found that smoking was linked to significantly increased risks of infection, kidney disease, intestinal disease caused by inadequate blood flow, and heart and lung ailments not previously attributed to tobacco.
Even though people are already barraged with messages about the dangers of smoking, researchers say it is important to let the public know that there is yet more bad news. "The smoking epidemic is still ongoing, and there is a need to evaluate how smoking is hurting us as a society, to support clinicians and policy making in public health," said Brian D Carter, an epidemiologist at the American Cancer Society and the first author of an article about the study. "It's not a done story."
Carter said he had been inspired to dig deeper into the causes of death in smokers after taking an initial look at data from five large health surveys being conducted by other researchers. The participants were 421,378 men and 532,651 women 55 and older, including nearly 89,000 current smokers. As expected, death rates were higher among the smokers. But diseases known to be caused by tobacco accounted for only 83% of the excess deaths in people who smoked. "I thought, 'Wow, that's really low,' " Carter said. "We have this huge cohort. Let’s get into the weeds, cast a wide net and see what is killing smokers that we don't already know."
Analysing deaths among the participants from 2000 to 2011, the researchers found that, compared with people who had never smoked, smokers were about twice as likely to die from infections, kidney disease, respiratory ailments not previously linked to tobacco, and hypertensive heart disease, in which high blood pressure leads to heart failure. Smokers were also six times more likely to die from a rare illness caused by insufficient blood flow to the intestines. Carter said he had confidence in the findings because, biologically, it made sense that those conditions were related to tobacco. Smoking can weaken the immune system, increasing the risk of infection, he said. It is also known to cause diabetes, high blood pressure and artery disease, all of which can lead to kidney problems. Artery disease can also choke off the blood supply to the intestines. Lung damage from smoke, combined with increased vulnerability to infection, can lead to multiple respiratory illnesses.
Two other observations supported the findings, he said. One was that the more heavily a person smoked, the greater the added risks. The second was that among former smokers, the risks diminished over time. In general, such effects, known as a dose response, suggest that an observed correlation is more than a coincidence.
The study also found small increases in the risks of breast and prostate cancer among smokers. Carter said those findings were not as strong as the others, adding that additional research could help determine whether there were biological mechanisms that would support a connection.
A major study by an international team, including the Montreal Neurological Institute at McGill University and the University of Edinburgh, shows new evidence that long-term smoking could cause thinning of the brain's cortex. The cortex is the outer layer of the brain in which critical cognitive functions such as memory, language and perception take place. Interestingly, the findings also suggest that stopping smoking helps to restore at least part of the cortex's thickness.
The study involved 244 male and 260 female subjects – five times larger than any previous similar research on smoking and cortical thickness. Their average age was 73. The test group included current smokers, ex-smokers and non-smokers. All of the subjects were examined as children in 1947 as part of the Scottish Mental Survey. Researchers used health data gathered during recent personal interviews with the subjects, and also analysed data from MRI scans showing the current state of the subjects’ brain cortices.
"We found that current and ex-smokers had, at age 73, many areas of thinner brain cortex than those that never smoked. Subjects who stopped smoking seem to partially recover their cortical thickness for each year without smoking," says the study's lead author Dr Sherif Karama, assistant professor of psychiatry at McGill, psychiatrist at the Douglas Mental Health University Institute and an affiliate of the Montreal Neurological Institute. The apparent recovery process is slow, however, and incomplete. Heavy ex-smokers in the study who had given up smoking for more than 25 years still had a thinner cortex.
Although the cortex grows thinner with normal ageing, the study found that smoking appears to accelerate the thinning process. A thinner brain cortex is associated with adult cognitive decline. "Smokers should be informed that cigarettes could hasten the thinning of the brain’s cortex, which could lead to cognitive deterioration. Cortical thinning seems to persist for many years after someone stops smoking," says Karama.
Smoking impairs the response to biological drugs used to treat inflammatory arthritis affecting the lower back, known as axial spondyloarthritis, or AxSpA, for short, Science Daily reports new research reveals. Smoking is known to heighten the risk of developing rheumatoid arthritis, and several drugs don't seem to work as well in smokers with the condition. But as AxSpA is a relatively newly defined form of arthritis, it's not clear what impact smoking has.
The researchers led by A Ciurea tracked the treatment response to a class of biological drugs known as tumour necrosis factor inhibitors in just under 700 patients with confirmed AxSpA in the Swiss Clinical Quality Management Cohort (SCQM), between 2005 and 2014. Almost two thirds (62%) were smokers; 38% were non-smokers. Their response to treatment was assessed using recognised criteria to quantify disease activity (BASDAI and ASDAS scores) 1-2 years later.
In all, complete data on treatment response and smoking status were available for just under 500 (70%) patients. As the impact of treatment on BASDAI scores is likely to be affected by several factors, such as age, sex, symptom duration, weight, and exercise, these were all accounted for in the analysis. Having smoked in the past didn't affect the response to treatment, but current smoking did.
Compared with the non-smokers, current smokers responded significantly less well to their drug treatment and achieved significantly smaller reductions in the BASDAI and ASDAS scores. This difference was particularly noticeable among those who had higher levels of an inflammatory marker (C reactive protein or CRP) to begin with. Between 10% and 20% fewer current smokers than non-smokers achieved a 50% fall in their baseline disease activity score (BASDAI) after a 1 year of treatment.
A study from the University of California, Davis, and the Berkeley non-profit Public Health Institute has found that children exposed to tobacco smoke from their parents while in the womb are predisposed to developing diabetes as adults.
In the study, women whose mothers smoked while pregnant were two to three times as likely to be diabetic as adults. Dads who smoked while their daughter was in utero also contributed to an increased diabetes risk for their child, but more research is needed to establish the extent of that risk.
"Our findings are consistent with the idea that gestational environmental chemical exposures can contribute to the development of health and disease," said lead author Michele La Merrill, an assistant professor of environmental toxicology at UC Davis.
The study analysed data from 1,800 daughters of women who had participated in the Child Health and Development Studies, an ongoing project of the Public Health Institute. The CHDS recruited women who sought obstetric care through Kaiser Permanente Foundation Health Plan in the San Francisco Bay Area between 1959 and 1967. The data was originally collected by PHI to study early risk of breast cancer, which is why sons were not considered in this current study.
In previous studies, foetal exposure to cigarette smoke has also been linked to higher rates of obesity and low birth weight. This study found that birth weight did not affect whether the daughters of smoking parents developed diabetes. "We found that smoking of parents is by itself a risk factor for diabetes, independent of obesity or birth weight," said La Merrill. "If a parent smokes, you're not protected from diabetes just because you're lean."
Plain tobacco packaging may, meanwhile, reduce the likelihood of smokers seeking to obtain cigarettes by almost 10% compared to branded packs, according to research from the Universities of Exeter and Bristol.
The findings come amidst debate over whether a law introducing plain cigarette packaging in England and Wales could come into force in 2016. Last month ministers said MPs would be asked to vote on the plan before May's general election, following a series of public consultations on the issue.
In the experiments, smokers had to choose between pressing a key that might earn cigarettes or a key that might earn chocolate, and were uncertain about which key was most likely to pay off in each trial. Just before participants made each choice, they were presented with either a picture of a branded cigarette pack, a picture of a plain cigarette pack, or nothing. The results showed that whereas branded packs increased the probability of participants making the cigarette choice by 10% compared to when nothing was presented, the plain packs did not. The implication is that plain packs are less effective at prompting smokers to purchase cigarettes compared to branded packs.
Associate Professor Lee Hogarth, the lead author of the study from the University of Exeter, explained: "The key finding was that plain cigarette packs were about 10% less likely to prompt participants to make the tobacco choice compared to branded packs. In fact, the plain packs promoted no more tobacco choice than when nothing was presented. These findings provide experimental support for the idea that introducing plain packaging might reduce tobacco purchasing or consumption."
However, the researchers also advise caution when interpreting these results. As Professor Marcus Munafo, a co-author of the study from the University of Bristol, explained: "The experimental procedure only modelled the ability of pack stimuli to promote a cigarette-seeking choice. In the natural environment, smoking may be governed by a whole range of factors, including tobacco withdrawal, the presence of other people smoking, time of day, and so on. It is not clear to what extent plain packaging will reduce smoking when these other factors are at play". Hogarth added: "Our study demonstrated that, under some circumstances, plain packaging can reduce cigarette-seeking behaviour. Policy makers must consider how much weight to place on this observation when considering the potential pros and cons of introducing plain packing as a national policy".Full report in The New York Times New England Journal of Medicine abstract McGill University release Molecular Psychiatry abstract Full Science Daily report Annals of the Rheumatic Diseases abstract University of California – Davis release Journal of Developmental Origins of Health and Disease abstract Universities of Exeter and Bristol release Addiction abstract