Why Smokers Gain Weight When They Quit Smoking

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Most smokers put on a couple of kilos when they quit smoking.

Eighty per cent of quiters put on seven kilos on average. Their weight increases even if their calorie intake remains the same or even falls compared to the level before quitting smoking.

Changes in Intestinal Flora

Researchers attribute the cause to a changed composition of the bacterial diversity in the intestine. The bacterial strains that also prevail in the intestinal flora of obese persons take the upper hand in people giving up smoking.

While the bacterial diversity in the faeces of smokers and non-smokers changed only little over time, giving up smoking resulted in the biggest shift in the composition of the microbial inhabitants of the intestines. The Proteobacteria and Bacteroidetes fractions increased at the expense of representatives of the Firmicutes and Actinobacteria phyla. 

The new gut flora apparently used the energy contained in the nutrition more efficiently.

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The above story is based on the August 29, 2013 news release by the Swiss NationalScience Foundation.

The research has been published in PLOS ONE, an inclusive, peer-reviewed, open-access resource from the PUBLIC LIBRARY OF SCIENCE:

Biedermann L et al. Smoking Cessation Induces Profound Changes in the Composition of the Intestinal Microbiota in Humans. PLoS ONE, 2013; 8 (3): e59260

Click HERE for the full text.

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Thirdhand Smoke Causes DNA Damage

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Thirdhand smoke -- the noxious residue that clings to virtually all surfaces long after the secondhand smoke from a cigarette has cleared out -- causes significant genetic damage in human cells!

This is the findings of a study led by researchers from Lawrence Berkeley National Laboratory

“Tobacco-specific nitrosamines, some of the chemical compounds in thirdhand smoke, are among the most potent carcinogens there are. They stay on surfaces, and when those surfaces are clothing or carpets, the danger to children is especially serious,” said Lara Gundel, co-author of the study.

The study also found that chronic exposure is worse than acute exposure, with the chemical compounds in samples exposed to chronic thirdhand smoke existing in higher concentrations and causing more DNA damage than samples exposed to acute thirdhand smoke, suggesting that the residue becomes more harmful over time.

Thirdhand smoke is extremely difficult to eradicate. Studies have found that it can still be detected in dust and surfaces of apartments more than two months after smokers moved out. Common cleaning methods such as vacuuming, wiping and ventilation have not proven effective in lowering nicotine contamination.

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The above story is based on the June 23, 2013 news release by DOE/Lawrence Berkeley National Laboratory. http://www.lbl.gov/

This paper was published in the journal Mutagenesis:     

Hang B, Sarker AH, Havel C, Saha S, Hazra TK, Schick S, Jacob P 3rd, Rehan VK, Chenna A, Sharan D, Sleiman M, Destaillats H, Gundel LA. Thirdhand smoke causes DNA damage in human cells. Mutagenesis. 2013 Jul;28(4):381-91. doi: 10.1093/mutage/get013.

* Nitrosamines - when nicotine in thirdhand smoke reacts with nitrous acid it undergoes a chemical transformation and forms carcinogenic tobacco-specific nitrosamines, such as NNA, NNK and NNN. Nicotine can react with ozone to form ultrafine particles, which can carry harmful chemicals and pass through human tissue. Humans can be exposed to thirdhand smoke through inhalation, ingestion or skin contact.

 

Cancer-Promoting Mechanisms of Overlooked Components in Secondhand Smoke

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Tobacco smoke, diesel exhaust and oil combustion carry polycyclic aromatic hydrocarbons -- PAHs that are known to cause cancer.

But of these PAHs, the obviously dangerous high-molecular-weight PAHs like benzo[a]pyrene (BaP) have received the vast majority of research attention. Their low-molecular-weight cousins have been largely overlooked, in part because studies have shown that these compounds alone aren't very successful at mutating genes in cancer-causing ways.

A University of Colorado Cancer Center study explores two of these low-molecular-weight (LMW) PAHs -- 1-methylanthracene (1-MeA) and 2-methylanthracene (2-MeA) -- and shows that while they don't necessarily cause cancer, 1-MeA promotes conditions that will likely allow cancer to grow.

There's a big distinction between initiating cancer and promoting it,

says Asst Prof Alison Bauer, CU Cancer Center investigator.

Her study showed that in a mouse cell model using a progenitor cell of lung cancer, the LMW 1-MeA promoted inflammation and increased mitogenic pathways, both of which are linked to tumor promotion. 2-MeA, while nearly structurally identical, did not.

Among other effects, Bauer and colleagues found that 1-MeA disrupts communication between cells, affecting the "gap junctions" across which adjoining cells pass information. 1-MeA also upregulates the gene COX2, which has been shown in other studies to create an over-aggressive inflammatory response -- and this inflammation in turn can promote tumor growth.

There are many different PAHs in secondhand smoke

Bauer says. "Some are obviously dangerous like BaP, which directly mutates genes. Others, like 1-MeA, we known very little about. Think about all these PAHs like chess pieces -- first you have to know how each piece moves and then you can start looking at how they all work together."

"With smoking rates decreasing, we think this problem is going away, but high levels of secondhand smoke still exist in the U.S., for example in some apartment buildings," Bauer says. "And around the world, in China, Russia, Poland and many other countries, secondhand smoke is still a major issue. Knowing the effects of these LMW PAHs like 1-MeA could help us prevent or treat cancers associated with them."

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The above story is based on the June 25, 2013 news release reprinted from materials provided by University of Colorado Denver.

The study has been published in the journal PLoSOne:                                                                

Osgood RS, Upham BL, Hill T, Helms KL, Velmurugan K, Babica P, Bauer AK. Polycyclic Aromatic Hydrocarbon-Induced Signaling Events Relevant to Inflammation and Tumorigenesis in Lung Cells Are Dependent on Molecular Structure. PLoS ONE, 2013; 8 (6): e65150 DOI: 10.1371/journal.pone.0065150

Smoking Leads to Five-Fold Increase in Heart Disease and Stroke in Under-50s

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Preventing smoking among teens and young adults could help lower health complications associated with smoking.

Smokers who are under 50 years of age have a fivefold increased risk of having a heart disease or stroke. The risk of these chronic condition doubles for smokers who are over 60 years of age, says the European Society of Cardiology.

Stopping young people taking up smoking is a key goal of the ESC joint guidelines on prevention of cardiovascular disease. Other recommendations are to avoid smoking and exposure to passive smoking, and that all smokers should be given advice and help to quit.

Passive smoking at home or in the work place increases the risk of CVD by 30%. However, smoking bans lead to rapid and sizeable reductions in hospitalizations for acute myocardial infarction. People who stop smoking also rapidly reduce their risk of CVD.

Professor Tell said: "Passive smoking is much more dangerous than many people think. Increasing exposure to cigarette smoke, either active or passive, is significantly associated with atherosclerosis.''

She concluded: "Prevention of smoking is the most cost-effective way to treat and prevent cardiovascular disease. This is particularly important for children and adolescents who are susceptible to tobacco promotion and find it more difficult to quit smoking."

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The above story is based on the May 31, 2013 news release by European Society of Cardiology (ESC).

Smoking immediately upon waking may increase risk of lung and oral cancer

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'Wake-Up' Cigarette May Raise Risk for Lung, Mouth Cancers

The sooner a person smokes a cigarette upon waking in the morning, the more likely he or she is to acquire lung or oral cancer, a new study reveals.

Penn State researchers analyzed data from nearly 2,000 adult smokers who took part in the U.S. National Health and Nutrition Examination Survey. The participants provided blood samples and information about their smoking behaviour.

The investigators found that about 32% of the participants smoked their first cigarette of the day within five minutes of waking. Among the others, 31% smoked within 6 to 30 minutes, 18% smoked within 31 to 60 minutes, and 19% smoked more than an hour after waking.

Highest levels of cancer-linked substance found in blood of those who light up first thing in morning.

People who had a cigarette immediately after waking had higher levels of NNAL -- a byproduct of a tobacco-specific cancer-causing substance called NNK -- in their blood than those who smoked a half hour or more after waking, regardless of how many cigarettes they smoked in a day, the study authors reported.

The research team also found that NNAL levels in the participants' blood was also associated with factors such as their age, their gender, the age they started smoking, and whether or not another smoker lived in their home.

"Most importantly, we found that NNAL level was highest among people who smoked the soonest upon waking, regardless of the frequency of smoking and other factors that predict NNAL concentrations," study co-author Steven Branstetter, an assistant professor of biobehavioral health, said in a Penn State news release.

"We believe these people who smoke sooner after waking inhale more deeply and more thoroughly, which could explain the higher levels of NNAL in their blood, as well as their higher risk of developing oral or lung cancer," he added. "As a result, time to first cigarette might be an important factor in the identification of high-risk smokers and in the development of interventions targeted toward early morning smokers."

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The above story is based on the March 29, 2013 news release by Penn StateUniversity.

The study was published in the journal Cancer Epidemiology, Biomarkers and Prevention:

Branstetter SA, Muscat JE. Time to First Cigarette and 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanol (NNAL) Levels in Adult Smokers; National Health and Nutrition Examination Survey (NHANES), 2007–2010.Cancer Epidemiol Biomarkers Prev April 2013 22:615-622; doi:10.1158/1055-9965.EPI-12-0842

More information

The U.S. National Cancer Institute has more about the harms of smoking.