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. 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. The authors acknowledged funding from the National Cancer Institute.
Smoking accounts for more than a third of cases of the most severe and common form of rheumatoid arthritis, indicates research published online in the Annals of the Rheumatic Diseases. And it accounts for more than half of cases in people who are genetically susceptible to development of the disease, finds the study.
The researchers base their findings on more than 1,200 people with rheumatoid arthritis and 871 people matched for age and sex, but free of the disease. The patients came from 19 health clinics in south and central Sweden, while their healthy peers were randomly selected from the population register. All the participants were aged between 18 and 70. They were quizzed about their smoking habits and grouped into three categories, depending on how long they had smoked. Blood samples were taken to assess all the participants' genetic profile for susceptibility to rheumatoid arthritis and to gauge the severity of their disease, as indicated by their antibody levels.
More than half of those with rheumatoid arthritis (61%) had the most severe form of the disease, which is also the most common form, as judged by testing positive for anticitrullinated protein/peptide antibody (ACPA). Those who were the heaviest smokers – 20 cigarettes a day for at least 20 years – were more than 2.5 times as likely to test positive for ACPA. The risk fell for ex-smokers, the longer they had given up smoking. But among the heaviest smokers, the risk was still relatively high, even after 20 years of not having smoked.
Based on these figures, the researchers calculated that smoking accounted for 35% of ACPA positive cases, and one in five cases of rheumatoid arthritis, overall. Although this risk is not as high as for lung cancer, where smoking accounts for 90% of cases, it is similar to that for coronary artery heart disease, say the authors. Among those with genetic susceptibility to the disease, and who tested positive for ACPA, smoking accounted for more than half the cases (55%). Those who smoked the most had the highest risk.
The authors point out that several other environmental factors may contribute to an increased risk of rheumatoid arthritis, including air pollutants and hormonal factors. But they suggest that their findings are sufficient to prompt those with a family history of rheumatoid arthritis to be advised to give up smoking.
A new UK research has found that more than a third believe cancer is down to fate and there is nothing they can do to avoid it. Cancer Research UK stated that one in five men and women feared cancer ahead of debt, knife crime, Alzheimer's disease and losing their job whereas 34 percent believed the disease was down to fate, rising to 41 percent of those aged 55 to 64.
The findings come in the midst of growing evidence suggesting lifestyle factors such as losing weight, taking exercise, reducing alcohol consumption and quitting smoking can significantly reduce the risk of developing cancer.
The survey questioned more than 2,000 adults aged 16 and over. Those questioned were asked to choose what they feared most from a list including developing Alzheimer's, being in debt, old age, being the victim of knife crime, cancer, being in a plane crash, motor neurone disease, being in a car accident, having a heart attack, losing your job and losing your home.
More people (20 per cent) overall chose cancer than anything else, followed by 16 per cent who feared Alzheimer's disease the most. Among adults up to the age of 44, cancer was feared most by 25 per cent while 7.5 per cent feared Alzheimer's most. For those aged over 65, Alzheimer's was feared most by 30 per cent while 14 per cent feared cancer most.
John Fyall, Cancer Research UK's spokesman for Scotland, said: “It's absolutely vital for us to get the message out that people can do something to alleviate their emphatic fear of cancer. Cancer is no longer the death sentence people still seem to dread,” the Scotsman quoted, John Fyall, Cancer Research UK's spokesman for Scotland, as saying. “Spotting early signs and symptoms of what could be cancer – but probably isn't – and getting these checked out by a doctor means that the disease can be diagnosed more quickly,” he added.
Teresa Nightingale, general manager of the World Cancer Research Fund, said, “It is a concern that so many people think cancer is a matter of fate, because there is now strong scientific evidence that people can make relatively simple changes to reduce their risk.” “Scientists estimate about a third of the most common cancers in the UK could be prevented just by eating a healthy, plant-based diet, being regularly physically active and maintaining a healthy weight. This includes about 40 per cent of breast and bowel cancer cases,” she added. Nightingale further informed that, “The strong evidence that diet, activity and weight affect our risk, together with other well-known risk factors such as smoking and sunburn, means that cancer is actually a largely preventable disease.” (ANI)
Steering clear of full-fat, fried, and processed foods is not just good for overall health, it could help prevent chronic lung conditions, a large UK study has revealed.
Led by Seif Shaheen, Professor of Respiratory Epidemiology at Barts and The London School of Medicine, the study – involving 1,551 men and 1,391 women with an average age of 66 – showed that those whose diet favoured fresh fruit and vegetables, oily fish and wholegrain products had far better lung function than those who chose a diet high in fat, sugar and processed food.
The diets of those involved were investigated to assess what kinds of food they consumed on a regular basis. Their lung function was also tested using a spirometer, a device which measures the amount of air that a person can blow out of their lungs in one second. This simple test illustrates how healthy the lungs are, and determines whether any blockage or obstruction exists in the airways. If the airways are obstructed, the person is diagnosed with Chronic Obstructive Pulmonary Disease (COPD).
The study also revealed that the beneficial effects of the sensible diet were particularly strong in men who smoked.
Lung health in particular may be positively affected by a sensible diet because of the antioxidants contained in fruit and wholegrains, and the omega-3 fatty acids found in oily fish – that protect the lungs against the adverse effects of smoking.
Professor Shaheen said: “Whilst cessation of smoking is still the number one way to improve lung health, this study is important because it suggests that cases of COPD might be prevented if people, especially male smokers, ate more fruit and vegetables, oily fish and wholegrain cereals, and less white bread, sugar, full fat dairy products, fried food and processed meat. However, the only way to confirm this would be to carry out a randomised controlled trial.”
NAFLD is the most common cause of liver disease worldwide and research suggests the number of cases will climb given an increasing trend toward higher fat diets, obesity, decreased physical activity, and a rise in diabetes. Past studies indicate that more than 30 million Americans have NAFLD and approximately 8 million may have nonalcoholic steatohepatitis (NASH).
In the first study, Ramón Bataller, M.D., and colleagues from the Hospital Clínic in Barcelona, Spain investigated the effects of cigarette smoking (CS) in obese rats. Rats were divided into 4 groups (n=12 per group): obese smokers, obese non-smokers, control smokers and control non-smokers. Smoker rats were exposed to 2 cigarettes/day, 5 days/week for 4 weeks. Researchers found that obese rats exposed to CS showed a significant increase in ALT serum levels (indicating liver disease), while this effect was not observed in control rats.
“Our results show that CS causes oxidative stress and worsens the severity of NAFLD in obese rats,” said Dr. Bataller. “Further studies should investigate longer exposures to CS, and assess whether this finding also occurs in patients with obesity and NAFLD.”
In her editorial, also published in Hepatology this month, Claudia Zein, M.D., from the Cleveland Clinic, noted that “the importance of these results is that taken together with other experimental and clinical data, they support that cigarette smoking appears to aggravate liver injury in patients with liver disease.” Dr. Zein added, “Studies characterizing the effects of cigarette smoking in human NAFLD will be crucial because of the vast number of patients that may benefit from modification of this risk factor.”
Additionally, prior studies suggest an over consumption of high fructose corn syrup (HFCS), primarily in the form of soft-drinks, have contributed to weight gain and the rise in obesity, particularly in children and adolescents. Table sugar (sucrose) and HFCS are the two major dietary sources of fructose. Over the past 40 years, consumption of dietary fructose has increased 1,000% according to Bray et al, and doctors believe it to be a major cause of NAFLD.
Researchers from Duke University studied 341 adults enrolled in the NASH Clinical Research Network who responded to a Block food questionnaire within 3 months of a liver biopsy. Fructose consumption was estimated conservatively by including that found in beverages, which accounts for 50% of dietary fructose intake. Results showed that 27.9% of participants consumed at least 1 fructose-containing beverage per day, 52.5% had 1 to 6 beverages with fructose per week, and 19.7% drank no beverages with fructose.
“In patients with NAFLD, daily fructose ingestion was associated with reduced fatty liver (steatosis), but we found increased fibrosis,” noted Manal Abdelmalek, M.D., M.P.H, and lead author of the study. “Further dietary intervention studies are needed to evaluate whether a low-fructose diet improves metabolic disturbances associated with NAFLD and improves patient outcomes for those at risk of disease progression,” concluded Dr. Abdelmalek.
A second fructose study led by Ling-Dong Kong, M.D., from Nanjing University in China investigated the effects of curcumin on fructose-induced hypertriglyceridemia and fatty liver in rats. Curcumin, a compound derived from turmeric (curcuma root), is sold as an herbal supplement and is believed to have anti-inflammatory, anti-tumor, and anti-viral properties. Researchers observed a hyperactivity of hepatic protein tyrosine phosphatase 1B (PTP1B), which is associated with defective insulin and leptin signaling, in fructose-fed rats.
For the first time this study demonstrated that curcumin inhibited hepatic PTP1B expression and activity in fructose-fed rats. “Our results provide novel insights into the potential therapeutic mechanisms of curcumin on fructose-induced hepatic steatosis associated with insulin and leptin resistance,” said Dr. Kong.
These studies indicate modifying risks such as smoking and fructose consumption offer potential benefits for those with liver diseases. Further studies are needed to explore these benefits in preventing the progression of liver disease.