A new study has found that active smoking and exposure to passive smoking during childhood, adolescence, and even young adulthood increase the risk of developing chronic obstructive pulmonary disease (COPD), a condition that damages the lungs and makes it much harder for people to breathe.
Researchers from the University of Copenhagen (Denmark) inform that roughly half the COPD cases that medical professionals encounter are found in people whose lungs aged normally but started adulthood with poor breathing capacity, and thus led to the development of other, more serious problems.
Dr. Peter Lange, lead author and professor over at the University of Copenhagen’s (Denmark) department of health gave a statement to Reuters Health informing that lung capacity is typically maxed out somewhere between the ages of 20 and 30, but that smoking (active or passive) can stunt their development.
“If you then observe them for 20 or 30 years, you find that their risk for having COPD will be 3 or 4 times greater than if they had normal lung function as young adults”.
He went on to stress that it is very important to achieve normal growth in lung function during early adulthood if people are to avoid serious risk in the future. Some of the measures of prevention he listed include not smoking during teenage years, treating asthma even in childhood, and reduce one’s exposure to damaging agents such as passive smoking.
Dr. Ralph Panos, chief of medicine from Cincinnati VA Medical Center, is an expert who was not involved in the study, but gave a statement of his own, saying that the study proved that there are several ways to develop chronic obstructive pulmonary disease (COPD).
Traditionally speaking, doctors have believed that COPD a sign of accelerate aging, caused by an unexplainable, quick decline in lung capacity. But the new study has revealed that this decline in lung capacity, which researchers measure with the help of a test that looks at forced expiratory volume (FEV-1), or how much air an individual can quickly exhale, is only responsible for half the cases encountered by professionals.
The other trajectory is related to how lung function is subatomicaly developed during childhood and adolescence.
For their study, the researchers looked at data gathered from three (3) separate population studies, and split subject into two (2) groups – one had starting FEV-1s that were above 80 percent (80%) of the expected lung capacity, the other had starting FEV-1s that were below 80 percent (80%).
Twenty-two (22) years later, the results showed that 26 percent (26%) of the subjects that started the study with a low FEV-1 did end up developing COPD, while just 7 percent (7%) of the subjects that started the study with a high FEV-1 suffered the same fate.
COPD is one of the most often cited causes of death today, with active smoking responsible for roughly 85 percent (85%) of all cases.
The study was published in the New England Journal of Medicine, and the research team hopes that their findings will aid in the development of better tests that can help assess better treatments.
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John Davidson Jr says
………….The inconvenient truth is that the only studies of children of smokers suggest it is PROTECTIVE in contracting atopy in the first place. The New Zealand study says by a staggering factor of 82%.
“Participants with atopic parents were also less likely to have positive SPTs between ages 13 and 32 years if they smoked themselves (OR=0.18), and this reduction in risk remained significant after adjusting for confounders.
The authors write: “We found that children who were exposed to parental smoking and those who took up cigarette smoking themselves had a lower incidence of atopy to a range of common inhaled allergens.
“These associations were found only in those with a parental history of asthma or hay fever.”
They conclude: Our findings suggest that preventing allergic sensitization is not one of them.”
The Journal of Allergy and Clinical Immunology
Volume 121, Issue 1 , Pages 38-42.e3, January 2008
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This is a Swedish study.
“Children of mothers who smoked at least 15 cigarettes a day tended to have lower odds for suffering from allergic rhino-conjunctivitis, allergic asthma, atopic eczema and food allergy, compared to children of mothers who had never smoked (ORs 0.6-0.7)
John Davidson Jr says
………..In 2008 this paper was produced in America and concludes that nictotine and hence active smoking and passive smoking leads to less asthma. It also gives the aetiology (causation) why nicotine and the biologial process that reduces asthma in recipients.
The results unequivocally show that, even after multiple allergen sensitizations, nicotine dramatically suppresses inflammatory/allergic parameters in the lung including the following: eosinophilic/lymphocytic emigration; mRNA and/or protein expression of the Th2 cytokines/chemokines IL-4, IL-5, IL-13, IL-25, and eotaxin; leukotriene C4; and total as well as allergen-specific IgE. unequivocally show that, even after multiple allergen sensitizations, nicotine dramatically suppresses inflammatory/allergic parameters in the lung including the following: eosinophilic/lymphocytic emigration; mRNA and/or protein expression of the Th2 cytokines/chemokines IL-4, IL-5, IL-13, IL-25, and eotaxin; leukotriene C4; and total as well as allergen-specific IgE. ”
John Davidson Jr says
……………Manufacturing the science to meet the agenda, in black on white. Does anyone still have doubts?
”Bal laughs when asked about the role of scientific evidence in guiding policy decisions. “There was no science on how to do a community intervention on something of this global dimension,” he says. “Where there is no science, you have to go and be venturesome—you can’t use the paucity of science as an excuse to do nothing. We created the science, we did the interventions and then all the scientists came in behind us and analyzed what we did.”
Read under the title :
Tobacco Control: The Long War—When the Evidence Has to Be Created
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