Life expectancy for people born in 1941, when Lawson (age 72) was born, is 63.5. Hence smoking most likely extended his life by 8.5 years relative to
his birth cohort.
Note also that tobacco smoke is a potent anti-inflammatory substance
and the statistical association of smoking with COPD is due to
-- people with chronic lung inflammation (which eventually results in COPD in more advanced age), or those genetically
susceptible to general inflammations, will be more likely to start smoking and will have harder time quitting under pressures to quit, since tobacco
smoke provides perceptible relief from the inflammatory symptoms. Hence, the statistical associations on non-randomized samples
(which is what
antismoking "science" is based on) is due to self-medication
For example, Rheumatoid Arthritis is positively associated with smoking and doctors will strongly urge and pester RA patients to quit smoking and
switch to synthetic corticosteroids (instead of using their own, stimulated by tobacco smoke). Yet, when animal experiments are conducted, such as
recent RA mice experiment
, where mice with induced RA, were divided into 3 groups, smoking
group, nicotine group and controls (not exposed to either), there was a little "surprise." The smoking group had the longest delay before the onset of
RA and had the least damage to the joints. The next was the nicotine group, while the "healthy living" controls had the earliest RA onset and the most
damage to their joints (see
references & further discussion).
While no such experiments are done on humans, the closest to well controlled comparison is in environments where there is common harmful
pro-inflammatory lung exposure, such as industrial toxins in a factory or in mines. In those situations the smokers end up with the least lung damage
(such as 6x lower rates of emphysema). This "paradoxical" effect is so strong that it has it has its own "scientific" name, the "strong smoker
i.e. it is assumed that those who still smoke despite such harsh conditions, are genetically stronger, more resilient to lung damage. Of
course, no has ever conducted any research to verify that kind of wishful conjecture. It is simply handwaved to explain away the facts that don't fit.
(See 2nd half of this post
for references and
Of course, there is a hard science that genuinely explains the protective effect -- besides the above anti-inflammatory effects, tobacco smoke also
strongly upregulates the three main antioxidant and detox enzymes in human body, glutathione by 80%, catalase and SOD (superoxide dismutase) by nearly
100%. With nearly doubled detox rates, along with the anti-inflammatory effects, the smokers enjoy strong protection against the harsh conditions
compared to non-smokers.
As in the case of RA, the same protective effect is also the mechanism behind the statistical associations on non-randomized samples
smoking and "smoking related diseases" (such as COPD and lung cancer) -- due to self-medication confounding (which never taken into account since such
therapeutic effects of smoking are a strong taboo in antismoking "science"), increased smoking rates among people living or working in harsh
conditions is merely a statistical marker or a proxy for exposure to industrial or environmental toxins.
edit on 28-1-2014 by nightlight7
because: (no reason given)
edit on 28-1-2014 by nightlight7 because: (no reason given)