Cannabis smokers show greater lung
capacity and lower cancer levels than non-smokers
by Raw
Michelle
For many years, the demonizing
claims being made against cannabis have been crumbling as research slowly dispels
them. Fifty years ago people earnestly believed that the consumption of
cannabis was directly linked to the development of an array of mental
illnesses, and violent and hypersexual behavior.
Medical opinion must be guided by research
But these prejudices are still
hanging on.
Today, an individual who responsibly informs their doctor of their marijuana
use, because, as with any medicine, chemical interactions may change the
resulting chemical behavior, are most frequently urged to cut back. Various
reasons are given for a physicians concern. Some, who appear to have fallen
behind on the research, still express concern about "brain cell
damage" a remnant from the Reagan era's Just Say No campaign.
The main objection, that even the most well-informed physicians feel justified in making, is that even if cannabis itself is not particularly harmful, its most common method of ingestion, smoking, is bad for the lung tissue, regardless of the harmlessness of the substance being smoked. The belief piggybacked its way in on the back of growing opposition to tobacco, and the understanding that tobacco obstructs pulmonary flow and shortens breath.
The main objection, that even the most well-informed physicians feel justified in making, is that even if cannabis itself is not particularly harmful, its most common method of ingestion, smoking, is bad for the lung tissue, regardless of the harmlessness of the substance being smoked. The belief piggybacked its way in on the back of growing opposition to tobacco, and the understanding that tobacco obstructs pulmonary flow and shortens breath.
When a chemical defined by its action doesn't act
Because some of the same
chemicals, which have identifiable carcinogenic impact in cigarettes, are also found
in cannabis smoke, many believe that the cancer-causing potential of cannabis is
proportionate to the amount of these chemicals. The fact that cannabis contains
four times more tar (or oil) than cigarettes sparked the 1990s claim that
smoking a joint was as bad for the lungs as smoking four cigarettes. This
extrapolation makes perfect sense at face value, but doesn't hold up when
compared to actual cancer rates.
Rewriting the medical records
The results of a new government-run research program are now forcing medical authorities to overturn these beliefs. The study has been ongoing for the past twenty years, following the smoking habits of over 5000 people. Researchers found that, contrary to popular belief, smoking cannabis, does not interfere with lung function or capacity. This holds true for ongoing regular -even including daily- and long term consumption. Curiously, as a general rule, cannabis smokers had better lung function than nonsmokers, which researchers attribute to the smoking action itself, rather than the cannabis. Pot smokers inhale deeply and hold those breaths to make the most of their supply, expanding the lung's capacity.
Dr. Tashkin found that, in almost all instances, cannabis consumers had rates of cancer that were no different from those who didn't smoke cannabis. The one exception to this rule was between cannabis smokers and individuals who didn't smoke anything (including tobacco), in which marijuana smokers actually had lower levels of lung cancer.
From Natural News @ http://www.naturalnews.com/035980_cannabis_smokers_cancer.html
Association Between Marijuana Exposure and
Pulmonary Function Over 20 Years
Mark J. Pletcher, MD, MPH; Eric Vittinghoff, PhD;
Ravi Kalhan, MD, MS; Joshua Richman, MD, PhD; Monika Safford, MD; Stephen
Sidney, MD, MPH; Feng Lin, MS; Stefan Kertesz, MD
…The 5115
CARDIA participants recruited in 1985-1986 contributed 20 777 total visits
that included pulmonary function testing. Of these, 959 visits were excluded
for lack of complete information on smoking behavior, 114 for lack of height or
waist measurements, and 1 for an unknown visit date, leaving 19 703 visits
(95%) with complete data from 5016 participants (98%). Participants contributed
3.9 visits/participant on average; attrition was more common in tobacco smokers
but not associated with marijuana use. FEV1 and FVC varied across
participants, increased slightly with age through the late 20s, and declined
slowly thereafter (Figure
1).
Figure 1. Pulmonary Function Measurements by Age
Participants
(n = 5017) contributed an average of 3.9 measurements per person
(n = 19 705 total) over the course of 20 years. A lowess
smoother was used to calculate the smoothed average. FEV1 indicates
forced expiratory volume in first second of expiration; FVC, forced vital
capacity.
View Large | Save
Figure | Download
Slide (.ppt)
More than half
of participants (54%; mean age at baseline, 25 years) reported current
marijuana smoking, tobacco smoking, or both at 1 or more examinations (Table
1). Smoking patterns differed by race and sex, with black women most likely
to smoke tobacco only, white men most likely to smoke marijuana only, and black
men most likely to smoke both. Tobacco
smokers tended to have lower education and income and to be slightly shorter
and less active, whereas marijuana smokers tended to be taller and more active.
The median intensity of tobacco use in tobacco smokers was substantially higher
(8-9 cigarettes/d) than the median intensity of marijuana use in marijuana
smokers (2-3 episodes in the last 30 days). Although marijuana and tobacco
exposures were strongly correlated, our sample included 91 participants with no
tobacco exposure and more than 10 joint-years of marijuana exposure
(contributing 153 observations of pulmonary function), 40 (56 observations) of
whom had more than 20 joint-years of exposure.
Table 1.
Characteristics of CARDIA Participants With Pulmonary Function Test Results, by
Smoking Behavior
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Table | Download
Slide (.ppt)
In fully
adjusted models that considered 4-level categorizations of current and lifetime
exposure to tobacco and marijuana, tobacco smoking (both current and lifetime)
was associated with a lower FEV1 and current smoking with a lower
FVC (Table
2). For example, compared with zero exposure, FEV1 was 63 mL
lower (95% CI, −89 to −36; P < .001
for trend) and FVC was 69 mL lower (95% CI, −97 to −41; P < .001
for trend) with current tobacco exposure of more than 20 cigarettes per day and
101 mL lower (95% CI, −136 to −65; P < .001
for trend) with lifetime tobacco exposure of more than 20 pack-years.
Table 2.
Associations Between Categorized Exposure to Tobacco and Marijuana Smoke and
Pulmonary Function
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Table | Download
Slide (.ppt)
In contrast,
exposure to marijuana (both current and lifetime) was associated with higher
FVC and lifetime exposure with higher FEV1. For example, compared
with zero exposure, FVC increased with greater lifetime exposure in joint-years
(P = .01 for trend)
and FEV1 increased with greater lifetime exposure of up to 10
joint-years and then declined to 36 mL (95% CI, −6.5 to 79)
greater than the zero exposure level (P = .049
for trend). FVC increased with smoking intensity up to 20 marijuana smoking
episodes in the past 30 days and then declined to 20 mL greater than the zero
exposure level (P = .03
for trend). We found no statistically significant interactions between tobacco
and marijuana exposure for either FEV1 or FVC.
When we
modeled current and lifetime tobacco and marijuana exposure as continuous
exposures and permitted flexible nonlinear associations (via splines), we again
found strong, dose-related associations (P < .001)
between increasing exposure to tobacco and lower FEV1 and FVC (Figure
2), with no evidence of nonlinearity (Table
3). Declining slopes ranged as steep as −2.8 mL (95% CI, −4.8 to −0.7; P = .007) per additional cigarette smoked per
day and −7.0 mL (95% CI, −10 to −3.7; P < .001)
per additional pack-year for FEV1 and were of similar magnitude for
FVC (Table
3). At 50 pack-years of exposure, FEV1 was on average 332 mL
lower (95% CI, −401 to −263; P < .001)
and FVC was 229 mL lower (95% CI, −310 to −147; P < .001),
compared with no exposure.
Figure 2. Associations Between Continuous Smoothed Exposure to Current and Lifetime Tobacco and Marijuana and Pulmonary Function
Associations
between continuous current and lifetime exposure measurements and pulmonary
function were modeled via cubic splines (see “Methods”). All 4 exposure
measurements were included in each model (one model each for forced expiratory
volume in the first second of expiration [FEV1] and forced vital
capacity [FVC]). Mixed models with a random intercept and a random 3-knot age
spline were used to adjust for repeated measures, and fixed effects were
included for year, center and center-year (their interaction), race-sex
category, education, and asthma; cubic splines for age, height, waist
circumference, secondhand smoke exposure, and exposure to airborne particulate
matter less than 10 microns and less than 2.5 microns in size; and interactions
between the age spline variables and race-sex, asthma, waist spline variables,
and height spline variables. Point estimates and confidence intervals for
slopes and net associations at different exposure levels are provided in Table
3.
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Table 3.
Estimated Slopes and Net Associations Between Continuous Smoothed Exposure to
Current and Lifetime Tobacco and Marijuana and Pulmonary Function
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Table | Download
Slide (.ppt)
For marijuana,
we found strong statistical evidence that associations between marijuana use
and pulmonary function were nonlinear (Figure
2, Table
3). At low lifetime exposure levels, increasing marijuana use was
associated with a steep increase in both FEV1 (13 mL/joint-year
higher [95% CI, 6.4 to 20], P < .001)
and FVC (20 mL/joint-year higher [95% CI, 12 to 27], P < .001), but at higher levels
of exposure (>7 joint-years), the slope leveled or even turned downward. At
more than 10 joint-years of lifetime exposure, we found a nonsignificant
decline in FEV1 (−2.2 mL/joint-year [95% CI, −4.8 to 0.3], P = .08)
but a significant decline in FEV1 at more than 20 episodes of
marijuana use per month (−3.2 mL/episode [95% CI, −5.8 to −0.6], P = .02). Although net associations with FEV1
became negative at very high exposure levels (>40 joint-years or >25
episodes/mo), these negative deflections were not statistically significant (Table
3). FVC remained significantly elevated in even heavy users (eg, 76 mL [95%
CI, 34 to 117; P < .001]
at 20 joint-years).
From the Journal of the American Medical Association @ http://jama.jamanetwork.com/article.aspx?articleid=1104848#qundefined
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