Links to DU threads in other forums regarding cannabis issues

[RainDog]

2. Asthma Studies

This study from 1975 demonstrated the use of cannabis for asthma.

(I'm posting a link that goes directly to the article but it you google the title, you can obtain the study as a pdf doc.)

http://www.druglibrary.org/schaffer/hemp/medical/tashkin/tashkin1.htm

Effects of Smoked Marijuana in Experimentally Induced Asthma

After experimental induction of acute bronchospasm in 8 subjects with clinically stable bronchial asthma, effects of 500 mg of smoked marijuana (2.0 per cent Delta 9-tetrahydrodrocannabinol) on specific airway conductance and thoracic gas volume were compared with those of 500 mg of smoked placebo marijuana (0.0 per cent Delta 9-tetrahydrocannabinol), 0.25 ml of aerosolized saline, and 0.25 ml of aerosolized isoproterenol (1,250 ug).

Bronchospasm was induced on 4 separate occasions, by inhalation of methacholine and, on four other occasions, by exercise on a bicycle ergometer or treadmill. Methacholine and exercise caused average decreases in specific airway conductance of 40 to 55 per cent and 30 to 39 per cent, respectively, and average increases in thoracic gas volume of 35 to 43 per cent and 25 to 35 per cent, respectively.

After methacholine-induced bronchospasm, placebo marijuana and saline inhalation produced minimal changes in speci! fic airway conductance and thoracic gas volume, whereas 2.0 per cent marijuana and isoproterenol each caused a prompt correction of the bronchospasm and associated hyperinflation. After exercise-induced bronchospasm, placebo marijuana and saline were followed by gradual recovery during 30 to 60 min, whereas 2.0 per cent marijuana and isoproterenol caused an immediate reversal of exercise-induced asthma and hyperinflation.

Another study

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1429361/

Abstract
1 delta1-trans-tetrahydrocannabinol, (delta1-THC) produces bronchodilatation in asthmatic patients. 2 Administered in 62 microliter metered volumes containing 50--200 microgram by inhalation from an aerosol device to patients judged to be in a steady state, it increased peak expiratory flow rate (PEFR) and forced expiratory volume in 1 second (FEV1). 3 The rate of onset, magnitude, and duration of the bronchodilator effect was dose related.

Another one

Acute Effects of Smoked Marijuana on Specific Airway Conductance in Asthma Subjects
American Review of Respiratory Disease, Volume 109, 1974, p. 420-428

By Donald P. Tashkin, Bertrand J. Shapiro, and Ira M. Frank

SUMMARY: The acute effects of smoked 2 per cent natural marijuana (7 mg per kg) and 15 mg of oral delta-9-tetrahydrocannabinol (THC) on plethysmographically determined airway resistance (Raw) and specific airway conductance (SGaw) were compared with those of placebo in 10 subjects with stable bronchial asthma using a double-blind crossover technique. After smoked marijuana, SGaw increased immediately and remained significantly elevated (33 to 48 per cent above initial control values) for at least 2 hours, whereas Sgaw did not change after placebo. The peak bronchodilator effect of 1,250 mcg of isoproterenol was more pronounced than that of marijuana, but the effect of marijuana lasted longer.

After ingestion of 15 mg of THC, SGaw was elevated significantly at 1 and 2 hours, and Raw was reduced significantly at 1 to 4 hours, whereas no changes were noted after placebo. These findings indicated that in the asthmatic subjects, both smoked marijuana and oral THC caused significant bronchodilation of at least 2 hours' duration.

Introduction

In the nineteenth century, one of the medicinal uses of marijuana was in the therapy of bronchial asthma (1); however, no definite evidence of its effectiveness as a bronchodilator was adduced until recent studies demonstrated significant airway dilatation in healthy young men after both the smoking of marijuana (2,3) and the ingestion of its principal psychoactive ingredient delta-9-tetrahydrocannabinol (THC) (3). Whether similar effects could be elicited in subjects with bronchospastic disease was of interest because the irritant effect of marijuana smoke, which is probably responsible for the symptoms of bronchitis attributed to heavy or chronic marijuana smoking (4,5), might outweigh the bronchodilator properties of delta-9-THC, thereby resulting in bronchospasm in patients with hyper-reactive airways. Consequently, the acute effects of both inhaled marijuana smoke and oral delta-9-THC on specific airway conductance (SGaw) were investigated in a group of patients with clinically stable bronchial asthma.

It is counter intuitive to assume any smoked material might have a positive effect - with current uses of vaporizers or sublingual cannabis meds, tho, smoking can be avoided.

Cannabis that contains CBD as well as THC seems to be useful b/c of the anti-inflammatory and anti-anxiety properties of CDB.