Using Cannabis to Treat Asthma and COPD
Although some may cringe at the mere thought of smoking something to treat pulmonary disease, it is not a new idea. In fact, for centuries European ‘healers’ prescribed smoked thornapple to relieve bronchospasm. Just recently, viewers of the popular series Outlander, which takes place in the Scottish Highlands, witnessed a character prescribing thornapple to a severe asthmatic. You could clearly see the relief he experienced as he drew in his first cloud of smoke.
If you saw that episode, you got a feeling of the power of a smokable herb that remarkably and immediately induced bronchodilation along with immediate relief. Even though the two herbs cannabis and thornapple (AKA Jimson weed) have very different chemicals: the former THC and the latter atropine/scopolamine, the end result — bronchodilation — was similar. THC acts differently than the above ‘anticholinergics.’ THC acts on CB1 receptors, it is thought.
Let’s see if the literature supports the use of THC and THC containing products in the treatment of bronchospastic conditions.
There are several studies available. Once again, Dr. Tashkin (UCLA Medical Center) has contributory publications. In the first study back in 1977 he used THC, either smoked or inhaled, as one would do using a rescue inhaler. In this study, Dr. Tashkin was able to clearly demonstrate a significant bronchodilator effect using both forms of THC.
Here’s the best part: in one arm of the study they compared THC to isoproterenol, AKA Isuprel. Isuprel is a non-specific beta agonist. That means that when administered, the patient’s heart rate may be stimulated as much as the bronchodilation effect. This is considered an unwanted side effect. As any asthmatic may attest, a racing heart rate after using one’s rescue inhaler isn’t fun, and it can be dangerous in some populations.
Dr. Tashkin was able to show that after 5 to 20 mg of aerosolized Δ9-tetrahydrocannabinol (THC) airway conductance (the greater the conductance the more significant the bronchodilation) increased immediately. It reached a maximum after 1 to 2 hours, and remained significantly greater than placebo values for 2 to 3 hours. Although the bronchodilator effect of aerosolized THC was less than that of isoproterenol after 5 min, it surpassed the clinical effects of Isuprel and was found to be significantly greater than that of isoproterenol after 1 to 3 hours. The magnitude of bronchodilatation after all doses of aerosolized Δ9-tetrahydrocannabinol was comparable. Lower doses (5 mg THC) produced less tachycardia than the highest dose (20 mg).
The drawback was that they found aerosolized THC produced a local irritant effect in about 20% of the test subjects which led to a worsening of bronchospasm, cough, and chest discomfort. Thus aerosolized THC in this form may not be proper in spite of the fact that the THC itself produced marked bronchodilation.
Smoke cannabis on the other hand produced greater intoxication and tachycardia along with bronchodilation.
Previous studies support the medical use of THC, and possibly CBD, for COPD or asthma. They have found that THC is about equipotent to commonly used bronchodilators such as albuterol (adrenergic beta agonist) or ipratropium bromide (an anticholinergic drug very similar to atropine, one of the active ingredients in thornapple).
The New England Journal of Medicne published a study in 1973:
“Marihuana smoke, unlike cigarette smoke, causes broncho-dilation rather than broncho-constriction [narrowing of the air passages] and, unlike opiates, does not cause central respiratory depression.”
A very well conducted study was published in 2006 again by Dr. Tashkin. This landmark study proved that cannabis smoke appears to have little in common with cigarette smoke as far as lung function goes. In fact, to their astonishment low to moderate cannabis smokers actually had better lung function and lung volumes both of which increased with each ‘joint year.
That certainly was an unexpected conclusion, especially since Dr. Tashkin receives his funding from the National Institute for Drug Abuse (NIDA) and related institutions. These governing bodies generally look for harms from illegal drug use, not benefits.
Another interesting finding is that orally ingested THC products produce better degrees of bronchodilation than smoking or aerosolized preparations. Both produce about 2-3 hours of bronchodilation, similar to a conventional inhaler.
Further investigations by the Respiratory Pharmacology Laboratory in Paris have shown that CB1 receptor stimulation (using THC) inhibits cholinergic (parasympathetic) bronchospasm in a concentration-dependent fashion.
What they found was that THC blocks the neurotransmitter acetylcholine at the muscarinic receptors located on smooth muscle lining the bronchioles of asthmatics. This end result is identical to the effects of the prescription drug ipratropium bromide which acts as an anticholinergic drug.
TWO WAYS TO CAUSE BRONCHOSPASM
There are two mechanisms for inducing bronchospasm in asthmatics, healthy subjects, and in patients with COPD. One way is to block sympathetic stimulation of beta receptors located in bronchiolar smooth muscle. When blocked it causes bronchospasm, hence using a beta receptor stimulant such as Alupent effectively induces bronchodilation.
The other way is by stimulating cholinergic receptors (called muscarinic receptors) which induces bronchospasm. In fact, using a certain cholinergic agonist — methacholine — induces a predictable bronchospasm in test subjects, and is often used in many clinical trials. Therefore, if you block cholinergic innervation to respiratory bronchioles you also get bronchodilation. Atrovent is one such drug.
Drug companies take advantage of this by sometimes using both an anti-cholinergic and an ‘adrenergic’ drug together for a synergistic bronchodilator effect. Drugs such as Combivent come to mind.
THE PROBLEM USING CONVENTIONAL DRUGS
The problem with all of these preparations are the enormous side effects that patients must endure. They run from severe tachycardia (racing heart rate), insomnia and tremulousness, to dry mouth and urinary retention. There are many more side effects.
I recall trying a combination inhaler once since I suspected mild bronchospasm in the dry, dusty air where I was living. Yes, it vastly improved my run but 12 hours later my heart was still racing at about 140 beats per minute. Honestly, I cannot imagine dealing with that every time you needed an inhaler.
The point I wish to stress is that THC is a decent bronchodilator, as good as many that are currently marketed. All that needs to change is the law. After that patients suffering from COPD and asthma can choose which is the best medication for their particular problem. The obvious advantage of a THC preparation is that none of the above mentioned side effects can occur.
It means that cannabis offers a significant alternative to conventional drugs.
The DEA has given the US their latest imbroglio that cannabis should stay a schedule I drug. Meaning that it’s a dangerous, addicting, medically worthless plant. I’m curious if Big Pharma had any say in this matter behind closed doors? It may be a while before you see a safer inhaler available by prescription. You know, the THC-type inhaler that works as well as anything else on the market?
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