also, most smokers are smoking 20-30 cigarettes per day, I would guess that the average marijuana smoker smokes one joint or one bowl a day at most, so I don't see how you ccan compare the two.
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- Thread starter edubz
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I agree that the use of a water pipe for filtering and also the tar delivered in a pin joint are alot different than the person who rips the filter off of their Camels or Marlboroughs.
Surprisingly, the initiation of lung, and head and neck cancers is tied to expression of a variety of nuclear receptors, among them the ERalpha and beta (Estrogen receptor) and also Rev-erb, a retinoid receptor, who action is primarily activated by arachidonic acid - the muscle building and also cancer initiating factor in prostate and breast tissue hyperplasia.
My guess is that there are PAHs, polyaromatic hydrocarbons, that are locally converted by lung microsomal cytochrome P450s (some of which were cloned in a lab I worked in long ago at Vanderbilt U) to compounds that structurally mimic arachidonic acid. Must be sorta the same case for Rev-erb (meaning that the retinoid gene that is shut off is detuning the immune control of run away cell turnover).
In the case of THC, also a lipid, its binding to and positively activating this receptor, and that could be the difference between that apoptosis, programmed cell death, that keeps tumors from forming in chronic pot smoking.
Now that is fucking cool, this connection... I just happened to be reading about this estrogen receptor and retinoid receptor binding today, after finding a funny ass article on ER control of strong myosin chain control in muscle cell.
Who wudda thunk. You mess with ER gene regulation with certain androgens analogs, and you get softer muscles (more water mass) but with less functional strength.
And here all this time, the thinking was, estrogen production was upregulated.
Nope. All that messing with SERMs.
Surprisingly, the initiation of lung, and head and neck cancers is tied to expression of a variety of nuclear receptors, among them the ERalpha and beta (Estrogen receptor) and also Rev-erb, a retinoid receptor, who action is primarily activated by arachidonic acid - the muscle building and also cancer initiating factor in prostate and breast tissue hyperplasia.
My guess is that there are PAHs, polyaromatic hydrocarbons, that are locally converted by lung microsomal cytochrome P450s (some of which were cloned in a lab I worked in long ago at Vanderbilt U) to compounds that structurally mimic arachidonic acid. Must be sorta the same case for Rev-erb (meaning that the retinoid gene that is shut off is detuning the immune control of run away cell turnover).
In the case of THC, also a lipid, its binding to and positively activating this receptor, and that could be the difference between that apoptosis, programmed cell death, that keeps tumors from forming in chronic pot smoking.
Now that is fucking cool, this connection... I just happened to be reading about this estrogen receptor and retinoid receptor binding today, after finding a funny ass article on ER control of strong myosin chain control in muscle cell.
Who wudda thunk. You mess with ER gene regulation with certain androgens analogs, and you get softer muscles (more water mass) but with less functional strength.
And here all this time, the thinking was, estrogen production was upregulated.
Nope. All that messing with SERMs.
Yeah, what she said...
Ditto
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