Marihuana inhibits dihydrotestosterone binding to the androgen receptor.

I thought this might be a fun study to post:



Marihuana inhibits dihydrotestosterone binding to the androgen receptor.
Purohit V, Ahluwahlia BS, Vigersky RA.

Abstract
Marihuana and its constitutents delta 9-tetrahydrocannabinol (delta 9-THC) and cannabinol (CBN) were tested for their ability to interact with the androgen receptor in rat prostate cytosol. Smoked marihuana condensate, delta 9-THC, and CBN inhibit specific binding of dihydrotestosterone (DHT) to the androgen receptor with a dissociatin constant of the inhibitors (Li) of 2.1-5.8 X 10(-7)M. in addition, other metabolites of delta 9-THC were also androgen antagonists. This data suggests that the anti-androgenic effects associated with marihuana use results, at least in part, from inhibition of androgen action at the receptor level.

misterE - This makes good sense, since this some studies have suggested better blood sugar and cardiovascular protection.

Here's a site that has videos and information on its medicinal purposes, mostly cancer. The interesting thing is that they distill the entire plant, THC and all and concentrate the oil. When taken by mouth, there are no psychogenic effects.

http://www.phoenixtears.ca/article/rick-simpson/articles/make-the-medicine.html

misterE wrote:
Marihuana inhibits dihydrotestosterone binding to the androgen receptor.

That's why marihuana cause erectyl disfonction in some cases?

All I know is that my best friend smokes everyday and has done so for the past 10 years (he's 28) and he's losing hair at a fast clip.

I don't know if it makes it worse but it's definitely not helping his hair.

The only concern about weed is the cannabinoid effect relative the CB1 receptor. This is what mediates neurogenic inflammation. When under stress we produce endocannabinoids, or we can get exogenously from weed.

So far it has already been shown that hair growth can be stimulated by using CB1 receptor antagonists.

The natural form of this is resveratrol and curcumin.

Here's more info on the role hair growth by endo- and exocannabinoids.

http://www.fasebj.org/cgi/content/full/21/13/3534

CS - I am comfused, I thought Cayenne worked the Cannabinoid receptor ? Can you please explain the difference between the function of Cayenne and Res/Cur ?

NrwgnKID - Cayenne is pretty confusing, here's why. In small amounts it can raise IGF-1, which can be helpful in cases when low IGF-1 is a factor for hair loss.

When cayenne is used topically, over time it can block substance P, which is a neuropeptide.

When taken internally in moderate to larger amounts, it appears to bring on neurogenic inflammation.

http://ajp.amjpathol.org/cgi/content/full/166/4/985

http://www.if-pan.krakow.pl/pjp/pdf/2006/1_13.pdf

CausticSymmetry wrote:NrwgnKID - Cayenne is pretty confusing, here's why. In small amounts it can raise IGF-1, which can be helpful in cases when low IGF-1 is a factor for hair loss.

CS, when you talk about IGF-1 will you please specify if its protein-bound or free?

misterE - In this context, it involved a subcutaneous administration of capsaicin with and without soy isoflavones, which resulted in the an increased expression of IGF-I in the dermal papilla

Here's more info on this below:

Growth Horm IGF Res. 2007 Oct;17(5):408-15. Epub 2007 Jun 13.
Administration of capsaicin and isoflavone promotes hair growth by increasing insulin-like growth factor-I production in mice and in humans with alopecia.

Harada N, Okajima K, Arai M, Kurihara H, Nakagata N.

Department of Translational Medical Science Research, Nagoya City University, Graduate School of Medical Sciences, Kawasumi 1, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan.


OBJECTIVE: Insulin-like growth factor-I (IGF-I) plays an important role in hair growth. Capsaicin activates vanilloid receptor-1, thereby increasing the release of calcitonin gene-related peptide (CGRP) from sensory neurons, and CGRP has been shown to increase IGF-I production. We recently reported that isoflavone, a phytoestrogen, increases production of CGRP by increasing its transcription in sensory neurons. These observations raise the possibility that administration of capsaicin and isoflavone might promote hair growth by increasing IGF-I production. In the present study, we examined this possibility in mice and humans with alopecia. DESIGN: Dermal IGF-I levels, immunohistochemical expression of IGF-I in the skin and hair regrowth were examined after capsaicin and isoflavone administration to wild-type (WT) mice and CGRP-knockout mice. Plasma levels of IGF-I and promotion of hair growth were evaluated in 48 volunteers with alopecia after administration of capsaicin and isoflavone for 5 months. RESULTS: Subcutaneous administration of capsaicin significantly increased dermal IGF-I levels at 30 min after administration in WT mice (p < 0.01), but not in CGRP-knockout mice. Dermal levels of IGF-I were significantly higher in WT mice administered capsaicin and isoflavone for 4 wks than in those administered capsaicin alone for 4 wks (p < 0.01) and in those administered neither of them (p < 0.01). Immunohistochemical expression of IGF-I at dermal papillae in hair follicles was increased in WT mice administered capsaicin and isoflavone and in those administered capsaicin alone at 4 wks. Hair regrowth was clearly more accelerated in WT mice administered capsaicin and isoflavone for 4 wks than in those administered capsaicin alone for 4 wks and in those administered neither of them. Plasma levels of IGF-I were significantly increased from baseline levels in 31 volunteers with alopecia at 5 months after oral administration of capsaicin (6 mg/day) and isoflavone (75 mg/day) (p < 0.01), while they were not increased in 17 volunteers with alopecia administered placebo. The number of volunteers with alopecia who showed promotion of hair growth at 5 months after administration was significantly higher among volunteers administered capsaicin and isoflavone (20/31: 64.5%) than among those administered placebo (2/17: 11.8%) (p < 0.01). CONCLUSIONS: These observations strongly suggested that combined administration of capsaicin and isoflavone might increase IGF-I production in hair follicles in the skin, thereby promoting hair growth. Such effects of capsaicin and isoflavone might be mediated by sensory neuron activation in the skin.

Also, the benefit of increasing IGF-1, maybe related to hypertensive patients. For instance, in androgen blockade therapy, patients would not get any hair growth if their IGF-1 levels were depressed. It's possible that hypertension depresses IGF-1 levels.

Here's more info on this theory:

Growth Horm IGF Res. 2008 Feb;18(1):75-81. Epub 2007 Aug 10.
Effect of capsaicin on plasma and tissue levels of insulin-like growth factor-I in spontaneously hypertensive rats.

Harada N, Okajima K.

Department of Translational Medical Science Research, Nagoya City University, Graduate School of Medical Sciences, Nagoya, Japan.
Abstract

OBJECTIVE: Plasma levels of insulin-like growth factor-I (IGF-I), an important substance for maintaining cardiovascular homeostasis, are lower in spontaneously hypertensive rats (SHR) than in normotensive Wistar Kyoto rats (WKY). Calcitonin gene-related peptide (CGRP) increases IGF-I production in vitro and in vivo, suggesting that stimulation of sensory neurons might increase the production of IGF-I in SHR. DESIGN: Levels of CGRP and IGF-I in plasma, kidneys and heart in WKY and SHR and cellular cyclic AMP levels in dorsal root ganglion neurons (DRGs) isolated from WKY and SHR were measured by an ELISA-based method. RESULTS: Levels of CGRP and IGF-I in plasma, kidneys and heart of SHR were about half of those of WKY. Administration of capsaicin significantly increased levels of CGRP and IGF-I in plasma and tissues of SHR to the levels in WKY and these increases were completely reversed by pretreatment with capsazepine, an inhibitor of vanilloid receptor-1 activation. CGRP release and cellular levels of cAMP in DRGs isolated from SHR were significantly lower than those in DRGs isolated from WKY. Capsaicin increased both CGRP release and cellular cAMP levels in DRGs isolated from SHR to the levels in DRGs isolated from WKY. CONCLUSIONS: Sensory neuron activation might be lower in SHR than in WKY probably due to decreased production of cAMP in sensory neurons, explaining why IGF-I levels in plasma and tissues are lower in SHR than in WKY.

I'm assuming it's protein-bound.

One of my best friends smoked pot from when he was a teen up until his early 30's. His wife made him quit as a condition on the marriage.

He reluctantly quit, gained close to 75 pounds and was just diagnosed as a diabetic at 35. He's now on a slew of diabetes medications. I tried to talk to him about natural routes for treating his situation, but he tells me he feels great on the diabetes meds and he's finally taking control of his health.

I sat back with my wife the other night and said, "in retrospect he would have been better off sticking with pot than what he's doing now".

hadrion - I totally agree!

Also, diabetes drugs make everything worse. Patients are actually better off not taking them, despite having higher blood sugar. Of course, diabetes is really a result of an electron shortage--it's quite easy to fix.

More:

http://books.google.com.br/books?id=fxoJPVNKYUgC&pg=PA94&lpg=PA94&dq=Marijuana+inhibits+dihydrotestosterone+binding+to+the+androgen+receptor.&source=bl&ots=w2RcQP-aWE&sig=C3XqyFl-Mm_yPk3oE7-kers-7wU&hl=pt-BR&ei=IvEDTNOxB8-JuAeqi833DQ&sa=X&oi=book_result&ct=result&resnum=1&ved=0CB0Q6AEwAA#v=onepage&q=Marijuana%20inhibits%20dihydrotestosterone%20binding%20to%20the%20androgen%20receptor.&f=false

http://www.docstoc.com/docs/21012384/Endocrine-Effects-of-Marijuana

CausticSymmetry wrote:hadrion - I totally agree!

Also, diabetes drugs make everything worse. Patients are actually better off not taking them, despite having higher blood sugar. Of course, diabetes is really a result of an electron shortage--it's quite easy to fix.

IH,

Not to get off topic, but what would be the easy fix. This is one of my best friends. He was the best man at my wedding. I'd like to really sit him down and offer him some solutions/advice. He's seen the physical changes I've made over the years. I want to take a shot at helping him. He was diagnosed type II.

hadrion - I'm planning to write an indepth article on diabetes in the future, but to summarize I would suggest that for diet, he check into his potential metabolic type.

http://www.naturalhealthyellowpages.com/metabolic/self_test.html

Avoiding eating anything in a package. This pretty much eliminates all the processed food.

Ask him if he has any root canals. If so, this could be a source of electron depletion.

The following articles will provide other information on drugs (not using them) and blood sugar control).

http://www.immortalhair.org/apps/blog/show/1800363-problems-with-insulin

http://www.immortalhair.org/apps/blog/show/1910518-diabetes-drugs-offer-zero-benefits

http://www.immortalhair.org/apps/blog/show/1917110-more-on-diabetes-treatment

hadrion wrote:



Not to get off topic, but what would be the easy fix. This is one of my best friends. He was the best man at my wedding. I'd like to really sit him down and offer him some solutions/advice. He's seen the physical changes I've made over the years. I want to take a shot at helping him. He was diagnosed type II.

Dr. Neal Barnard has reversed diabetes with a low-fat/high-fiber carbohydrate based vegan diet. He wrote about how to do it in his book called: Dr. Neal Barnard's Program for Reversing Diabetes. Which you can read here.

The thing about weed makes such SENSE!

Man like, you always see people who smoke weed and they have proper good heads of hair, and then those who drink... no hair!

I know it's a vast generalization and there are other factors, but on some subconscious level... this is kinda something that always occurred to me in the past

Good find misterE!

Diabetologia. 2010 Mar;53(3):406-18. Epub 2010 Jan 5.

Optimal dietary approaches for prevention of type 2 diabetes: a life-course perspective.
Buyken AE, Mitchell P, Ceriello A, Brand-Miller J.

Nutrition and Health Unit, Research Institute of Child Nutrition, Heinstück 11, 44225 Dortmund, Germany. buyken@fke-do.de

Abstract
In recent years, several alternative dietary approaches, including high-protein and low-glycaemic-load diets, have produced faster rates of weight loss than traditional low-fat, high-carbohydrate diets. These diets share an under-recognised unifying mechanism: the reduction of postprandial glycaemia and insulinaemia. Similarly, some food patterns and specific foods (potatoes, white bread, soft drinks) characterised by hyperglycaemia are associated with higher risk of adiposity and type 2 diabetes. Profound compensatory hyperinsulinaemia, exacerbated by overweight, occurs during critical periods of physiological insulin resistance such as pregnancy and puberty. The dramatic rise in gestational diabetes and type 2 diabetes in the young may therefore be traced to food patterns that exaggerate postprandial glycaemia and insulinaemia. The dietary strategy with the strongest evidence of being able to prevent type 2 diabetes is not the accepted low-fat, high-carbohydrate diet, but alternative dietary approaches that reduce postprandial glycaemia and insulinaemia without adversely affecting other risk factors.

Thanks for the response IH. I'll keep an eye out for that article. Right now my friend is raving about how these diabetes drugs have saved his life, his marriage, etc. He thinks he's finally in control of his health. I asked him if looked into the side effects and he got angry at me.

I then told him there were natural alternatives along with diet changes and he didn't want to hear it.

When you post that article, I'm just going to forward it to him and let him read it and tell him I won't bother him about it again.

When this thread was posted today it resonated with me since all of this man's health issues came crashing down on him once he gave up marijuana. Now some could say that was a coincidence since he was hitting his mid 30's, but after he gave it up he started to look like a walking corpse.

Hoppy wrote:
"The thing about weed makes such SENSE!

Man like, you always see people who smoke weed and they have proper good heads of hair, and then those who drink... no hair!

I know it's a vast generalization and there are other factors, but on some subconscious level... this is kinda something that always occurred to me in the past

Good find misterE!"

I know plenty of bald dudes who are a chronic. Two bothers, NW7. Both have been smoking since junior high. If it were only as simple....

I strongly feel that cannabis helped my hair to thin!
I have always had a widows peak until I started smoking green, I look back at pictures close to the time before I started and then to now and put a checkpoint on where I started losing my hair! About a year of smoking and my hair is noticably, I have stopped now and can finally relize that either... Cannabis speeds up MPB or causes hair to thin when using regularly.

Some people find using it makes thier hair grow quicker, while some say it has made thier hair thinner and the majority of people dont get this side effect...

Not only the smoke and drug, but eating habits, diet, stoned sleep, psychology changes and stress masked by the drug all play a big part...

FATE? wrote:I strongly feel that cannabis helped my hair to thin!
I have always had a widows peak until I started smoking green, I look back at pictures close to the time before I started and then to now and put a checkpoint on where I started losing my hair! About a year of smoking and my hair is noticably, I have stopped now and can finally relize that either... Cannabis speeds up MPB or causes hair to thin when using regularly.

I agree with you. My hairloss looks like classic MPB : thinning crown, less density vertex. But MPB is genetics. The problem is : my father (55yo) NW1, both my grandfathers (>85yo) slight recession but very amount of hair considering their ages , my uncles and brothers (>30 yo) : NW1. Almost 20 men in my family, not even one of them shows any sign of balding. How can this stuff can be genetics ?

And my hairloss has started when I was smoking cannabis like crazy.

Did you notice any change after you gave up getting high?

[/quote]Did you notice any change after you gave up getting high?[/quote

I heavily smoked every weekend for 5months and first I noticed my hair would curl/bend in some areas, like sides and back of neck and hair was more lifeless... I did not put this down to smoking at all untill I stopped! (I have noticed a few friends that toke also have the same curly type areas of hair and crown thinning!)

Then 8months after I finally stopped as I know it either started my hair loss or speeded it up!

Now that I have stopped compleatly (also any other drugs... alcohol, caffine...) and follow my healthy regiem, I am in a much better off... I cycle a lot now and no joke! I feel a greater satisfactinal high than I ever got from smoking! I'm a stronger person inside as I finally can deal with stress. My hair was looking healthier within 2-3 weeks of stopping, I did say to myself that I would only smoke once a month, but now looking back I could not care if I never smoked again! I know it made me stress a lot more about my hair in the end...

Yeah, it made a huge difference overall to my hair...

FATE? wrote:
Yeah, it made a huge difference overall to my hair...

What do you mean by huge difference ?
Did the hairloss stop and/or regrow or your hair just looks more healthier ?
I think hair regrowth is a very slow process if done naturally : no more smoking, better diet, physical exercices...
It can take many months even years if the person has been having a very bad hygiene for many years.
This is probably why vey few people are able to regrow hair using a natural method. They are too lazy to make major lifestyle changes over a long period of time.