Theory: Cooked Fat =DHT(Dihydrotestosterone) Baldness

[Bryan]

Which brings me to the point of what causes DHT at high concentrations. the answer to this imo is cooked fat which increases alpha reductase activity and then DHT activity.

I second what Michael just got through saying: post a legitimate medical reference or citation for that claim, not something you found on a Web site that's trying to sell something to gullible readers.

I'm not saying that it's completely out of the question that certain kinds of fat _might_ tend to increase the production of androgens (I'm somewhat less inclined to accept the claim about greater 5a-reductase activity), but I want to see a scientific treatise on that so we can get some idea of the extent to which it happens. Is the (alleged) increase in DHT significant, or is it just something like a 1% increase? :wink:

Out best bet is to keep DHT/reductase levels normal through the correct diet and maintenance of hormonal balance.

Sorry, but I don't buy it. Not without some serious SCIENTIFIC evidence.

Bryan

 

[The Gardener]

I agree with Bryan.

I am SURE that certain elements of diet might create spikes in hormone levels, but I have a hard time believing that these changes would persist long enough to disrupt or exacerbate the male pattern baldness mechanism. I'd think that the body would get the levels back to some sort of baseline fairly quickly through some sort of internal regulation.

 

[DammitLetMeIn]

I'm looking for a specific medical study...

19. Sebaceous Gland Hypothesis of Androgenetic Alopecia (Inaba 1985; Inaba and Inaba 1992a)

http://www.med-estetica.com/Cientifica/ ... droAlo.htm

I thought M.Barry's post at the bottom of this thread was interesting:

http://www.gourmetstylewellness.com/discussions ... eb8e5c17cc

OK, this isn't a medical source but it refers to a medical study:

Recently, a group of Japanese researchers reported a correlation between excessive sebum in the scalp and hair loss. Excessive sebum often accompanying thinning hair is attributed to an enlargement of the sebaceous gland. They believed excessive sebum causes an high level of 5-alpha reductase and pore clogging, thus malnutrition of the hair root.

Although this condition could be hereditary, they believe diet is a more prominent cause.

http://www.psoriasiscafe.org/hairloss-male.htm

I think this study was actually carried out as its quoted in many websites. Its just a matter of finding it.

"We studied the effects of growth hormone (GH) and insulin-like growth factors (IGFs), alone and with androgen, on sebaceous epithelial cell growth...IGF-I was the most potent stimulus of DNA synthesis. These data are consistent with the concept that increases in GH and IGF production contribute in complementary ways to the increase in sebum production during puberty."

Endocrinology
1999 Sep, 140:9, 4089-94

http://www.all-creatures.org/aip/nl-21j ... kevin.html

I've written extensively about testosterone, culture and health in a previous column, but I should mention here that high testosterone is clearly implicated in hair loss and is closely related to various cultural factors that vary between societies. Cross cultural studies show that Japanese men who shift from their traditional vegetable based diet to a Western one high in animal foods begin to lose their hair. Prior to the introduction of animal fat into their diet after World War II Japanese people's hair was thick and healthy. High animal food intake raises cholesterol which contributes to male pattern baldness by increasing sebum production. Excess sebum that accompanies hair loss is due to enlargement of the sebaceous gland which is attached to each hair follicle. This increases sebum production, clogging pores, malnourishing the hair root and raising levels of the enzyme 5 alpha reductase which converts testosterone to the hormone DHT which causes follicles to shrink and hair to go into resting phase. Ex cess animal food in the diet also over-stimulates the adrenal glands, producing extra androgens, which raises testosterone levels in the scalp. Testosterone levels peak in the fall and are lowest in spring when hair grows most fully.

http://www.findarticles.com/p/articles/ ... 67857/pg_2

^^^
This is written by medic (i think, check it out)

The elevated lipid levels and anaerobic conditions in the comedones provide a suitable environment for P. acnes, and this organism increases in number. Propionibacterium acnes is the most important factor in the inflammatory process of acne. It produces bacterial lipases that hydrolyse the triglycerides in the sebum to form free fatty acids and low molecular weight neutrophil chemotactic factor. Neutrophils that are thus attracted to the hair follicles release active oxygen species. The free fatty acids and active oxygen species cause irritation and weakening of the follicular walls. The contents of the follicles enter the surrounding connective tissue because of the degradation of the follicles and the inflammation progresses from the formation of comedones to redness, papules, pustules, indurations and cysts.

http://www.jimronline.net/content/html/ ... icleID=213

^^
what do you think of this?

This is interesting:

Research has shown that sweat is much more effective than water at emulsifying fat located in the skin's sebaceous glands, and thus at removing the sebum and bacteria lodged in the fat.[citation needed] The vasodilation caused by the high temperatures also allow essential fluids to be transported to the skin's surface. This enhances the development of collagen, giving the skin a continued elasticity and wrinkle-free complexion

http://en.wikipedia.org/wiki/Sauna

Essentially the sequence is going like this:

Excess animal fat = excess cholesterol = excess sebum production = excess 5 alpha reductase = excess DHT in that specified area (maybe not DHT levels in the entire body) = starvation of follicle = hair loss

A question. Prostate problems / male pattern baldness were low in Japan. Prostate Problems / male pattern baldness are high in America (and in 2nd gen. jap/americans). surely diet has to be implicated?

 

[michael barry]

Dammitletmein,

I hope you read this post CLOSELY.

You actually make some interesting points about the Japanese.


But is it higher carbohydrates or higher fats? Thats what we have to identify for certain, to wit:

That old post of mine was based on an online article I had read at about that time that claimed animal fats were the reason for higher baldness and more oily Japanese scalps, and more androgen related disorders in the Japanese population like acne and prostate-hyperplasia. Since then, Ive learned that insulin-resistance gets the adrenal gland to make more testosterone. There is also alpha five reductase enyzmes right in the adrenal glands, so some of it gets turned into DHT right there. Bear in mind, the Japanese cosumption of soy isoflavones (which might bind to circulating DHT, and "handcuff it", and inhbits inlfammatory PKC cytokines) and less green tea (a STRONG inhbitor of alpha five reductase type one, a weaker inhibitor of alpha five type two, a substance that "does something" to DHT after its created of either kind of manufacture, and a weak receptor blocker), less fish (hence fish oil consumption is down, fish oil inhibits TNF-alpha), and less vegetables and rice oils (less beta sitosterol, a substance that is alot like estrogen in the body), ................................and you have some reasons for baldness increases right there.

Keep in mind insulin-resistance building diets help induce less globulin in the blood. 98% of your testosterone is supposed to be bound up by globulin as it travels through your blood stream. If you are insulin resistant however, there is less globulin.................and perhaps only 96% of your testosterone is "bound", and there is alot more of it available to bind and make DHT and bind to hair receptors themselves, there would be more testosterone made PERIOD by the adrenals also, there is more PKC in the blood, more TGF-beta (because green tea inhibits that also, as well as TNF alpha)................................are you getting this.

The old Japanese diet was very hair-healthy, ours is very hair "unhealthy"



But are fats in meats the cause, or all the things I outlined above????


Keep in mind that eskimos eat ALOT of meats. Rural eskimos eat meat and milk ALMOST EXCLUSIVELY. I dont think Ive ever seen a balding eskimo.


Could it be that the white bread on a hamburger bun, the french fries, the cola (high sugar, high fructose corn syrup-----which is about the unhealthiest damn thing you can digest), the pastas, the processed foods, the caramel dyes, and all the insulin-resistance building modern food additives be much worse for your hair than the cooked meat.

Cooked meat has been with us for thousands of years, but this other stuff has not.


However, Dammitletmein, I will be the first to conceed that we dont know the long term implications of of all the added hormones and steroids that we have cows and chickens and hogs on these days. A man might be better off restricting his meat consumption to organic meats and fish if he is concerned about that.




There would only be one way to test your idea.....................get a set of twins and raise one vegan and the other allowed to eat meats but not processed foods and check their hair at 30 and see who had more.
That ain't gonna happen though, and its one reason researchin' hair is so frustrating.



Im sure Bryan can tell you how infuriating it is that no major medical concern has tested topical spironolactone out on 30 guys or so and took before and after pictures of their success at one and two years so we can really compare it to finasteride, etc. The lack of studies and our having to extrapolate from hamster flank organ data, and forehead sebum secretion data, and murine follicle data is frustrating.


By the way,,,,,,,,,,,,,,,,,,did you know that OVEREATING contributes to insulin resistance, and that mice that were deliberately UNDERFED not only live longer, but have shinier, thicker coats? Interesting stuff.....

 

[DammitLetMeIn]

Apparently a the presence of a high amount of fat in the diet builds insulin resistance as well. Fat also causes the limitation of that binding globulin.

HEre is a GREAT article on that particular issue tat may be worth reading:

http://www.mesomorphosis.com/articles/i ... diet02.htm

So in effect the best diet for treating baldness might be one which includes:

Low glycemic natural carbs (oats, basmati brown rice), Soy Protein, wheatgrass juice, ion-exhanged microfiltrated whey protein, soymilk (altho dubious), green tea (altho dubious), flaxseed oil/flaxseed lignans.

Our cooked meat today is not even like that of the 1920's it is terribly imbalanced in terms of fat. All meat is supposed to have the same fat content as Game such as venison but instead farmers have fed the animals up on carbohydrates producing really fatty cuts which when cooked create a bit of a disaster health wise.

The meat which the Eskimos eat is better balanced with regard to fat as it is not domesticated. They eat wild (I could be wrong). And isn't it true that the eskimos ate raw meat until the 60's? Raw meat has a 1:1 ratio of Omega 3 to Omega 6 whereas our cooked meats have 1:6 ratio. Bear in mind that good fats are 5 alpha reductase inhibitors...

In fact the eskimo point is a great one. Eskimos actually do not go bald or at least, they didn't. I've read that the literal translation of eskimo is 'he who eats raw'.

'Eskimo means, "one who eats raw." While living forcenturies on a diet that consisted primarily of whale or seal blubber, Eskimosdeveloped no arterial sclerosis. They had almost no heart disease or stroke, and nohigh blood pressure. Established nutritional doctrine would predict a high incidence ofthese ailments, but even raw blubber will digest itself completely if it is not cookedand its enzymes are not destroyed. But once you heat even the finest olive oil above118 degrees, you will not be able to digest it completely. It will clog you up'


In theory, if we just ate as the Japs/Eskimos did, we should grow good hair and be in better balance.


But what about the link there is with food and sebaceous glands with regard to acne?

The bigger the sebaceous gland gets the more DHT right?

 

[abcdefg]

If someone is very sensitive to DHT it doesnt take a large amount of DHT to lose hair though. I am 24 almost 25 and I have no back hair, like 15 chest hairs, and not a ton of facial hair. When I got more facial hair I noticed my head hair starting to thin out. It could be a coincidence though.
The western diet thing causing hairloss is just dumb. I mean male pattern baldness has been around how long? Think how many civilizations and cultures with all there own unique diets dealt with hairloss. Obviously diet has no profound effect on male pattern baldness. I mean how do we know its the diet and not a million other things? Hell the temperature changes, el nino, air pollution could be responsible. Theres way to many things to narrow it down to diet for a disease that science says relates to a cascade of effects having to do in part with DHT.

 

[docj077]

Docj are you a doctor? Why not get a job doing research or something if you know this much about cellular biology and such?

Whats the best way to safely lower or stop the downstream effects of tgf-beta? Im scared of propecia I love my dht and I dont want to mess up my hormonal system.

No, I'm not a doctor. I'm a 55 year old mother of five that is really concerned about male pattern baldness.

But, seriously, I used to be a research assistant and that was a great job. It's pretty easy work and you learn a lot. I'm trained to do Southern Blots, Northern Blots, PCR, Fusion PCR, electrophoresis, mini-preps, etc.

As for lowering TGF-beta using a drug that is not FDA approved, I really don't have an answer for that one. There are a lot of herbs out there that claim to do a lot of different miraculous things. Unfortunately, most herbs aren't ingested in large enough concentrations to make a difference. So, for right now the only means of lowering both DHT and TGF-beta that I know of that is approved by the FDA (for lowering DHT, anyway) is the use of 5AR inhibitors.

EDIT: The topical use of Minoxidil has also been shown to decrease the effects of TGF-beta on the hair follicle.

 

[abcdefg]

Ah one more thing docj since I have your attention. Do you think from what you know that 5ar2 inhibition is safe long term? Do you think the hormone changes like higher T, higher E are safe? It crosses blood brain barrier, and was originally intended for cancer as you know. Im just curious what you think of its safety.

 

[DammitLetMeIn]

Finally found a little bit of science linking DHT and diet composition:

(pending)

Seshadri P 2005 Dietary fat and androgens. J Clin Endocrinol Metab 90:3802 (Letter)[Free Full Text]

Wang C, Catlin DH, Starcevic B, Heber D, Ambler C, Berman N, Lucas G, Leung A, Schramm K, Lee PWN, Hull L, Swerdloff RS 2005 Low-fat high-fiber diet decreased serum and urine androgens in men. J Clin Endocrinol Metab 90:3550–3559[Abstract/Free Full Text]

Also interesting:

Anorexia Nervosa; Characterized by voluntary starvation. The adrenal gland secretes extra androgen to compensate for the lack of strength. Consequently, additional hair is produced.

 

[Bryan]

Here's the abstract of that second study. Interesting that they found a 12% reduction in serum androgens:

To validate our hypothesis that reduction in dietary fat may result in changes in androgen metabolism, 39 middle-aged, white, healthy men (50-60 yr of age) were studied while they were consuming their usual high-fat, low-fiber diet and after 8 wk modulation to an isocaloric low-fat, high-fiber diet. Mean body weight decreased by 1 kg, whereas total caloric intake, energy expenditure, and activity index were not changed. After diet modulation, mean serum testosterone (T) concentration fell (P < 0.0001), accompanied by small but significant decreases in serum free T (P = 0.0045), 5 alpha-dihydrotestosterone (P = 0.0053), and adrenal androgens (androstendione, P = 0.0135; dehydroepiandrosterone sulfate, P = 0.0011). Serum estradiol and SHBG showed smaller decreases. Parallel decreases in urinary excretion of some testicular and adrenal androgens were demonstrated. Metabolic clearance rates of T were not changed, and production rates for T showed a downward trend while on low-fat diet modulation. We conclude that reduction in dietary fat intake (and increase in fiber) results in 12% consistent lowering of circulating androgen levels without changing the clearance.

 

[DammitLetMeIn]

I think I pretty much understand baldness now.

The fact that starvation causes a release of DHT which causes hirutism and baldness is especially revealing.

In such an instance it is the CHANGE up in the level of DHT in the body which causes the condition.

Thereby, one can really conclude that there has been an increase in DHT which the biochemistry (body) of that specific individual is not comfortable with.

Essentially, what needs to be done is to cut down DHT whilst maintaining normal T levels. This is why drugs such as Dutasteride and Finasteride work. Unfortunately, they cut it down TOO much and cause feminising side-effects.

Basically, what the body needs to do is find out its ideal natural resting level of DHT. It can do this by making the appropriate changes to the diet as can be explained/deciphered in the following two links:

http://www.mesomorphosis.com/articles/i ... iet-01.htm

http://www.mesomorphosis.com/articles/i ... diet02.htm

^^^
All the science is in the footnotes to those links.

It would appear that the macronutrient breakdown is of particular importance.

 

[bubka]

I think I pretty much understand baldness now.

The fact that starvation causes a release of DHT which causes hirutism and baldness is especially revealing.

In such an instance it is the CHANGE up in the level of DHT in the body which causes the condition.

Thereby, one can really conclude that there has been an increase in DHT which the biochemistry (body) of that specific individual is not comfortable with.

Essentially, what needs to be done is to cut down DHT whilst maintaining normal T levels. This is why drugs such as Dutasteride and Finasteride work. Unfortunately, they cut it down TOO much and cause feminising side-effects.

Basically, what the body needs to do is find out its ideal natural resting level of DHT. It can do this by making the appropriate changes to the diet as can be explained/deciphered in the following two links:

http://www.mesomorphosis.com/articles/i ... iet-01.htm

http://www.mesomorphosis.com/articles/i ... diet02.htm

^^^
All the science is in the footnotes to those links.

It would appear that the macronutrient breakdown is of particular importance.

well good luck with all that then, write back when you are a NW7

 

[Old Baldy]

Bubka, Bubka, Bubka - :lol: :lol: :shock:

You have to admit though that a lousy diet might play a role in male pattern baldness for some guys. I don't think it's a major player but WTF do I really know!? :lol:

You know, we have always heard about Japanese men experiencing more baldness once switching to a Western diet. That might be due to bad blood vessel health developing, like Doctor Proctor stated in a quote I pasted from alt.baldspot, rather than from the direct effect of cooking oil consumption on androgen levels?

(I mean is a 12 percent reduction in T going to make that much of a difference? I wouldn't think so but WTF do I really know? Why would that decrease in T reduce the amount of DHT in our bodies? Guys taking finasteride., reduce DHT production and the body compensates by making more T. Why not the opposite if T is reduced? Bryan?)

Btw, Bryan thanks for answering my questions in a previous post. I thought 5AR enzymes came from one chromosome.

Either way, lousy diets can't help IMHO. It just makes sense to me what Doctor Proctor said. Keep your blood vessels healthy, it can only help.

I mean we all know that consuming too much cooked oil ain't good for our overall health. And that's more important to me than male pattern baldness.

DLM my brother, who was a NW7 by 30 years old does eat worse than me. I just have a real hard time believing his diet is the reason my balding was MUCH less severe and occurred MUCH later in life. But like I said previously, WTF do I really know!

 

[docj077]

Ah one more thing docj since I have your attention. Do you think from what you know that 5ar2 inhibition is safe long term? Do you think the hormone changes like higher T, higher E are safe? It crosses blood brain barrier, and was originally intended for cancer as you know. Im just curious what you think of its safety.

???

5AR inhibitors weren't originally designed for cancer. They do not demonstrate any effect in androgen sensitive cancers as far as know. Chemical castration or surgery are usually the only true remedies in such situations.

The long term effects of 5AR inhibition are not known, but their use really has no health benefits, either. They are efficacious when used in benign prostate hyperplasia, but the periurethral region that this disease impacts is not the same region in which prostate cancer develops (peripheral). However, I would not rule out the fact that 5AR inhibitors prevent the conversion of progesterone to dihydroprogesterone as being a negative side effect. Afterall, dihydroprogesterone is a neuroactive steriod.

 

[Old Baldy]

But Doctor, how do you explain the 25 percent reduction in prostate cancer for men using finasteride? (You know the study I'm talking about.)

I'm NOT talking about high-grade prostate cancer.

 

[docj077]

But Doctor, how do you explain the 25 percent reduction in prostate cancer for men using finasteride? (You know the study I'm talking about.)

I'm NOT talking about high-grade prostate cancer.

25% reduction in androgen sensitive prostate cancer or an overall reduction?

 

[Old Baldy]

But Doctor, how do you explain the 25 percent reduction in prostate cancer for men using finasteride? (You know the study I'm talking about.)

I'm NOT talking about high-grade prostate cancer.

25% reduction in androgen sensitive prostate cancer or an overall reduction?

Overall reduction is how I remember it going.

 

[docj077]

[quote="Old Baldy":31ae9]But Doctor, how do you explain the 25 percent reduction in prostate cancer for men using finasteride? (You know the study I'm talking about.)

I'm NOT talking about high-grade prostate cancer.

25% reduction in androgen sensitive prostate cancer or an overall reduction?

Overall reduction is how I remember it going.[/quote:31ae9]

Hell of a question. I have no idea how a decrease in DHT can prevent the formation of non-hormone dependent prostate cancer.

All that I know is that BPH does not lead to prostate cancer.

 

[DammitLetMeIn]

I think I pretty much understand baldness now.

The fact that starvation causes a release of DHT which causes hirutism and baldness is especially revealing.

In such an instance it is the CHANGE up in the level of DHT in the body which causes the condition.

Thereby, one can really conclude that there has been an increase in DHT which the biochemistry (body) of that specific individual is not comfortable with.

Essentially, what needs to be done is to cut down DHT whilst maintaining normal T levels. This is why drugs such as Dutasteride and Finasteride work. Unfortunately, they cut it down TOO much and cause feminising side-effects.

Basically, what the body needs to do is find out its ideal natural resting level of DHT. It can do this by making the appropriate changes to the diet as can be explained/deciphered in the following two links:

http://www.mesomorphosis.com/articles/i ... iet-01.htm

http://www.mesomorphosis.com/articles/i ... diet02.htm

^^^
All the science is in the footnotes to those links.

It would appear that the macronutrient breakdown is of particular importance.

well good luck with all that then, write back when you are a NW7

how about you actually read whats in those two links. it tells you how diet relates to DHT and how it is the bioavailability of testosterone which is impt.


Read this and tell me it isn't relevant:

Given the variety of diets that people follow and the variety of prescription medications and over-the-counter drugs people take, the logical progression was to look at how altering the macronutrient composition of the diet affected drug metabolism. It turns out that a higher ratio protein diet, a diet with more calories from protein than carbohydrates or fat, metabolizes some drugs faster, thus decreasing the clearance time of the drug. Since diet can affect drug metabolism, perhaps it could affect liver enzymes involved in the metabolism of endogenous steroids. Sure enough, it was found that a high ratio protein diet decreased the reduction of T (14). Reducing the reduction of T could mean a potential decrease in DHT and/or androsterone in the blood, which is good by most accounts. However, DHT levels were not measured and, more importantly, urinary T excretion increased, although it was not statistically significant. These subjects were not in ketosis, so perhaps ketones do not increase T excretion rates. Regardless of the exact mechanism, there is sufficient evidence in the literature that when protein intake exceeds carbohydrate intake, T clearance increases by excretion in the urine.

A cross over design study used seven normal men from 23-43 years of age and compared a high protein diet to a high carbohydrate diet (15). This study has been referenced many times and cited as proof that high protein diets lower total T levels in the blood. The high carbohydrate diet from this study will be covered in Part II. The high protein diet consisted of 44% protein, 35% carbohydrate, and 21% fat and supplied between 2400 and 2500 kilocalories per day (kcals/d). Let’s assume it was an even 2450 kcals/d. The men also had bodyweights that ranged from 64-72 kg. If we assume the mean was 68 kg, then this would give us an average body weight of about 150 pounds. This means these guys were eating [(2450 kcals/d times .44) (divide by 4)] 270 grams (g) of protein, [(2450 x.350 /4] 215 g of carbohydrates (CHO) and [(2450 x .21) /9] 58 g of fat per day.

However, total T is not that big of a deal. The more important measure is the bioactive fraction of T. (Earlier in the overview of the HPT Axis, it was mentioned that SHBG-bound T is not considered bioactive, while the other fractions of T are). While subjects followed the high protein diet, their total T levels were 28% lower than on the higher CHO diet (15). This is important because T decreased in all seven subjects, although the magnitudes of the decrease ranged from 10 to 93%. For the same seven subjects, their SHBG levels decreased about 39% with a range from 19 to 64%. Looking at this data gives the impression that the actual bioactivity of T was higher while the subjects were on a high protein diet. SHBG-bound T and fT were not measured, so it is not known for sure. On the surface it appears that a mean decrease of 39% in the SHBG values and only a 28% in the T would leave more T available for binding to tissues. However, if we calculate out the actual changes in the hormones using the data from the study, we see something different. The mean and standard error (M±SE) for T was 371 ± 23 ng/dL. The currently used units in clinical chemistry are nmol/L. Multiplying the mean T by the conversion factor of 0.0347 gives us about 12.9 ± .8 nmol/L. The M±SE SHBG was 23.4 ± 1.6 nmol/L. If we assume that the amount of T bound to SHBG averages 44%, then .44 x 12.9 ± .8 nmol/L gives us 5.7 ± .4 nmol/L of T bound to SHBG. That leaves 7.2 ± .4 nmol/L of T to interact with tissues in the body. However, we don’t know from the data if the amount of SHBG bound T decreased below or increased above the normal 44%, in which case there would be more or less T available to interact with tissues.

From work by the same group of researchers using the exact same diet (but different subjects) we see that the ratio of 5a - reduction to 5b - reduction (5a /5b ) of T is reduced by about 50%, with the decrease being attributed to lower rates of 5a - reduction (14). The T values that have been used thus far (15) already reflect any changes in altered T metabolism, so the conversion to a 5a - reduced hormone (ie androsterone) is accounted for at this point. Note that even though there is a decrease in 5a - reduced hormone production, it does not show up as increased T levels. The decrease in androsterone probably shows up in small, but statistically insignificant increases in other metabolites of T (they were statistically insignificant perhaps due to the small sample size). Another interesting aspect is that there is an increase in the oxidation of estradiol on the higher protein diet by about 14-15% (14). Unfortunately estradiol levels were not measured in this paper. This could have given us clues as to the mechanism by which higher protein diets lower T (ie increased negative feedback on T levels via estradiol). At this point, this is only one study and it is still difficult to come to any final conclusions. However, if this is what really happens, then a high-protein diet may actually lower the anabolic actions of T in the body. Unfortunately, this has not been verified through laboratory research and is just a theory at this point. Perhaps the decrease in T is a result of increased excretion in the urine either as T or a sulfated metabolite, or increased conversion to estradiol and oxidation by the liver.

 

[bubka]

as i said, good luck with that then