Do you think it's possible I just had an increase in DHT? Simple as?

Because at the same time as I started having the stomach cramps and the bad skin change, whatever caused all this, I had a noticeable increase in body hair that has progressed ever since. And as my body hair has increased, my scalp hair has decreased.

Surely the only other explanation is that my body's RESPONSE to DHT has somehow become more sensitive, like the amount of DHT hasn't increased, but it's just reacting to it more. Is that possible?

Either way, you can see we I am opting for a DHT-lowering regimen and looking into an s-equol supplement...

Would be interested to hear your responses to this

Hoppi!

Hoppipolla wrote:Because at the same time as I started having the stomach cramps and the bad skin change, whatever caused all this, I had a noticeable increase in body hair that has progressed ever since. And as my body hair has increased, my scalp hair has decreased.

Surely the only other explanation is that my body's RESPONSE to DHT has somehow become more sensitive, like the amount of DHT hasn't increased, but it's just reacting to it more. Is that possible?

Either way, you can see we I am opting for a DHT-lowering regimen and looking into an s-equol supplement...

Would be interested to hear your responses to this

Hoppi!

Hoppi, your focus should be on free-testosterone, not DHT. You can inhibit DHT all day long, but if you do nothing to decrease free-testosterone, you will never really be solving the real-problem (low-SHBG). Try increasing SHBG and IGFBP's and lowering estrogen levels, then combat the inflammation (often caused by body-fat), fungus (Malassezia-furfur) and remove “build-up” on scalp (Dr. Bronners Magic Soap and scalp-exfoliation). Also don’t forget to reverse the “big-three” diseases associated with MPB; atherosclerosis, diabetes/insulin-resistance and prostate-enlargement.

misterE wrote:

Hoppipolla wrote:Because at the same time as I started having the stomach cramps and the bad skin change, whatever caused all this, I had a noticeable increase in body hair that has progressed ever since. And as my body hair has increased, my scalp hair has decreased.

Surely the only other explanation is that my body's RESPONSE to DHT has somehow become more sensitive, like the amount of DHT hasn't increased, but it's just reacting to it more. Is that possible?

Either way, you can see we I am opting for a DHT-lowering regimen and looking into an s-equol supplement...

Would be interested to hear your responses to this

Hoppi!

Hoppi, your focus should be on free-testosterone, not DHT. You can inhibit DHT all day long, but if you do nothing to decrease free-testosterone, you will never really be solving the real-problem (low-SHBG). ctions. I am sad to say I have , then combat the inflammation (often caused by body-fat), fungus (Malassezia-furfur) and remove “build-up” on scalp (Dr. Bronners Magic Soap and scalp-exfoliation). Also don’t forget to reverse the “big-three” diseases associated with MPB; atherosclerosis, diabetes/insulin-resistance and prostate-enlargement.

How does one do that?

Does not make sense to me. I have low T, lower Free T and am still prone to hairloss. If I increase SHBG, it will further reduce my Free T and I wll feel crap(per).

lund wrote:Does not make sense to me. I have low T, lower Free T and am still prone to hairloss. If I increase SHBG, it will further reduce my Free T and I wll feel crap(per).

SHBG has a receptor! Increasing SHBG will snatch up free-testosterone and prevent it from converting to estrogen in DHT keeping nice and bound to the SHBG-receptor... thus increasing your total-amount of testosterone.

Lambaugh wrote:

How does one do that?

The best way to increase SHBG is to increase IGFBP's (preferably IGFBP-3) because free-IGF-1 is the most powerful inhibitor of SHBG in the body! The quickest way to do that is to stay far away from dairy-products because the concentrated protein in milk is a massive stimulator of free-IGF-1 and this should come as no surprise considering milks role is to grow a calf into a steer. This is the main reason why dairy consumption is associated with cancer of the breast and prostate, besides the saturated-fat which ups the estrogen and insulin levels.

Next, decrease all animal-protein. Vegans are shown in numerous studies (which I can post for you if you would like) to have much higher SHBG and a much lower FAI, and higher IGFBP's. Animal-protein (and plant-protein to a much lesser extent) directly decreases SHBG.

Then I would limit fats and oils because they desensitize your sensitivity to insulin. Leaving sugar and insulin in the blood which both lowers SHBG. High-fat diets increases estrogen and the estrogens compete with testosterone (for SHBG), which is a fat-burning and insulin-sensitizing hormone, opposite of estrogen.

Getting rid of processed-food is a given.

Dietary-fiber is shown to correlate with higher SHBG levels and so does fasting, protein-restriction and aerobic-exercise. Certain foods also directly increase SHBG like green-tea, flaxseeds and other phytoestrogen-rich foods. Vegetable consumption is associated with higher levels of SHBG and conversely with red-meat or milk consumption.

Hope this helps.

Why not just test your SHBG and TT?

You don't want SHBG to be high or low...

Thyroid hormone t3 will increase T3

SHBG around 20-25 is good

i mean t3 will increase SHBG

blackjack wrote:i mean t3 will increase SHBG

I think optimizing thyroid function is the best way to increase SHBG. Eating wild caught fish and sea weed along with what mistere adovcates will definitely increase SHBG.

Hoppi - Using finasteride or other chemical DHT blockers is an invitation to disaster.

If one measures their DHT levels on finasteride, they will vary. And they will vary dramatically even up to 2 years post finasteride cessation.

In my opinion, the worst thing someone can do is to experiment with a lot of methods in an ultra short period of time, because to see a result takes a very long time.

Homeostasis (balance the body seeks) can take a while. When a drug is introduced, results are vary hard to predict.

I want to second what CS says about giving treatments time. It's rare for a supplement or regimen to give me instant relief. It's a gradual process that takes time, experimentation and a calm spirit to combat the tendency to panic. It's all about staying cool.

CausticSymmetry --

While DHT is not the sole culprit in hair loss, what do you recommend for younger people who want to block DHT "naturally"?

I mean the thing is, something fairly core must have changed in my body to suddenly start me losing hair and growing more body hair.. you know?

I mean, I've been eating junky food on and off since like.. well, for as long as I could open my mouth! lol

So.. you know and inflammation.. that hasn't suddenly come along in the last year.

So something must have fundamentally changed in my body that is upsetting my scalp hair. So... is it not feasible that I simply have more DHT in me now, which is upsetting my scalp?

Hm, I read somewhere that the trigger for increased DHT is an enlarged prostate O.O

I also read that it's estrogen, all this jazz O.O

Truth is, I do think I have an increase but.. I am fascinated to learn _why_ - and of course different people say different things so it's hard to know who to believe ._.

That's why often I just opt for the equol route, and leave it there lol.

The enlarged prostate idea.. that makes a kind of sense doesn't it? It explains the predictable loss of hair as we age. I dunno ._.

http://wiki.answers.com/Q/What_causes_increase_in_DHT_levels - is this true or nonsense? O.O

Hoppi, your focus should be one controlling IGF-1. When IGF-1 is "free" it affects hormonal-homeostasis in the body in a very negative way. Free-IGF-1 is shown to increase 5-alpha-reductase, lower SHBG, stimulate the production of testosterone, increase testosterone conversion, activate the androgen-receptor, stimulate lipogenesis of the sebaceous glands, over stimulate keratinocyte proliferation and enlarge the sebaceous glands (and prostate). So my advice to you and every one reading this is to: attack the very top of the "chain of command" not the bottom. Why combat DHT when the reason you have excess DHT in the first place is due to low levels of IGFBP-3?

Hoppi please read this link, I think this will answer many of your questions. http://www.canibaisereis.com/download/milk-consumption-acne.pdf

Hm

I mean erm, to be honest even though I do find myself swaying recently towards the more mainstream HLT way of thinking, I am very drawn in and interested by people like you misterE who say you have had such success without needing to use treatments. I am just wary of having my hair dictate my lifestyle _too_ much, as I like having a bit of freedom to live how I would like hehe

I will read that pdf and do some catching up soon I think!

Hoppi - Prostate enlargement occurs due to too much estrogen (in most cases).

We do not see young men with BPH, but we do see older men with it.

Estrogen depresses testosterone levels and when this happens, the body produces more DHT to compensate.

I've always been curious about that. Main stream thinking says that the opposite occurs. When the body sense high estrogen, it decreases LH and consequently testosterone. My thinking is that while this does happen, estradiol causes androgen receptors to become more sensitive to the effects of DHT. Also while estradiol may lower testosterone levels, it does not stop the remaining testosterone from converting to DHT. I believe some of the beneficial 2 hydroxy estradiol metabolites inhibit 5ar.

Hm. On HLT the conclusion was largely reached that a change takes place in the way the follicles react to the DHT not in 5ar expression or receptor numbers but within the mechanism itself, which would explain why pre-MPB follicles don't always react to androgens yet they do when they're older and the change has happened. I dunno how true that is but it does seem to reflect a fair amount I've observed.

Ugh man I wish I knew what caused this change in me ._.

Yeah and I think it's elevated estradiol that causes the upregulation of androgen receptors to occur. If you look at the prostate for example, it won't enlarge without adequate estradiol. Same thing could be said about the macqaues (sp?). Juvenile macqaues haven't been exposed to large amounts of estradiol (or DHT) so their follicles don't respond to androgens while adult macques have.

Honestly I think your best bet Hoppi is to lower estradiol WITHOUT inhibiting aromatase. If you lower estradiol without affecting aromatase, DHT will also go down. I think phytoestrogens are the best way to do this.

Hm

Have you controlled your loss yet?

What are the best phytoestrogens? o.O

Oh, you mean like HMR lignans?

Estradiol Activates the Prostate Androgen Receptor and Prostate-specific Antigen Secretion through the Intermediacy of Sex Hormone-binding Globulin.


Abstract.

These experiments were designed to examine the relationship between the effects of steroid hormones mediated by classic intracellular steroid hormone receptors and those mediated by a signaling system subserved at the plasma membrane by a receptor for sex hormone-binding globulin. It is known that unliganded sex hormone-binding globulin (SHBG) binds to a receptor (RSHBG) on prostate membranes. The RSHBG·SHBG complex is rapidly activated by estradiol to stimulate adenylate cyclase, with a resultant increase in intracellular cAMP. In this paper we examine the effect of this system on a prostate gene product known to be activated by androgens, prostate-specific antigen. In serum-free organ culture of human prostates, dihydrotestosterone caused an increase in prostate specific antigen secretion. This event was blocked by the anti-androgens cyproterone acetate and hydroxyflutamide. In the absence of androgens, estradiol added to prostate tissue, whose RSHBG was occupied by SHBG, reproduced the results seen with dihydrotestosterone. Neither estradiol alone nor SHBG alone duplicated these effects. The estradiol·SHBG-induced increase in prostate-specific antigen was not blocked by anti-estrogens, but was blocked both by anti-androgens and a steroid (2-methoxyestradiol) that prevents the binding of estradiol to SHBG. Furthermore, an inhibitor of protein kinase A prevented the estradiol·SHBG-induced increase in prostate-specific antigen but not that which followed dihydrotestosterone. These data indicate that there is a signaling system that amalgamates steroid-initiated intracellular events with steroid-dependent occurrences generated at the cell membrane and that the latter signaling system proceeds by a pathway that involves protein kinase A.

Hoppipolla wrote:Oh, you mean like HMR lignans?

Phytoestrogens are found in all plant-based foods and are absent in animal-products (meats, dairy, eggs, etc.) and processed-foods (coconut-oil, Oreo-cookies, chips, Gatorade, brownies, etc.). The best source of phytoestrogens is, hands down, ground flaxseeds or flax-meal.

A plant-based-diet rich in fruit, vegetables, legumes, whole grains and flaxseed-meal will provide you with plenty of phytoestrogens, which will save you money on unneeded supplements.

misterE wrote: In the absence of androgens, estradiol added to prostate tissue, whose RSHBG was occupied by SHBG, reproduced the results seen with dihydrotestosterone. Neither estradiol alone nor SHBG alone duplicated these effects. The estradiol·SHBG-induced increase in prostate-specific antigen was not blocked by anti-estrogens, but was blocked both by anti-androgens and a steroid (2-methoxyestradiol) that prevents the binding of estradiol to SHBG.

Ketoconazole inhibition of testicular secretion of testosterone and displacement of steroid hormones from serum transport proteins.


Abstract.

In vivo perfusion of canine testes with ketoconazole inhibited the stimulation of testosterone production by human chorionic gonadotropin in a dose-dependent manner. Ketoconazole also selectively displaced steroids from serum-binding globulins. Dihydrotestosterone and estradiol binding to sex hormone-binding globulin were inhibited by ketoconazole. Cortisol binding to corticosteroid-binding globulin was unaffected. The concentrations of ketoconazole that inhibited human chorionic gonadotropin stimulation of testicular androgen production and displaced sex steroids from sex hormone-binding globulin were in the range of blood levels found in patients on higher therapeutic dosage regimens. Suppression of testicular testosterone synthesis and displacement of estrogens from sex hormone-binding globulin may decrease the androgen/estrogen ratio of the blood and contribute to the development of gynecomastia that has been reported in some ketoconazole-treated patients.