So... which stress response hormone increases the enzymes responsible for hair loss?

I am starting to agree that it's a stress response hormone that causes MPB.

So in my case with Candidiasis, my gut got distressed and perhaps this increased serotonin which increases... I believe ACTH and/or CRH... basically it all stimulates the HPA axis as a stress-coping mechanism and probably a hormone that's part of this increases the enzymes that produce more DHT in places like the hair follicles, prostate etc, and side effects to all this are MPB, BPH, annoying amounts of body hair, etc.

This would explain why my MPB started suddenly in the same WEEK that my IBS went from very mild (almost undetectable) to pretty bad.

The question therefore is which hormone is responsible for increasing those enzymes. ACTH? CRH? Serotonin? Cortisol? Something else?

Knowing is half the battle and while in the long run fixing the gut is the best solution, in the short term it might be beneficial to calm down the stress response and/or target the problematic hormone.

The enzymes it increases are numerous I think and include 5ar2.

So... do we wanna pin down this sucker?

Hoppi!

Hoppi,

If I were to tell you it was ACTH specifically, which in all likelihood it would be, as it is what signals the adrenal production of cortisol, that still probably wouldn't be of much use for you. Its not that we want to shut down our stress response, but eliminate what is promoting it.

That is unless you are dealing with a situation where you are producing too much due to some kind of tumor, whether it be pituitary or some ectopic tumor. But those conditions present with some very, very recognizable symptoms and you'd know something was wrong. Cushings is a good approximation.

But then there is the issue of the endocrine system of the skin, which CS posted about recently. If high ACTH were present along with high levels of 11b-HSD in the skin, it could create cycle of excess cortisol in the skin.

anthonyspencer54 wrote:Hoppi,

If I were to tell you it was ACTH specifically, which in all likelihood it would be, as it is what signals the adrenal production of cortisol, that still probably wouldn't be of much use for you. Its not that we want to shut down our stress response, but eliminate what is promoting it.

That is unless you are dealing with a situation where you are producing too much due to some kind of tumor, whether it be pituitary or some ectopic tumor. But those conditions present with some very, very recognizable symptoms and you'd know something was wrong. Cushings is a good approximation.

But then there is the issue of the endocrine system of the skin, which CS posted about recently. If high ACTH were present along with high levels of 11b-HSD in the skin, it could create cycle of excess cortisol in the skin.

I know, and I did say this in my initial post that in the long term the solution is to fix the underlying problem (for example Candidiasis).

I just thought if we could specify hormones we might be in a better position to quick fix it or progress in general.

Danny Roddy has some great stuff though on calming the GI system by eating easily digestible foods. Perhaps this is a good quick fix, as even if for example the Candida is still there, by eating easily digestible and gut-friendly foods we can stop the digestive system releasing as much of the hormone which triggers the stress response (be it serotonin or whichever one it is...).

I might try that, as it seems logical enough in the mean time before I get rid of Candidiasis.

I just think that understanding the EXACT hormonal chain is a very good idea!

For example serotonin -> ACTH -> increase of enzymes -> DHT -> hair loss

That would be great and we would understand things far more specifically.

There is a chance of course that, say, serotonin AND CRH both increase ACTH, but that's ok, we can just acknowledge that too

EDIT -- To be honest, if simply keeping the gut calm with things like more easily digestible foods as a method of reducing the hormonal trigger is an option, then one would imagine that manually reducing the stress response at a similarly early point is... most likely fine. I certainly think there is a good chance that manually lowering as a temporary solution it is completely safe and possibly even healthy. But that requires more research to make a call one way or the other

No I understand, and being that the gut is a major , if not one of the most major, sources of stress hormones it would probably be a big step to reducing stress there. The chain is probably highly complex but oversimplifying it would look like:

CRH > ACTH > Cortisol (adrenal)
[In order to produce cortisol requires several different enzymes that convert the steroids down that particular pathway, some of the same enzymes that also interact to produce testosterone and DHT. Logically, if a stress response is upregulating the production of cortisol we could probably expect an increase in DHT, not to mention DHT seems to be upregulated anyway during times of cellular stress in a direct way as well]

In the kidney and liver: Cortisol via 11b-HSD1 > cortisone

In the liver, adipose, nervous system, and skin: cortisol via 11b-HSD2 > cortisol

For Serotonin:
L-tryptophan via tryptophan hydroxylase > 5-hydroxytryptophan via dopa decarboxylase > serotonin

So you can see just how complex the issue becomes when you have different organs that will differentially express the 11b-HSD (1 and 2) enzyme. That makes it difficult to control and problems with these organs or just genetic variation could mean someone has vastly different levels in different tissues, especially the skin.

Sreotonin acts down a different pathway entirely that seems to be produced during periods of stress and inflammation. Many things can increase tryptophan hydroxylase.

Why is it that no matter how out of wack our bodies are, that we don't lose hair on the sides of our heads?

Why is it that Placebo reduces scalp DHT levels by 15%, but not serum levels.

...That reducing scalp muscle tension arrests it?

That damn question.

But I do agree there is something that must explain it, and the studies you've posted recently do a good job of showing hypoxia induces DHT. There's definitely something to that.

anthonyspencer54 wrote:That damn question.

But I do agree there is something that must explain it, and the studies you've posted recently do a good job of showing hypoxia induces DHT. There's definitely something to that.

LOL

SlowMoe wrote:Why is it that no matter how out of wack our  bodies are, that we don't lose hair on the sides of our heads?

Why is it that Placebo reduces scalp DHT levels by 15%, but not serum levels.

...That reducing scalp muscle tension arrests it?

Because only the galea is affected negatively by the hormonal/enzymatic shift due to lessened bloodflow o.O

anthonyspencer54 wrote:No I understand, and being that the gut is a major , if not one of the most major, sources of stress hormones it would probably be a big step to reducing stress there. The chain is probably highly complex but oversimplifying it would look like:

CRH > ACTH > Cortisol (adrenal)
[In order to produce cortisol requires several different enzymes that convert the steroids down that particular pathway, some of the same enzymes that also interact to produce testosterone and DHT. Logically, if a stress response is upregulating the production of cortisol we could probably expect an increase in DHT, not to mention DHT seems to be upregulated anyway during times of cellular stress in a direct way as well]

In the kidney and liver: Cortisol via 11b-HSD1 > cortisone

In the liver, adipose, nervous system, and skin: cortisol  via 11b-HSD2 > cortisol

For Serotonin:
L-tryptophan via tryptophan hydroxylase > 5-hydroxytryptophan via dopa decarboxylase > serotonin

So you can see just how complex the issue becomes when you have different organs that will differentially express the 11b-HSD (1 and 2) enzyme. That makes it difficult to control and problems with these organs or just genetic variation could mean someone has vastly different levels in different tissues, especially the skin.

Sreotonin acts down a different pathway entirely that seems to be produced during periods of stress and inflammation. Many things can increase tryptophan hydroxylase.

Wow that's fascinating.. do you think the DHT increase is accidental? o.O

And yeah I just meant that if a tablet or something could calm the stress response manually then we could halt hair loss in the drop of a hat, and then later focus on the gut!

I think DHT could be directly and indirectly increased by stress. Indirect because of the cross-functionality of the enzymes, and directly because certain kinds of stress (general and mitochondrial hypoxia) raise DHT. Its really about a ratio of the hormones. Slowmoe has posted a few studies showing the detrimental effects of DHT in the scalp tend to happen when the ratio of DHT to estradiol is too high.

As far as a one-size fits all tablet solution. That one will be tough, being that stress can come from so many different angles. I am a broken record with this by now but we have to address stress at the macro and micro level: cellular, tissues/organs, and entire organism. We have to acknowledge the entire biological and psychological experience of the person.

For me a big part is the mitochondria and membrane integrity. If you look at the body like one big cell, then the gut showcases the importance of membrane integrity. As another example, hypoxia in the scalp (thanks to Slowmoe again) is another tissue level stress that is implicated in hair loss. We also have to factor in psychological stress and that also means addressing the psychosocial variables. As you can well imagine, this entire picture can be totally different from person to person.

What makes me wanna pull my hair out  is that stress at each level can promote or increase stress at each other level. Psychological stress which increases the stress hormones will have an indirect effect on things due to the inflammatory and anti-metabolic nature of the stress hormones. Stress at the level of the mitochondria could lead to psychological stress if it promotes insulin resistance and blood sugar problems.

Hoppi,

As I'm having trouble answering your specific question, I guess my question to you would be where you want to put your focus. Ultimately it requires a total body strategy, but again the profile of stress can be different from person to person. You could choose to place your focus on very specific things and see how you do. Honestly, if you ask me what is going to have the biggest bang for the buck (and not including the use of drugs), it would be to reduce hypoxia in the scalp, use natural substances to try to promote a better DHT:Estradiol ratio (in lieu of drugs), heal the gut and remove all offending foods, balance the gut microflora, optimize oxidative respiration, lower the amount of substrate that leads to inflammatory products, lower psychological stress and try to reduce total levels of stress hormones through all of the aforementioned.

Neuropeptides. 1993 Sep;25(3):161-7.
The effect of salt-loading on corticotropin releasing hormone and arginine vasopressin mRNA levels in the mouse hypothalamus: a quantitative in situ hybridization analysis.
Tracer HL, Loh YP.

Section on Cellular Neurobiology, National Institutes of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892.

Previously, we showed that during salt-loading in mice there was an acute rise in plasma ACTH levels after 2 days followed by a transient decrease after 4 and 9 days. Pro-opiomelanocortin (POMC) mRNA levels in the anterior pituitary increased after 2 days and returned to normal thereafter. In this study, changes in hypothalamic CRH and AVP mRNA levels during salt-loading were investigated using quantitative in situ hybridization histochemistry. CRH mRNA was expressed only in the paraventricular nucleus (PVN), while AVP mRNA was expressed in both the supraoptic (SON) and paraventricular nuclei. CRH mRNA levels were unchanged after 2 days salt-loading, but declined to 77% of control levels after 9 days. AVP mRNA levels rose to 260% and 634% of control levels in the SON, and to 352% and 522% of control levels in the PVN, after 2 and 9 days salt-loading, respectively. These data suggest a major role of AVP in the acute stimulation of ACTH secretion and POMC mRNA levels seen after 2 days salt-loading. Desensitization of AVP receptors at the corticotroph level and a centrally mediated inhibition of CRH release may account for the decrease of ACTH secretion and POMC mRNA levels in the anterior pituitary with prolonged salt-loading.

Incidentally, it has been shown that increased salt (via a 5% hypertonic saline injection) actually increases the stress markers in diabetics. I'm trying to connect this to oxidative cellular stress. It would appear that when oxidative stress is present (like in diabetics), ACTH response is actually higher. I'm trying to put together some research on this, but it looks like the mechanism is through the mineralcorticoid receptor and aldosterone. The mineralcorticoid receptor complex in the brain is actually inflammatory and increases NADPH oxidase, a huge player in vascular endothelial oxidative stress and for athersclerosis. Trying to connect the dots between the glucocorticoids, mineralcorticoids, stress, and the mitochondria is complex.

As a note, an NADPH inhibitor apocynin has been shown to reduce several of the negative effects of increased ACTH. Vanillin (synthetic form is vanilla extract that we use for flavoring) is the structural analogue of apocynin and has been shown to reduce these effects also.

I believe progesterone actually works to inhibit this as well, and a progesterone derivative used in certain contraceptives is even more effective. As a side effect they tend to mildly anti-androgenic, which is curious to me too as it tends to suggest a connection between this pathway and the androgens. I've got so many questions marks to get answered now...

anthonyspencer54 - Yes, with diabetics it's a little different...mainly because they have a nutrient wasting disease that tends to dump potassium, magnesium and some B-vitamins. Also, diabetics (type II) are normally sedentary who do not lose a lot of sodium through sweating. Of course the ones that do will balance blood sugar better.

In other words, salt sensitive people tend to be diabetic.

Endocrinology. 1994 Sep;135(3):1171-7.
Histaminergic activation of the hypothalamic-pituitary-adrenal axis.
Kjaer A, Larsen PJ, Knigge U, Warberg J.

Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark.

Centrally administered histamine (HA) stimulates the secretion of adenohypophysial POMC-derived peptides, which subsequently cause release of corticosterone. The effect of HA on POMC-derived peptide release is indirect, and it is possible that hypothalamic neurons containing corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), or oxytocin (OT) are involved in the mediation of this response. We studied the effect of HA on: 1) expression of CRH, AVP, and OT messenger RNA (mRNA) at the hypothalamic level; 2) expression of c-fos and POMC mRNA at the pituitary level; and 3) peripheral plasma levels of AVP, OT, ACTH, beta-endorphin (beta-END), and corticosterone. HA (270 nmol) infused intracerebroventricularly increased the expression of CRH, AVP, and OT mRNA in the paraventricular nucleus as well as that of OT mRNA in the supraoptic nucleus of the hypothalamus. At the pituitary level the expression of mRNA for c-fos and POMC increased in the anterior but not in the intermediate lobe in response to HA. Plasma levels of AVP, OT, ACTH, beta-END, and corticosterone all increased in response to central HA administration. Circulating levels of AVP and OT peaked after 5 min, ACTH and beta-END after 15 min, whereas corticosterone levels were highest after 30 min. In concert with our earlier discoveries, the present data support the hypothesis that HA-induced secretion of ACTH and beta-END is mediated via central activation of hypothalamic neuroendocrine neurons containing CRH, AVP, and/or OT.

Do we have studies showing the levels of various relevant enzymes in the presence of hormones like ACTH?

I'm trying to work out a way to calm down the HPA axis manually. I mean if one can do it by doing little more than calming down the digestive tract, it really can't be that difficult or risky.

So... wait...

The entire stress response starts with CRH... right?

http://en.wikipedia.org/wiki/Corticotropin-releasing_hormone

"CRH is secreted by the paraventricular nucleus (PVN) of the hypothalamus in response to stress."

It seems that serotonin simply increases due to a distressed gut and then this increases CRH and that kicks off the whole HPA axis.

http://www.jneurosci.org/content/27/26/6956.short
(Serotonin Activates the Hypothalamic–Pituitary–Adrenal Axis via Serotonin 2C Receptor Stimulation)

EDIT -- Hm, worked in mice...

http://www.diennet.com/hair_brochure.pdf (see the study they talk about and quote)

Hm, and lo and behold my IBS made me run to the loo again!

So that's serotonin amiright?

BAD serotonin! Triggering the HPA axis and making my hair fall out!

Serotonin... y u do dis? >.<

lol

Hoppi, you are certifiable haha.

Have you gotten a diagnosis of IBS? I'm just asking out of curiosity. If your IBS has certain triggers, serotonin could certainly be implicated. But then again, diarrhea could have several causes. Sodium intake, or even certain minerals. If I get too much magnesium is one sitting, I get diarrhea without question. Just suggesting other possible causes. What do you suspect are the triggers for your IBS?

anthonyspencer54 wrote:Hoppi, you are certifiable haha.

Have you gotten a diagnosis of IBS? I'm just asking out of curiosity. If your IBS has certain triggers, serotonin could certainly be implicated. But then again, diarrhea could have several causes. Sodium intake, or even certain minerals. If I get too much magnesium is one sitting, I get diarrhea without question. Just suggesting other possible causes. What do you suspect are the triggers for your IBS?

erm, yeah doctors just call it IBS. I think my gut is just sensitive due to what I perceive to be Candidiasis

It's sensitive to lots of things like eggs, lactose, acidic foods, starch etc.

Also I don't have diarrhea... well, not unless I eat foods that really disagree with me like mayonnaise, but I never eat them anyway

Its funny, the foods I tend to be the most sensitive are those same foods. A history of lactose intolerance runs in the family, as does celiac.

There are a few things that can lead to those symptoms that aren't always candida related (not saying you absolutely don't have it, just suggesting some alternatives for you to research):

Small Intestinal Bacterial Overgrowth (SIBO); since doing a 4 week course of antibiotics a lot of my general GI distress has completely disappeared (symptoms are general bloating especially after meals, gas, abdominal distension) This condition, as well as the presence of H Pylori can reduce stomach acid and cause you to not digest food properly and when some sugars (lactose) get further into the intestine they cause reactions. (Betaine HCL can help) There are often skin manifestations too, particularly with H Pylori, things like eczema, rosacea or psoriasis. Hydrogen breath test can identify if this is the culprit.

A general gut flora imbalance could result in these symptoms also.

Perhaps you have an undiagnosed food allergy. Have you gotten tested for this?

I'd get tested for food allergies and also get the hydrogen breath test for SIBO.

I think a lot of people on this forum confuse symptoms of IBS with Candidiasis. Candida is most likely the culprit for your sub-optimal digestion. In my case, my digestion was always excellent even when under Candida, the problems started happening when I started chelating and taking anti-candida supplements then my digestion went out of whack. If not for this forum, I would be treating IBS purely based on the symptoms, but I'm 100% positive that's it's the candida that's messing everything apart.

anthonyspencer54 wrote:Its funny, the foods I tend to be the most sensitive are those same foods. A history of lactose intolerance runs in the family, as does celiac.

There are a few things that can lead to those symptoms that aren't always candida related (not saying you absolutely don't have it, just suggesting some alternatives for you to research):

Small Intestinal Bacterial Overgrowth (SIBO); since doing a 4 week course of antibiotics a lot of my general GI distress has completely disappeared (symptoms are general bloating especially after meals, gas, abdominal distension) This condition, as well as the presence of H Pylori can reduce stomach acid and cause you to not digest food properly and when some sugars (lactose) get further into the intestine they cause reactions. (Betaine HCL can help) There are often skin manifestations too, particularly with H Pylori, things like eczema, rosacea or psoriasis. Hydrogen breath test can identify if this is the culprit.

A general gut flora imbalance could result in these symptoms also.

Perhaps you have an undiagnosed food allergy. Have you gotten tested for this?

I'd get tested for food allergies and also get the hydrogen breath test for SIBO.

I do have a lot of Candida symptoms (that aren't common symptoms of SIBO), however peroxide kills all bacterial and fungal infections along with their biofilms (and parasites don't like it at all either, or viruses) AFAIK, so I don't think it really matters which one(s) I have!

hoppipolla wrote:
I do have a lot of Candida symptoms (that aren't common symptoms of SIBO), however peroxide kills all bacterial and fungal infections along with their biofilms (and parasites don't like it at all either, or viruses) AFAIK, so I don't think it really matters which one(s) I have!

Hoppy H2O2 is a strong compound. You shouldn't just play with hydrogen peroxide. If you really believe H2O2 can help you, buy good quality unheated honey. Honey has enzymatic and H2O2 action. To ensure you do not lose these benefits of honey, do not mix honey in foods and drinks above 40-45 deg C, and do not dilute it too much in water. Rest you can look up with the help of google and nsa.

9rugrats5 wrote:

hoppipolla wrote:
I do have a lot of Candida symptoms (that aren't common symptoms of SIBO), however peroxide kills all bacterial and fungal infections along with their biofilms (and parasites don't like it at all either, or viruses) AFAIK, so I don't think it really matters which one(s) I have!

Hoppy H2O2 is a strong compound. You shouldn't just play with hydrogen peroxide. If you really believe H2O2 can help you, buy good quality unheated honey. Honey has enzymatic and H2O2 action. To ensure you do not lose these benefits of honey, do not mix honey in foods and drinks above 40-45 deg C, and do not dilute it too much in water. Rest you can look up with the help of google and nsa.

I'm happy with peroxide for now (I researched it a lot)

However I'm very interested in the potential of enzymes like nattokinase and serrapeptase to remove biofilms too - I'm researching that!