Flaxseeds, & other potential ways of "balancing" hormones :)

[47thin]

Who are these people who have no stress? How can I join this leisure class? Almost 80 % of the country is in bad shape, one way or another, financially, but you don't see a bunch of bald people.

I saw an article that said they found some 3000 year old mans corpse, up in Iceland. He was thought to be in his late 20's/ early 30's- and he had the baldness gene. No preservatives, no post modern stress, etc, but he still had hairloss.

Honestly, we all want to keep it, but hair is, in terms of modern survival, pretty low on the whole scale of necessities to get by. You can still find a mate, food, everything else, without it. You can reproduce, live to a nice old age, etc.

 

[OverMachoGrande]

Who are these people who have no stress? How can I join this leisure class? Almost 80 % of the country is in bad shape, one way or another, financially, but you don't see a bunch of bald people.

People handle stress differently.

I saw an article that said they found some 3000 year old mans corpse, up in Iceland. He was thought to be in his late 20's/ early 30's- and he had the baldness gene. No preservatives, no post modern stress, etc, but he still had hairloss.

But we weren't there to see his lifestyle, there could have been numerous other factors pertaining to hair loss, and that's usually how hair loss works.

 

[LewdBear]

They do, here are a few,

Why are you selectively citing symptoms of Cushing's Syndrome? We're talking about healthy people.

Let's understand something as one big happy group, male pattern baldness, is associated with heart disease, enlarged prostate and diabetes, and these conditions are linked to unnatural hormone levels, (I think that's what male pattern baldness has a basis around, something about too much DHT, but hey, who knows..., elevated blood pressure and high LDL, low HDL, can easily result in free-radicals morphing LDL into arterial plaque.

What the association is remains unclear. A lot of people have this idea that male pattern baldness is frequently part of a larger syndrome, and I fail to understand why.

There is obviously a subset of individuals who, for reasons yet unknown, experience premature balding and insulin resistance, heart disease etc. I've already provided a possible explanation why. But you have chosen to ignore it in favor of this 'male pattern baldness is a commonly part of a metabolic syndrome' idea.

http://www.articlesbase.com/health-arti ... 48622.html

There's a link

That website appears to let anyone submit an article.

If that is the quality of evidence you plan on producing, I'm through debating with you.

Take a look at viewtopic.php?f=32&t=57572

I do a step by step review on exactly what happens there.

I asked for references, not a link to your other thread. I'm not concerned with your hypotheses, but rather supporting evidence.

I don't know dude, seems pretty obvious to me.

That's because you accept your about.com reference without question. I don't.

So here is a challenge..

If psychosocial stress-related cortisol elevations are a well-known common cause of all of those things in otherwise healthy people (without medically elevated levels of cortisol), it shouldn't be hard to find other medical sources which support that.

I want to see supporting evidence from a mainstream medical/science or journal site (Elsevier, ScienceDirect, Nature.com, WebMD, BMJ etc.). Alternatively, references to studies indexed by pubmed or offline journal references are acceptable. I will not accept or debate any articles from non-medical sources, non-doctors or non-scientists.

There is one caveat, however. In some cases there can be something known as "subclinical cushing's" (although this condition is still somewhat controversial.) It means that someone has medically elevated cortisol without other features of Cushing's.

For example this editorial on cortisol and osteoporosis (http://www.annals.org/content/147/8/I-48.full) :

"219 people referred to 2 medical centers for osteoporosis testing. Most participants were women."
[...]
"Seven apparently healthy people with osteoporosis had high cortisol levels. None of the people without osteoporosis had high levels. All 7 people with high levels had tumors that increased the levels."

That would not constitute 'evidence' of healthy people, with normal cortisol levels, being 'stressed out' to the point of having osteoporosis.

Occult or single symptom conditions with elevated cortisol are therefore excluded.

 

[Hoppi]

Who are these people who have no stress? How can I join this leisure class? Almost 80 % of the country is in bad shape, one way or another, financially, but you don't see a bunch of bald people.

People handle stress differently.

[quote:xru4o691]I saw an article that said they found some 3000 year old mans corpse, up in Iceland. He was thought to be in his late 20's/ early 30's- and he had the baldness gene. No preservatives, no post modern stress, etc, but he still had hairloss.

But we weren't there to see his lifestyle, there could have been numerous other factors pertaining to hair loss, and that's usually how hair loss works.[/quote:xru4o691]

Plus, some people it is just triggered by age, IMO. It seems to be triggerable by many things

 

[Bryan]

Some hormones such as DHT (and later estrogen) it is useful to lower more drastically in order to help control and stop male pattern baldness...

Are you saying you think that estrogen contributes to male pattern baldness?

 

[Hoppi]

Some hormones such as DHT (and later estrogen) it is useful to lower more drastically in order to help control and stop male pattern baldness...

Are you saying you think that estrogen contributes to male pattern baldness?

No, I probably don't think it does personally, I'm just saying that it might be helpful to later lower estrogen to limit side effects of drugs like Finasteride.

 

[OverMachoGrande]

Why are you selectively citing symptoms of Cushing's Syndrome? We're talking about healthy people.

:shock: ?!

You said...,

[/quote]

Also, do you not find it slightly weird that this hypothesized 'stress-induced' mild hypercortisolism would be so selective in its symptoms?

Cushing's Syndrome, for example, can cause a moon face, buffalo hump (non-HIV-ARV related lipodystrophy) and purpura.

Why would people under chronic stress not experience mild versions of these symptoms as well?

Then I said...,

They do, you idiolog, I gave you many different, non-'selective' symptoms, moron, take a look, and read the words,

Stress does not have to only have a few selective outputs.

They do, here are a few,

https://health.google.com/health/ref/Cushing+syndrome,

Men may have:
Decreased fertility
Decreased or no desire for sex
Impotence

Other symptoms that may occur with this disease:
Mental changes, such as depression, anxiety, or changes in behavior
Fatigue
Headache
High blood pressure
Increased thirst and urination

These are MILD VERSIONS of your full out "Cushings Symdrome", WHICH PEOPLE UNDER STRESS, WOULD BE SUFFERING FROM, if YOUR IDEA that Cortisol, HAS to be linked to Cushing's symdorme,

What I am telling you, and what everyones mom, and grandmother knows.

stress causes illness, stress is bad, :nono:

OMG REALLY??! NO WAY!!! EVER NOTICED PEOPLE THAT ARE CONSTANTLY STRESSED GET SICK EASIER, ARE ON EDGE, LOSE HAIR?!

Anyone who has any idea about hair loss understands stress can be a cause.

"Oh no, but stress is okay!" "Heart attacks are good for you!"
"Cortisols great!" "Are car keys the same?"

Are you insane?

Go ask your mom, if stress will cause hair loss. WHAT I'M HELPING YOU LEARN, IS INCREASED CORTISOL DOESN'T HAVE TO LEAD TO CUSHING SYNDROME.

THE ACTION OF STRESS, INCREASE CORTISOL, AMONG OTHER HORMONES, OVER-WORKS THE LIVER AND HEART, AND IS UNHEALTHY IN EXCESS.

Any doctor can EASILY grasp this, and tell you THE SAME THING.

I learned this in elementary school, but you're claiming stress can't hurt people, and can't lead to MANY problems in the body. Are you out of your mind?

What the association is remains unclear. A lot of people have this idea that male pattern baldness is frequently part of a larger syndrome, and I fail to understand why.

Because the health of your hair, is an indicator of overall health in the body, AT LEAST referring to the health of those epithelial cells.

That website appears to let anyone submit an article.

If that is the quality of evidence you plan on producing, I'm through debating with you.

Lol, if you 'being like Bryan' ironically, are going to ignore comments I made back, taking them out of context, then your a waste of air.

What is this, 1984?, an Orwellian nightmare?

I'll tell you when I'm done debating with you.

I asked for references, not a link to your other thread. I'm not concerned with your hypotheses, but rather supporting evidence.

Oh, okay

J Eur Acad Dermatol Venereol. 2009 Jun;23(6):673-7. Epub 2009 Feb 24.
Is androgenetic alopecia a risk for atherosclerosis?
Dogramaci AC, Balci DD, Balci A, Karazincir S, Savas N, Topaloglu C, Yalcin F.
Department of Dermatology, Faculty of Medciine, Mustafa Kemal University, Hatay, Turkey. catahan85@yahoo.com
BACKGROUND: Several studies have demonstrated the presence of an association between androgenetic alopecia (Androgenetic Alopecia) and cardiovascular disease. The aim of this study was to evaluate subclinical atherosclerosis in patients with Androgenetic Alopecia and healthy controls by the incorporation of carotid intima-media thickness (IMT) and high-sensitive C-reactive protein (hs-CRP) along with echocardiography (ECHO) and exercise electrocardiography (ExECG). METHODS: We performed a case-control study in 50 male patients with Androgenetic Alopecia and 31 age-matched healthy male controls with normal hair status. Both the Androgenetic Alopecia patients and controls with a history of diabetes mellitus, cigarette smoking, hypertension, cardiovascular or cerebrovascular disease, and renal failure were excluded. Androgenetic Alopecia was classified according to the Hamilton-Norwood scale. Serum lipids, serum hs-CRP, total testosterone, and dehydroepiandrosterone sulphate were examined in all study subjects. Carotid ultrasonography was used to measure the IMT of the common carotid arteries (CCA). ECHO and ExECG were performed in all subjects. RESULTS: IMT of the CCA was found to be significantly higher in patients with severe vertex pattern Androgenetic Alopecia when compared to patients with other patterns of Androgenetic Alopecia and healthy controls (P < 0.05). Hs-CRP in patients with any group of Androgenetic Alopecia was not significantly different from those healthy controls (P > 0.05). ECHO showed that cardiac structural and functional measures were in normal ranges. ExECG was also normal in all subjects. CONCLUSION: Severe vertex pattern Androgenetic Alopecia should be considered to have an increased risk of subclinical atherosclerosis. For this reason, CCA IMT measurement can be recommended as a non-invasive and early diagnostic method.


Clin Endocrinol (Oxf). 2009 Oct;71(4):494-9.
Androgenetic alopecia and insulin resistance in young men.
González-González JG, Mancillas-Adame LG, Fernández-Reyes M, Gómez-Flores M, Lavalle-González FJ, Ocampo-Candiani J, Villarreal-Pérez JZ.
Servicio de Endocrinologia, Dr Jose Eleuterio Gonzalez University Hospital, Facultad de Medicina, Universidad Autonoma de Nuevo Leon, Ave. Madero y Gonzalitos S/N, Monterrey, Mexico. jgonzalezg@fm.uanl.mx
BACKGROUND: Epidemiological studies have associated androgenetic alopecia (Androgenetic Alopecia) with severe young-age coronary artery disease and hypertension, and linked it to insulin resistance. We carried out a case-control study in age- and weight-matched young males to study the link between Androgenetic Alopecia and insulin resistance using the homeostasis model assessment of insulin resistance (HOMA-IR) index or metabolic syndrome clinical manifestations. METHODS: Eighty young males, 18-35 years old, with Androgenetic Alopecia > or = stage III in the Hamilton-Norwood classification, and 80 weight- and age-matched controls were included. Alopecia, glucose, serum insulin, HOMA-IR index, lipid profile and androgen levels, as well as metabolic syndrome criteria, were evaluated. RESULTS: The HOMA-IR index was significantly higher in cases than controls. Nonobese cases had a higher mean diastolic blood pressure and a more frequent family history of Androgenetic Alopecia than nonobese controls. A borderline difference in the HOMA-IR index was found in obese Androgenetic Alopecia cases vs. obese controls [P = 0.055, 95% confidence interval (CI) 2.36-4.20 vs. 1.75-2.73]. Free testosterone values were significantly higher in controls than cases, regardless of body mass index (BMI). A statistically significant additive effect for obesity plus alopecia was found, with significant trends for insulin, the HOMA-IR index, lipids and free testosterone when BMI and alopecia status were used to classify the participants. CONCLUSIONS: Our results support the recommendation for assessing insulin resistance and cardiovascular-related features and disorders in all young males with stage III or higher Androgenetic Alopecia, according to the Hamilton-Norwood classification.
PMID: 19094069 [PubMed - indexed for MEDLINE]



Endocr Regul. 2005 Dec;39(4):127-31.
Premature androgenic alopecia and insulin resistance. Male equivalent of polycystic ovary syndrome?
Starka L, Duskova M, Cermakova I, Vrbiková J, Hill M.
Institute of Endocrinology, Narodni 8, CZ 116 94 Prague 1, Czech Republic. lstarka@endo.cz
BACKGROUND: Polycystic ovary syndrome (PCOS), the most frequent endocrinopathy in women with estimated prevalence of 5-10 %, is characterised by a hormonal and metabolic imbalance of polygene autosomal trait. The complexity of symptoms and genetic base started up the hypothesis on the existence of male equivalent of PCOS. Precocious loss of hair before 30 years of age was suggested as one of the male symptoms of this syndrome. OBJECTIVES: The aim was to confirm the association of lower levels of follicle stimulating hormone (FSH) and sexual hormone binding globulin (SHBG) or higher free androgen index (FAI) in premature balding men with a reduced insulin sensitivity. PATIENTS/METHODS: The study included 30 men with premature hair loss (defined as grade 3 vertex or more on the alopecia classification scale by Hamilton with Norwood modification) starting before 30 years of age. The hormonal values of the investigated group were compared with those regarded as normal reference values obtained in a group of 256 males in the age of 20-40 years during the Czech population study of iodine deficiency. In all men with premature baldness besides hormonal level determinations insulin tolerance test was carried out. RESULTS: The observed group was divided into two subgroups. The first one showed similar hormonal changes as women with PCOS, namely subnormal SHBG, FSH or increased FAI. The other had either no anomalies in steroid spectrum or only lower SHBG. The groups did not differ either in BMI or in age. The group with hormonal profile resembling that of women with PCOS, showed significantly higher insulin resistance than the group without these changes. CONCLUSIONS: The findings are consistent with the hypothesis that at least a part of the men with premature androgenic alopecia could be considered as a male equivalent of the polycystic ovary syndrome of the women. These premature balding men represent a risk group for the development of impaired glucose tolerance or diabetes mellitus type 2.




Lancet Oncol. 2007 Jan;8(1):21-5.
Effect of 1 mg/day finasteride on concentrations of serum prostate-specific antigen in men with androgenic alopecia: a randomised controlled trial.
D'Amico AV, Roehrborn CG.

Department of Radiation Oncology, Brigham and Women's Hospital and Dana-Faber Cancer Institute, Boston, MA 02215, USA. adamico@lroc.harvard.edu
Comment in:

Nat Clin Pract Urol. 2007 Aug;4(8):412-3.
Lancet Oncol. 2007 Feb;8(2):94-5.
Lancet Oncol. 2007 Jan;8(1):4-5.
BACKGROUND: Use of 5 mg/day finasteride (Proscar) for benign prostatic hyperplasia is known to affect serum concentrations of prostate-specific antigen (PSA). When men taking this treatment undergo screening for prostate cancer, a compensatory adjustment of the PSA concentration (to multiply the value by two) is recommended. Whether this recommendation should apply to men taking 1 mg/day finasteride (Propecia) for the treatment of androgenic alopecia is unknown. We aimed to assess the effect of 1 mg/day finasteride on serum PSA in men aged 40-60 years with male-pattern hair loss. METHODS: Between March 13, 1998, and Jan 12, 2000, 355 men aged 40-60 years with male-pattern hair loss were stratified by age decade (40-49 years and 50-60 years), and randomised in a ratio of four to one to 1 mg/day finasteride or placebo. The primary endpoint was the effect of this treatment for 48 weeks on serum PSA concentration compared with placebo. This trial is in the process of being registered on the US National Institutes of Health website . Analyses were according to protocol. FINDINGS: Within 48 weeks of randomisation, men aged 40-49 years and 50-60 years who were assigned 1 mg/day finasteride had a median decrease in serum PSA concentration of 40% (95% CI 34-46) and 50% (44-57), respectively. In men assigned placebo, the median changes were 0% [-14 to 14] and a median increase of 13% [2 to 24], respectively. INTERPRETATION: In men aged 40-60 years, 1 mg/day finasteride for 48 weeks lowers serum PSA concentration. Therefore, the existing recommendation for the adjustment of serum PSA concentration in prostate-cancer screening in men taking 5 mg/day finasteride should also apply to men taking the 1 mg/day preparation for male-pattern hair loss. Research is needed to assess the effect of 1 mg/day finasteride preparation beyond 48 weeks of treatment.

PMID: 17196507 [PubMed - indexed for MEDLINE]


The evidence is over-whelming that these 3 diseases are associated with male pattern baldness.

That's because you accept your about.com reference without question. I don't.

No, you fool, this is common knowledge, if you're going to waste my time with defending stress, then I'm done educating you.

There is one caveat, however. In some cases there can be something known as "subclinical cushing's" (although this condition is still somewhat controversial.) It means that someone has medically elevated cortisol without other features of Cushing's.

For example this editorial on cortisol and osteoporosis (http://www.annals.org/content/147/8/I-48.full) :

"219 people referred to 2 medical centers for osteoporosis testing. Most participants were women."
[...]
"Seven apparently healthy people with osteoporosis had high cortisol levels. None of the people without osteoporosis had high levels. All 7 people with high levels had tumors that increased the levels."

That would not constitute 'evidence' of healthy people, with normal cortisol levels, being 'stressed out' to the point of having osteoporosis.

Occult or single symptom conditions with elevated cortisol are therefore excluded.

This study had to do with osteoporosis, I don't care about osteoporosis, at least mine was more prevalent with wound healing.

And this was mainly about women with osteoporosis, wow....

No, the only thing excluded is your mind numbing way of obviously dodging the fact that stress kills.

Now, I'm done educating you, if you have any more questions if cortisol and stress kills, go ask your doctor or mommy, Shills.

 

[Hoppi]

No, you fool, this is common knowledge, if you're going to waste my time with defending stress, the I'm done educating you.

Quote of the thread? lol

 

[OverMachoGrande]

Some hormones such as DHT (and later estrogen) it is useful to lower more drastically in order to help control and stop male pattern baldness...

Are you saying you think that estrogen contributes to male pattern baldness?

No Way, excess estrogen in the body produces more Testosterone to compensate for the imbalance?? What?!

Uh-oh Bryan, looks like people are starting to learn more than what your company wants them to.

Hey, by the way, I was thinking back on my form, when I told you I'd need to see a document signed and dated by Merck & Company, regarding if Propecia was created with male pattern baldness in mind, and is not an accidental discovery.

Did you get the document I ordered you to get?

I mean, Dr. Fromme and you shouldn't have to much of a problem having the company tell the TRUTH, and get you that paper, I mean, they wouldn't have any issue, unless it wasn't TRUE, right...?

Besides it would make their shriveling drug look at least a little better, wouldn't it?

 

[Hoppi]

Psst! Justin! Finasteride is the most successful male pattern baldness treatment of all time!



Oh, and does Bryan actually work for them (Merck & Company)? O.O

 

[OverMachoGrande]

Psst! Justin! Finasteride is the most successful male pattern baldness treatment of all time!



Oh, and does Bryan actually work for them (Merck & Company)? O.O

You don't say?

Nat Prod Res. 2009 Sep 16:1-12. [Epub ahead of print]
Effect of Citrullus colocynthis Schrad fruits on testosterone-induced alopecia.
Dhanotia R, Chauhan NS, Saraf DK, Dixit VK.
Department of Pharmaceutical Sciences, Dr H.S. Gour Vishwavidyalaya, Sagar, India.
Alopecia is a psychologically distressing phenomenon. Androgenetic alopecia (Androgenetic Alopecia) is the most common form of alopecia, which affects millions of men and women worldwide, and is an androgen driven disorder. Here, the Citrullus colocynthis Schrad fruit is evaluated for hair growth activity in androgen-induced alopecia. Petroleum ether extract of C. colocynthis was applied topically for its hair growth-promoting activity. Alopecia was induced in albino mice by testosterone administration intramuscularly for 21 days. Its inhibition by simultaneous administration of extract was evaluated using follicular density, anagen/telogen (A/T) ratio and microscopic observation of skin sections. Finasteride (5alpha-reductase inhibitor) solution was applied topically and served as positive control. Petroleum ether extract of C. colocynthis exhibited promising hair growth-promoting activity, as reflected from follicular density, A/T ratio and skin sections. The treatment was also successful in bringing a greater number of hair follicles in anagenic phase than the standard finasteride. The result of treatment with 2 and 5% petroleum ether extracts were comparable to the positive control finasteride. The petroleum ether extract of C. colocynthis and its isolate is useful in the treatment of androgen-induced alopecia.




J Cosmet Dermatol. 2008 Sep;7(3):199-204.
Effect of Cuscuta reflexa Roxb on androgen-induced alopecia.
Pandit S, Chauhan NS, Dixit VK.
Department of Pharmaceutical Sciences, Dr. Harisingh Gour University, Sagar, Madhya Pradesh, India.
BACKGROUND: Alopecia is a psychologically distressing condition. Androgenetic alopecia, which affects millions of men and women, is an androgen-driven disorder. Here, Cuscuta reflexa Roxb is evaluated for hair growth activity in androgen-induced alopecia. METHODS: Petroleum ether extract of C. reflexa was studied for its hair growth-promoting activity. Alopecia was induced in albino mice by testosterone administration for 20 days. Its inhibition by simultaneous administration of extract was evaluated using follicular density, anagen/telogen ratio, and microscopic observation of skin sections. To investigate the mechanism of observed activity, in vitro experiments were performed to study the effect of extract and its major component on activity of 5alpha-reductase enzyme. RESULTS: Petroleum ether extract of C. reflexa exhibited promising hair growth-promoting activity as reflected from follicular density, anagen/telogen ratio, and skin sections. Inhibition of 5alpha-reductase activity by extract and isolate suggest that the extract reversed androgen-induced alopecia by inhibiting conversion of testosterone to dihydrotestosterone. CONCLUSIONS: The petroleum ether extract of C. reflexa and its isolate is useful in treatment of androgen-induced alopecia by inhibiting the enzyme 5alpha-reductase.




J Altern Complement Med. 2002 Apr;8(2):143-52.
A randomized, double-blind, placebo-controlled trial to determine the effectiveness of botanically derived inhibitors of 5-alpha-reductase in the treatment of androgenetic alopecia.
Prager N, Bickett K, French N, Marcovici G.
Clinical Research and Development Network, Aurora, CO, USA.
Erratum in:
• J Altern Complement Med. 2006 Mar;12(2):199.
BACKGROUND: Androgenetic alopecia (Androgenetic Alopecia) is characterized by the structural miniaturization of androgen-sensitive hair follicles in susceptible individuals and is anatomically defined within a given pattern of the scalp. Biochemically, one contributing factor of this disorder is the conversion of testosterone (T) to dihydrotestosterone (DHT) via the enzyme 5-alpha reductase (5AR). This metabolism is also key to the onset and progression of benign prostatic hyperplasia (BPH). Furthermore, Androgenetic Alopecia has also been shown to be responsive to drugs and agents used to treat BPH. Of note, certain botanical compounds have previously demonstrated efficacy against BPH. Here, we report the first example of a placebo-controlled, double-blind study undertaken in order to examine the benefit of these botanical substances in the treatment of Androgenetic Alopecia. OBJECTIVES: The goal of this study was to test botanically derived 5AR inhibitors, specifically the liposterolic extract of Serenoa repens (LSESr) and beta-sitosterol, in the treatment of Androgenetic Alopecia. Subjects: Included in this study were males between the ages of 23 and 64 years of age, in good health, with mild to moderate Androgenetic Alopecia. RESULTS: The results of this pilot study showed a highly positive response to treatment. The blinded investigative staff assessment report showed that 60% of (6/10) study subjects dosed with the active study formulation were rated as improved at the final visit. CONCLUSIONS: This study establishes the effectiveness of naturally occurring 5AR inhibitors against Androgenetic Alopecia for the first time, and justifies the expansion to larger trials.





Biochem Pharmacol. 2002 Mar 15;63(6):1165-76.
Structure-activity relationships for inhibition of human 5alpha-reductases by polyphenols.
Hiipakka RA, Zhang HZ, Dai W, Dai Q, Liao S.
Department of Biochemistry and Molecular Biology, The Ben May Institute for Cancer Research, and The Tang Center for Herbal Medicine Research MC6027, University of Chicago, 5841 S. Maryland, Chicago, IL 60637, USA.
The enzyme steroid 5 alpha-reductase (EC 1.3.99.5) catalyzes the NADPH-dependent reduction of the double bond of a variety of 3-oxo-Delta(4) steroids including the conversion of testosterone to 5 alpha-dihydrotestosterone. In humans, 5 alpha-reductase activity is critical for certain aspects of male sexual differentiation, and may be involved in the development of benign prostatic hyperplasia, alopecia, hirsutism, and prostate cancer. Certain natural products contain components that are inhibitors of 5 alpha-reductase, such as the green tea catechin (-)-epigallocatechin gallate (EGCG). EGCG shows potent inhibition in cell-free but not in whole-cell assays of 5 alpha-reductase. Replacement of the gallate ester in EGCG with long-chain fatty acids produced potent 5 alpha-reductase inhibitors that were active in both cell-free and whole-cell assay systems. Other flavonoids that were potent inhibitors of the type 1 5alpha-reductase include myricetin, quercitin, baicalein, and fisetin. Biochanin A, daidzein, genistein, and kaempferol were much better inhibitors of the type 2 than the type 1 isozyme. Several other natural and synthetic polyphenolic compounds were more effective inhibitors of the type 1 than the type 2 isozyme, including alizarin, anthrarobin, gossypol, nordihydroguaiaretic acid, caffeic acid phenethyl ester, and octyl and dodecyl gallates. The presence of a catechol group was characteristic of almost all inhibitors that showed selectivity for the type 1 isozyme of 5 alpha-reductase. Since some of these compounds are consumed as part of the normal diet or in supplements, they have the potential to inhibit 5 alpha-reductase activity, which may be useful for the prevention or treatment of androgen-dependent disorders. However, these compounds also may adversely affect male sexual differentiation.
PMID: 11931850 [PubMed - indexed for MEDLINE]

Read it Bryan.
Medicine is moving passed the 80's.

 

[OverMachoGrande]

Oh yeah, in regards to stress;

Cleve Clin J Med. 2009 Jun;76(6):361-7.
Diffuse hair loss: its triggers and management.
Harrison S, Bergfeld W.
Department of Dermatology, Cleveland Clinic, Cleveland, OH 44195, USA.
Diffuse hair loss can affect both sexes at any age. Anything that interrupts the normal hair cycle can trigger diffuse hair loss. Triggers include a wide variety of physiologic or emotional stresses, nutritional deficiencies, and endocrine imbalances. Loss of telogen-phase hairs is the most common. Hair loss during the anagen phase is usually caused by chemotherapy or radiation therapy. Finding the cause, or trigger, of the hair loss requires a thorough history and examination and will enable appropriate treatment. Patient education is key in the management of diffuse hair loss.

Just thought I'd toss that in there for fun,

 

[LewdBear]

It seems you can't debate without degenerating into personal insults, Lord_Justin.

I will say that it is incredibly ironic that you used this study : "Premature androgenic alopecia and insulin resistance. Male equivalent of polycystic ovary syndrome?" This is precisely what I was talking about in my earlier messages. See what I said about the possibility of a male PCOS state causing some of the male pattern baldness/insulin/heart disease associations. The feinberg.edu editorial I cited strongly suggests that this is a genetic condition.

If the about.com article you cited was indeed "common knowledge," then you should have no problem providing other sources of that information. As I said, the article appears to cite only one study regarding wound healing so I have no way of knowing what those claims are based upon. If elevations of cortisol, within the medically normal range, were contributing to all of those diseases, it should be trivial to corroborate. Did pubmed go down just as you were replying to that part of my post?

 

[Cassin]

Lord_Justin13

Seriously...calm down or you will be removed....we try to keep things civilized here.

 

[OverMachoGrande]

J Pathol. 2009 Jan;217(1):73-82.
5alpha-dihydrotestosterone (DHT) retards wound closure by inhibiting re-epithelialization.
Gilliver SC, Ruckshanthi JP, Hardman MJ, Zeef LA, Ashcroft GS.
Faculty of Life Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK.
The ongoing search for explanations as to why elderly males heal acute skin wounds more slowly than do their female counterparts (and are more strongly disposed to conditions of chronic ulceration) has identified endogenous oestrogens and androgens as being respectively enhancers and inhibitors of repair. We previously demonstrated that blocking the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) limits its ability to impair healing, suggesting that DHT is a more potent inhibitor of repair than is testosterone. The present study aimed to delineate the central mechanisms by which androgens delay repair. Whilst the contractile properties of neither rat wounds in vivo nor fibroblast-impregnated collagenous discs in vitro appeared to be influenced by androgen manipulations, the global blockade of DHT biosynthesis markedly accelerated re-epithelialization of incisional and excisional wounds and reduced local expression of beta-catenin, a key inhibitor of repair. Moreover, DHT retarded the in vitro migration of epidermal keratinocytes following scratch wounding. By contrast, it failed to influence the migratory and proliferative properties of dermal fibroblasts, suggesting that its primary inhibitory effect is upon re-epithelialization. These novel findings may be of particular significance in the context of chronic ulceration, for which being male is a key risk factor.


This is in regards to wound healing and DHT...

 

[OverMachoGrande]

It seems you can't debate without degenerating into personal insults, Lord_Justin.

I will say that it is incredibly ironic that you used this study : "Premature androgenic alopecia and insulin resistance. Male equivalent of polycystic ovary syndrome?" This is precisely what I was talking about in my earlier messages. See what I said about the possibility of a male PCOS state causing some of the male pattern baldness/insulin/heart disease associations. The feinberg.edu editorial I cited strongly suggests that this is a genetic condition.

If the about.com article you cited was indeed "common knowledge," then you should have no problem providing other sources of that information. As I said, the article appears to cite only one study regarding wound healing so I have no way of knowing what those claims are based upon. If elevations of cortisol, within the medically normal range, were contributing to all of those diseases, it should be trivial to corroborate. Did pubmed go down just as you were replying to that part of my post?

You must be kidding,

That's cool. You should make the "Lord_Justin13" anxiety inventory.

If that is the quality of evidence you plan on producing, I'm through debating with you.

That's because you accept your about.com reference without question. I don't.

It seems you can't debate without degenerating into personal insults, Lord_Justin.

Yet, all of these comments are personal insults in which you use a degrading attitude, which is very Hippo-critical.

Every time you'd make snide comments, I was responding without insults, in an informative way, yet you continuously try to make people who disagree with you as if they don't have any validity in their remarks.

You're statement holds no ground, seeing as you were indeed committing these acts before me.

Anyways, did you even read the posts I made? Everyone knows stress = bad, that's just life, don't be upset at me, I didn't create it.

 

[OverMachoGrande]

From http://www.mayoclinic.com/health/stress/SR00001

Understanding the natural stress response
If your mind and body are constantly on edge because of excessive stress in your life, you may face serious health problems. That's because your body's "fight-or-flight reaction" — its natural alarm system — is constantly on.

When you encounter perceived threats — a large dog barks at you during your morning walk, for instance — your hypothalamus, a tiny region at the base of your brain, sets off an alarm system in your body. Through a combination of nerve and hormonal signals, this system prompts your adrenal glands, located atop your kidneys, to release a surge of hormones, including adrenaline and cortisol.

Adrenaline increases your heart rate, elevates your blood pressure and boosts energy supplies.
Cortisol, the primary stress hormone, increases sugars (glucose) in the bloodstream, enhances your brain's use of glucose and increases the availability of substances that repair tissues. Cortisol also curbs functions that would be nonessential or detrimental in a fight-or-flight situation. It alters immune system responses and suppresses the digestive system, the reproductive system and growth processes.
This complex natural alarm system also communicates with regions of your brain that control mood, motivation and fear.

Cortisol is the primary stress hormone

Mayo Clin Womens Healthsource. 2004 Sep;8(9):4-5.
Your adrenal glands. Vital for your good health.
[No authors listed]

You probably don't think much about your adrenal glands, possibly not even what they are or what they do. Although tiny, these glands produce hormones such as cortisol and adrenaline, which help regulate crucial body functions, including your reactions to stress.

The adrenal glands are in charge of producing Cortisol, which are connected to the kidneys, by over stressing the adrenal glands hurts kidney function as well. Kindeys are very important in Hair loss.


And, what's this, an article examining the relationship between stress and increased cortisol levels.

Encephale. 2002 Mar-Apr;28(2):139-46.
[Study of the stress response: role of anxiety, cortisol and DHEAs]
[Article in French]
Boudarene M, Legros JJ, Timsit-Berthier M.
Bat G, N 266, Cité Djurdjura, Ville Nouvelle, Tizi Ouzou 15010, Algérie, France.
AIM OF THE STUDY: Several studies have exhibited the psychological processes that are implied in the stress response and have shown, according to Selye's research, the participation of the hypothalamic-pituitary-adrenal axis and the major role of cortisol. The possible action of another adrenal steroïd, dehydroepiandrosterone (DHEA), is increasingly documented. The beneficial effect of the latter and his antistress role would be related to an antagonistic action to that of cortisol. The aim of our study was, first to assess biological and psychological aspects of the stress response, then to define the relationships that exist between these two processes. POPULATION AND METHODOLOGY: 40 subjects (21 women) aged 42 +/- 12 years, who consulted within a clinic of stress (CITES Prevert, Liege, Belgium) were studied. They all felt stressed but, according to DSM IV, were without mental disorders and drug free when examined. Subjects were asked to accomplish simple cognitive tasks: 1 - to distinguish two different auditory stimulations. The first one was a high-pitched sound of 1 470 Hz, which was presented unfrequently (20%). The second one, a low frequency tone of 800 Hz, was presented more frequently (80%). The interval between both stimuli was 1 s. The subject had to press a button when the rare stimulus was recognized. 2 - to extinguish a light after a warning tone of 64 dB, 50 ms and 1 000 Hz. The light, which followed one second later the tone, consisted of a series of flashes of 18 c/s that the subject had to stop by pressing a button. The purpose of this second procedure was that the subject was warned and had to prepare and anticipate the most rapid response. After that, subjects were submitted to self-evaluation psychological tests. The impact of psychosocial factors was assessed by Amiel-Lebigre life events questionnaire. Personality features and emotional response (state anxiety, related to experimental situation) were assessed by Spielberger inventory (STAI: State and Trait Anxiety Inventory). Psychological tests are practised immediately after experimental situation. Cortisol and DHEAs (dehydroepiandrosterone sulfate) were measured in blood samples taken before (t1) and after (t2) the experimental test. Cortisol was measured by radio-immunology and expressed as ng/ml of plasma. DHEAs was measured by radio-immunoassay and expressed as g/liter of plasma. RESULTS AND DISCUSSION: The majority of subjects displayed high scores of trait anxiety (37 subjects had a score>42) and life events impact (35 subjects had a score>200). These data confirmed that the subjects were fragile and were obviously stressed. In response to the cognitive tasks, that constituted for each subject a new event with which it was necessary to cope, 25 subjects exhibited high level of state anxiety (score>42) and an increase of cortisol plasmatic concentrations occurred solely in 11 persons. Ten among them were in the group of subjects which displayed a score of state anxiety>42 (p=0,0223, Chi square). Base on these data three types of stress response were identified: 1 - the experimental situation was experienced without anxiety ( psychological silence ) and without any increase in cortisol level ( biological silence ). There was no stress and these subjects were, despite their vulnerability, close to a normal health state . 2 - high emotional reaction (high level of state anxiety) was observed. This response reveals a psychological vulnerability that can be considered as the expression of a consecutive psychological distress induced by a threatening experimental situation. There were no biological manifestations ( biological silence ). 3 - high state anxiety and increased plasma cortisol levels were observed. The corresponding subjects were obviously more vulnerable. CONCLUSION: These results allow us to propose that the emergence of state anxiety is the first stress response and the primary protest . Up to a certain level, a plateau level, anxiety remains stable. Then, nature of the stress response changes and takes a biological aspect. Increased of cortisol plasma levels, the secondary protest , is observed and gives evidence of an intensified and sustained stress response. Such a gradual phenomenon is particularly reported in elevated psychological distress which is associated with loss of control. It is important to note that identical scores of state anxiety (Mann Whitney test) were observed in anxious subjects with or without rise of plasma cortisol levels. DHEAs was also implied in the stress response. The enhancement of plasma levels of DHEAs were dependent on cortisol, as shown by the close correlation between both hormones (r=0,433, p=0,0033, Spearman test). The hypothesis of an antagonism between these two hormones is based on the fact that DHEAs opposes the action of cortisol and exerts a true anticortisol effect. This antagonism might be related to a competition in their synthesis and release by the adrenal gland. In the present case, high level of anxiety (state and trait) was associated with an increase of cortisol, while low level (of anxiety) was related to an exclusive rise of DHEAs. Intermediate anxious score was observed in subjects who showed increases of both cortisol and DHEAs (p=0,0225, Kruskall Wallis test). Furthermore, a close relationship (negative correlation: Spearman test), was observed between increases in DHEAS and scores of state anxiety (r=- 0,382, p=0,06) and trait anxiety (r=- 0,0097, p=0,527). This means that the worriness and the underlying anxious ruminations and negative anticipations, which characterize trait anxiety, were less important in subjects who increased plasma DHEAs levels. In addition, emotional tension and uneasiness, which accompanies state anxiety, were also less marked. There are no studies reporting a relation between DHEA(s) and state or trait anxiety. Nevertheless, many authors have proposed a beneficial action of DHEA on the feeling of well-being. This beneficial role could be related to a double action of DHEA: a direct effect provided by its transformation into sexual hormones, an indirect one mediated by its competition with cortisol, of which the synthesis and consequently the activity decrease.


This is clear, for people in a state of anxiety, (Stress), have elevated Cortisol Levels.

Stress. 2008;11(3):177-97.
Impact of stressors in a natural context on release of cortisol in healthy adult humans: a meta-analysis.
Michaud K, Matheson K, Kelly O, Anisman H.

Department of Psychology, Carleton University, Ottawa, Ont., Canada.
Comment in:

Stress. 2009;12(5):464-5.
Increased hypothalamic-pituitary-adrenal (HPA) activation, culminating in elevated circulating cortisol levels is a fundamental response to stressors. In animals, this neuroendocrine change is highly reliable and marked (approximately 5-10-fold elevations), whereas in humans, the increase of cortisol release is less pronounced, and even some potent life-threatening events (anticipation of surgery) only elicit modest cortisol increases. Meta-analysis of factors that influenced the increase of cortisol release in a laboratory context pointed to the importance of social evaluative threats and stressor controllability in accounting for the cortisol rise. The present meta-analysis, covering the period from 1978 through March 2007, was undertaken to identify the factors most closely aligned with cortisol increases in natural settings. It appeared that stressor chronicity was fundamental in predicting cortisol changes; however, this variable is often confounded by the stressor type, the stressor's controllability, as well as contextual factors, making it difficult to disentangle their relative contributions to the cortisol response. Moreover, several experiential factors (e.g. previous stressor experiences) may influence the cortisol response to ongoing stressors, but these are not readily deduced through a meta-analysis. Nevertheless, there are ample data suggesting that stressful events, through their actions on cortisol levels and reactivity, may influence psychological and physical pathology.

And that finishes it, If you can provide any real data on stress not elevating cortisol, (from PubMed, or another credible medical journal) Then I might take a look at it, Thank you for your time.

 

[LewdBear]

Yet, all of these comments are personal insults in which you use a degrading attitude, which is very Hippo-critical.

Do you know what a personal insult is?

In none of those quotes am I saying things like "Are you stupid?" Are you insane?" "You are a moron?". Those are personal insult. It insults the person, not something they've posted.

If you had a problem with any of my posts, you could have (and still can) report them.

And that finishes it, If you can provide any real data on stress not elevating cortisol, (from PubMed, or another credible medical journal) Then I might take a look at it, Thank you for your time.

It's a question of quantity. It's whether or not such an elevation can be considered abnormal enough (if it is abnormal at all) to induce clinical symptoms.

 

[OverMachoGrande]

First, I want to note when you replied to the article I highlighted by Elizabeth Scott M.S.,

Since the article you linked only seems to cite one source (regarding wound healing), I cannot know what some of those claims are based on.

Now I'd like to take a look at who she is, exactly,

Elizabeth Scott

Elizabeth Scott, M. S. has spent years counseling, coaching and educating families on effective strategies to manage stress, maintain healthy relationships, and live a balanced lifestyle. She's been interviewed on national television and radio shows, and in national publications like USA Today, Woman's Day as well as CNN.com. She's written hundreds of articles on various aspects of stress management for About.com, which can be found at: http://stress.about.com.

The article is submitted shows the potential harm of cortisol.

Are suggesting a national icon in stress, who posts her articles on stress.about.com, (where I pulled the article from), Is not credible?

Cortisol can do everything the article claims in disease states where it is medically abormal.

That was referring to your mayoclinic article regarding "Women with osteoporosis" ...yea...

But then I found this article;

J Biochem Biophys Methods. 2002 Oct-Nov;53(1-3):123-30.
Urinary steroids in men with male-pattern alopecia.
Poór V, Juricskay S, Telegdy E.

Central Research Laboratory, Faculty of Medicine, Pécs University Medical School, 12Szigeti út, 1Honvéd u. H-7643 Pécs, Hungary. Viktoria.Poor@AOK.PTE.hu
Enzyme hydrolysis, solid phase extraction, methoxym-silyl derivatization and capillary gas chromatographic analysis were used to examine the changes in urinary steroid metabolites in men with androgenic alopecia. A total of 23 men with androgenic alopecia and 7 age-matched control healthy men collected 24-h urine. Significantly increased values were found in the metabolites of testosterone (T): androsterone (A) (p<0.02), and etiocholanolone (E) (p<0.05) in patients with androgenic alopecia, compared to the control values. Elevated levels of 16-hydroxy-dehydroepiandrosterone (16-OHD) (p<0.03) and cortisol (F) (P<0.05) were found, but the levels of cortisol metabolites were unchanged. Calculating the ratio of total 5 alpha/5 beta metabolites provided information on the activity of 5 alpha-reductase. The ratio of total 5 alpha/5 beta metabolites was increased in the patients showing the increased 5 alpha-reductase activity. The elevated 16-OHD level could be indicative of patients who had mild hyperadrenal activity.

Wait, mild hyper-adrenal activity, and they have hair loss... :agree:
AND their cortisol is higher...

Also, do you not find it slightly weird that this hypothesized 'stress-induced' mild hypercortisolism would be so selective in its symptoms?

I proved to you, in TWO other articles (out of the many I've brought to the table), from PubMed, that stress does increase cortisol, and it's variety in outlets can be many.

I then gave you the list of symptoms which the disease your referring to can also cause, when you said;

Why would people under chronic stress not experience mild versions of these symptoms as well?

~They do, here are a few,

https://health.google.com/health/ref/Cushing+syndrome,

Men may have:
Decreased fertility
Decreased or no desire for sex
Impotence

Other symptoms that may occur with this disease:
Mental changes, such as depression, anxiety, or changes in behavior
Fatigue
Headache
High blood pressure
Increased thirst and urination

and then you tell me;

Lord_Justin13 wrote:
They do, here are a few,


Why are you selectively citing symptoms of Cushing's Syndrome? We're talking about healthy people.

You are running in circles as if anything I say with awesome references are wrong?

and here's symptoms of Cushing's on Wiki;

In humans
Symptoms include rapid weight gain, particularly of the trunk and face with sparing of the limbs (central obesity). A common sign is the growth of fat pads along the collar bone and on the back of the neck (buffalo hump) and a round face often referred to as a "moon face". Other symptoms include hyperhidrosis (excess sweating), telangiectasia (dilation of capillaries), thinning of the skin (which causes easy bruising and dryness, particularly the hands) and other mucous membranes, purple or red striae (the weight gain in Cushing's syndrome stretches the skin, which is thin and weakened, causing it to hemorrhage) on the trunk, buttocks, arms, legs or breasts, proximal muscle weakness (hips, shoulders), and hirsutism (facial male-pattern hair growth), baldness and/or cause hair to become extremely dry and brittle. In rare cases, Cushing's can cause hypercalcemia, which can lead to skin necrosis. The excess cortisol may also affect other endocrine systems and cause, for example, insomnia, inhibited aromatase, reduced libido, impotence, amenorrhoea/oligomenorrhea and infertility due to elevations in androgens. Patients frequently suffer various psychological disturbances, ranging from euphoria to psychosis. Depression and anxiety are also common.[3]
Other striking and distressing skin changes that may appear in Cushing's syndrome include facial acne, susceptibility to superficial dermatophyte and malassezia infections, and the characteristic purplish, atrophic striae on the abdomen.[4]:500
Other signs include polyuria (and accompanying polydipsia), persistent hypertension (due to cortisol's enhancement of epinephrine's vasoconstrictive effect) and insulin resistance (especially common in ectopic ACTH production), leading to hyperglycemia (high blood sugar) which can lead to diabetes mellitus. Untreated Cushing's syndrome can lead to heart disease and increased mortality. Cushing's syndrome due to excess ACTH may also result in hyperpigmentation, such as acanthosis nigricans in the axilla. This is due to Melanocyte-Stimulating Hormone production as a byproduct of ACTH synthesis from Pro-opiomelanocortin (POMC). Cortisol can also exhibit mineralcorticoid activity in high concentrations, worsening the hypertension and leading to hypokalemia (common in ectopic ACTH secretion). Furthermore, gastrointestinal disturbances, opportunistic infections and impaired wound healing (cortisol is a stress hormone, so it depresses the immune and inflammatory responses). Osteoporosis is also an issue in Cushing's syndrome since, as mentioned before, cortisol evokes a stress-like response. Consequently, the body's maintenance of bone (and other tissues) becomes secondary to maintenance of the false stress response. Additionally, Cushing's may cause sore and aching joints, particularly in the hip, shoulders, and lower back.

Elevated stress and cortisol does all of this, you can't turn from the evidence.

First you ask me, if my idea is weird because because your idea of stress can only lead to Cushing's Syndrome, I defended my initial knowledge of stress increasing cortisol, (I later cited PubMed).

Then you ask me if it's weird that mild stress/cortisol wouldn't exhibit similar features as the the symtoms you selected(Cushing's Syndrome, for example, can cause a moon face, buffalo hump (non-HIV-ARV related lipodystrophy) and purpura.
, but oddly these symptoms on wiki, and more on this link of cushing's do the things I've said, and more, it causes these three diseases I've noted, and many other problems.

http://www.google.com/imgres?imgurl...39&w=300&sz=68&tbnid=pLQceXxiH9jadM:&tbnh=12

Source: U.S. National Library of Medicine & National Institutes of Health

I don't know how much more blatant it can be!

I cited the symptoms, then ask why im citing selected examples of cushings syndrome, when I answered is it weird that mild stress/cortisol wouldn't exhibit similar features as the symptoms you selected, but those aren't the only symptoms, especially if it's mild, let alone it doesn't even have to be cushings, its elevated cortisol were are talking about. And even then!!, these same fats on the body, and other problems, among other main symptoms being listed under the link, are the diseases I mentioned, baldness, and more, cushings is another problem causing hair loss, I DID NOT KNOW THIS!

This proves the validity of everything I said!

All of these symptoms and it's a disease based on a hormone imbalance, just like male pattern baldness

As far as I'm concerned (and any sane human being reading this), this is another valid reason that bridges the gap further than what I knew before, stress, it's release of Cortisol, all tie into hormonal issues, and heart problems, and insulin resistance/diabetes, inflammation, BALDNESS, this cushings is a far advanced disease as is from insane amounts of cortisol over such a long period of time, causing elevated blood suger, and blood pressure, and all of these sick symptoms.

That thing you mentioned the study of women and osteoporosis, it also states;

Osteoporosis is also an issue in Cushing's syndrome since, as mentioned before, cortisol evokes a stress-like response. Consequently, the body's maintenance of bone (and other tissues) becomes secondary to maintenance of the false stress response

Simply going 'OMG I'm stressed!!' is not medically meaningful.

Yes it is, stress and cortisol release over and over is very much medically meaningful, it's too much for the body, it is not designed to live under and tear conditions 24/7.

Lord_Justin13 wrote:
Psychological stress, is much more important than people think, as soon as your brain is taxed this way, your opening a flood gate of potential disasters to your entire system.


You are now making very vague claims about "disasters" which I can't really comment on.

No I'm not, psychological stress releases cortisol as well.

Lord_Justin13 wrote:
True, but, regarding male pattern baldness, many guys losing hair, especially at a younger age, is an obvious physiological sign of many imbalances occurring at once, a few being unnatural hormone levels, elevated blood pressure, higher LDL/lower HDL etc...


Really? Where's the evidence of this imbalance in healthy men? Let me tell you where I think some of these disease associations are coming from.

Your hair, for one. Every organ and cell in the body is a complex network, which DOES interact with one another, yes, even hair loss is an indicator of a piece to your health.

To the best of my knowledge, there has been no male pattern baldness/heart disease/obesity/insulin resistance study which attempts to weeds out potential male PCOS partipants.

Oh, I got that covered too, in that form I made on "the big three, their correlated disease, and natures cure", I added 3 links at the bottom of my post, all full of articles from PubMed, linking all those diseases together with hair loss.

Take a look.

Quote:

Also, heart disease, enlarged prostate, and diabetes are three illness, which can help one anothers onset, but the one common precursor found is hair male pattern baldness, stress, increasing cortisol, have several promoting factors leading to these diseases.


Wow.. this is real mess of claims. male pattern baldness is the precursor? And cortisol? References please.


Links at the bottom of my form.
And Cushings, which you originally cited to try and prove my theory wrong that stress increases cortisol, and cortisol isn't harmful unless you have cushings, which does, and, this syndrome you cited which you asked me if people would have mild syndroms of if it were minor cortisol, effects the onset of the 3 diseases I state. Along with baldness, Due to it's Hormonal Imbalance on the kidneys, it stresses the heart and blood, and all those other things.

gg.

 

[OverMachoGrande]

First, I want to note when you replied to the article I highlighted by Elizabeth Scott M.S.,

Since the article you linked only seems to cite one source (regarding wound healing), I cannot know what some of those claims are based on.

Now I'd like to take a look at who she is, exactly,

Elizabeth Scott

Elizabeth Scott, M. S. has spent years counseling, coaching and educating families on effective strategies to manage stress, maintain healthy relationships, and live a balanced lifestyle. She's been interviewed on national television and radio shows, and in national publications like USA Today, Woman's Day as well as CNN.com. She's written hundreds of articles on various aspects of stress management for About.com, which can be found at: http://stress.about.com.

The article is submitted shows the potential harm of cortisol.

Are suggesting a national icon in stress, who posts her articles on stress.about.com, (where I pulled the article from), Is not credible?

Cortisol can do everything the article claims in disease states where it is medically abormal.

That was referring to your mayoclinic article regarding "Women with osteoporosis" ...yea...

But then I found this article;

J Biochem Biophys Methods. 2002 Oct-Nov;53(1-3):123-30.
Urinary steroids in men with male-pattern alopecia.
Poór V, Juricskay S, Telegdy E.

Central Research Laboratory, Faculty of Medicine, Pécs University Medical School, 12Szigeti út, 1Honvéd u. H-7643 Pécs, Hungary. Viktoria.Poor@AOK.PTE.hu
Enzyme hydrolysis, solid phase extraction, methoxym-silyl derivatization and capillary gas chromatographic analysis were used to examine the changes in urinary steroid metabolites in men with androgenic alopecia. A total of 23 men with androgenic alopecia and 7 age-matched control healthy men collected 24-h urine. Significantly increased values were found in the metabolites of testosterone (T): androsterone (A) (p<0.02), and etiocholanolone (E) (p<0.05) in patients with androgenic alopecia, compared to the control values. Elevated levels of 16-hydroxy-dehydroepiandrosterone (16-OHD) (p<0.03) and cortisol (F) (P<0.05) were found, but the levels of cortisol metabolites were unchanged. Calculating the ratio of total 5 alpha/5 beta metabolites provided information on the activity of 5 alpha-reductase. The ratio of total 5 alpha/5 beta metabolites was increased in the patients showing the increased 5 alpha-reductase activity. The elevated 16-OHD level could be indicative of patients who had mild hyperadrenal activity.

Wait, mild hyper-adrenal activity, and they have hair loss... :agree:
AND their cortisol is higher...

Also, do you not find it slightly weird that this hypothesized 'stress-induced' mild hypercortisolism would be so selective in its symptoms?

I proved to you, in TWO other articles (out of the many I've brought to the table), from PubMed, that stress does increase cortisol, and it's variety in outlets can be many.

I then gave you the list of symptoms which the disease your referring to can also cause, when you said;

Why would people under chronic stress not experience mild versions of these symptoms as well?

~~~~~~~~~~~~~