Swimmy

Hi Swimmy

 

I would be interested in learning about the new growth factors. Have you had experience using any of those? Have you heard about renokin...it seems to have good reviews

 

 

 

I haven't used RENONKIN but I heard they've gone to other forums and spammed their product...Not sure. Usually when I see companies do that its not a good sign. If the product is good at regrowing hair it would obviously speak for itself. But I'll wait and see the early results before I buy it. Right now I have a listo f stuff I want to try so I'll fit it in some where.

 

 

As for the growth factors

 

Dermaheal

 

Hair Concentrating Serum

 

 

 

Topical Stem C'rum HL, 5 vials 5 ml ech - HAIR CARE

 

 

This one is almost 500 dollars. There's a few people using it right now. So another product I'll wait and see on.

 

 

 

WorldLingo Website Translation

 

 

 

This one is DermatoPoietin. This is probably the next thing I'll try

 

 

The only one I used of these was Dermaheal. The first link. I only got to use it for a month so I wasn't able to get results.

Swimmy, don't get me wrong, I am as wishful as you are that it "makes sense" that supplements would address alopecia, consistently. But medical science is not done by just "putting the pieces together" but rather by controlled studies with numbers that show statistical significance. The articles you reference could allow one to put together an assumption that particular supplements may address hairloss...but scientists have not taken the next step....or perhaps they have and didn't find a clinical effect.

 

While it may sound sarcastic, its like me predicting that the redskins will beat the colts in a few weeks, simply because at halftime the redskins were beating the texans, who had beaten the colts the week before....

 

 

I respectfully disagree with your assumption that putting the assumptions of various studies together will result in a clinical benefit in humans worthy of spending hard earned money on.

 

Dr. Lindsey McLean VA

 

 

Actually I would like to clarify something here. This regimen isn't deigned to grow back full heads of hair.I believe that you will achieve some regrowth. But don't expect slick bald spots to be filled in. Unless you respond amazingly.

The regimen itself is designed to stop hair loss in its tracks, to keep the hair you have. The only thing I know that can fill in a nice slick bald spot is a hair transplant, and hopefully in the future histogen .

 

 

This theory is in practice. There's a forum dedicated to it. The evidence is mounting(in studies) for the underlying causes listed for MPB as the problem.. So far the supplements listed are good at fighting these underlying causes. Its near fact that inuslin plays a part in hair loss. Theres too many correlations. No offense doctor but I don't need a clinical study for them to tell me Lipoic+carniitine is beneficial for hair. I know that it has a positive effect on Insulin. (Which in itself lowers DHT and helps hair. That's just one benefit.

 

 

Now I don't recommend everyone should go out and buy a boatload of supplements I think whomever is interested should study it more deeply. I haven't even scratched the surface of this topic But I don't think people should buy them solely on what I said. To put it simply the rabbit hole goes very deep.

Well here's some info on that

 

 

"Androgenetic alopecia is considered to be associated with coronary heart disease but the explanation of this association remains unknown. Hypertension is highly prevalent in patients with coronary heart disease. Essential hypertension is linked to hyperaldosteronism and spironolactone, an antihypertensive drug which is a mineralocorticoid receptor antagonist, has been used for a long time in the treatment of androgenic alopecia." So does this mean Spironolactone is actually GOOD or BAD?

 

 

Chronic treatment with the mineralocorticoid hormone aldosterone results in increased anxiety-like behavior.

 

Hlavacova N, Jezova D.

Laboratory of Pharmacological Neuroendocrinology, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, Bratislava, Slovakia.

Abstract

 

Aldosterone is the last component of the renin-angiotensin-aldosterone system inducing its peripheral effects via mineralocorticoid receptors (MR). Brain MR bind preferentially glucocorticoids. So far, the role of MR in behavioral functions has been investigated almost exclusively in relation to glucocorticoids. Recently, aldosterone itself has been linked to affective disorders. The aim of this study was to test the hypothesis that chronic elevation of circulating levels of aldosterone leads to increased anxiety. We have investigated the effects of chronic aldosterone treatment on (1) anxiety-like behavior, and (2) basal and stress-induced levels of selected hormones. Forty male Wistar rats were subcutaneously implanted with osmotic minipumps and treated with aldosterone (2 microg/100 g/day) or vehicle for two weeks. Aldosterone concentrations in plasma showed a mild (approximately four-fold) increase at the end of two-week aldosterone treatment. This mild hyperaldosteronism resulted in a significant enhancement of anxiety as demonstrated by alterations in all indicators of anxiety-like behavior measured in the open field and elevated plus-maze tests, without significant changes in measures of general locomotor activity. Aldosterone treatment affected not only the spatiotemporal measures of anxiety, but also the ethological parameters related to exploration and risk assessment. Chronic treatment with aldosterone was associated with increased water intake and decreased plasma renin activity, but failed to modify basal or stress-induced activity of the hypothalamic-pituitary-adrenocortical axis. The results provide evidence on anxiogenic action of prolonged increase in circulating aldosterone concentrations. Thus, aldosterone may represent an important target for future antidepressant and anxiolytic drug development.

 

PMID: 18377905 [PubMed - indexed for MEDLINE]

 

 

 

 

Spironolactone blocks glucocorticoid-mediated hearing preservation in autoimmune mice.

 

Gross ND, Kempton JB, Trune DR.

Oregon Hearing Research Center, Department of Otolaryngology--Head & Neck Surgery, Oregon Health & Science University, Portland, Oregon 97201-3998, USA.

Abstract

 

HYPOTHESIS: Although autoimmune sensorineural hearing loss can be effectively treated with corticosteroids, little is known about how these drugs affect cochlear function. MRL/MpJ-Faslpr autoimmune mice treated with a mineralocorticoid (aldosterone) have previously been shown to have hearing improvement equal to those treated with a glucocorticoid (prednisolone). This suggested that the restoration of hearing with steroids was the result of an effect on sodium transport rather than an antiinflammatory or immunosuppressive role. We hypothesized that corticosteroids reverse autoimmune hearing loss through the mineralocorticoid receptor and that blocking the mineralocorticoid receptor will prevent glucocorticoid effects.

METHODS: Spironolactone, a mineralocorticoid receptor antagonist, was administered to MRL/MpJ-Faslpr autoimmune mice alone or in combination with corticosteroids. The four treatment groups were: spironolactone, spironolactone + aldosterone, spironolactone + prednisolone, and untreated water controls. Auditory brainstem response (ABR) thresholds were recorded before and during treatment (2, 3, and 4 mo) to measure the effect of steroids on hearing decline.

RESULTS: Hearing in spironolactone and spironolactone + prednisolone mice showed progressive decline in hearing similar to water controls. The hearing was preserved in spironolactone + aldosterone mice, presumably as a result of the fact that aldosterone has a higher affinity for the mineralocorticoid receptor than spironolactone. Thus, aldosterone was able to maintain cochlear function with autoimmune disease progression, similar to previous reports of aldosterone treatment effects.

CONCLUSIONS: Spironolactone effectively blocked prednisolone from improving hearing in MRL/MpJ-Faslpr autoimmune mice. This offers evidence that the inner ear mineralocorticoid receptor is the therapeutic target for corticosteroids used to treat autoimmune and sudden sensorineural hearing loss. Pharmacologic treatments that selectively target the mineralocorticoid receptor may provide greater clinical benefit with fewer systemic side effects than prednisone in patients with autoimmune sensorineural hearing loss.

 

PMID: 11889387 [PubMed - indexed for MEDLINE]

 

 

 

To blindly submit to the doctor’s request to take spironolactone increases susceptibility to acquire "age-related" hearing loss, as the hormone aldosterone is intimately involved in the sodium-potassium interaction in the inner ear. Many of those who start to lose their hearing could be deficient in aldosterone, or they could be taking an aldosterone receptor blocker like spironolactone.

 

 

If one is not taking spirolactone, the hearing loss could result from a deficiency of aldosterone, which is remedied by bio-identical aldosterone and would require the services of a qualified physician, preferably one educated in nutritional medicine.

The logic behind using spirolactone is simple enough, reducing excess aldosterone. After all, the correct balance of sodium and potassium in your body helps maintain the fluids in your body, transmits nerve impulses, and contracts and relaxes your muscles. Too much aldosterone causes sodium retention, which then causes water retention. This combination increases blood pressure and blood volume. However, reducing insulin will address the cause of excessive aldosterone.

Firstly, do you have any reason why you site finasteride as being hazardous to your health but believe Saw Palmetto to be safe and effective? My concern with Saw Palmetto is that, due to it's nature as a fairly unprofitable naturally occurring substance the clinical testing on it has been, at best, scant. Sure there are lot of 'reports' on the web but the only really reliable sorts of trials (and then 'reliable' is not an easy word to use) are large scale trials involving hundreds/thousands of people over a long period of time with thorough examination. I've read the odd report here and there but it's usually restricted to tens of people at most, or animals. Whilst these reports might have their usage they can't really be used to assess efficacy across the population. I was wondering if you had good evidence to demonstrate SPs effectiveness and safety.

 

Secondly, why do you feel finasteride is damaging? Yes, there have been some horror stories, but to my knowledge the best these qualify as is hearsay. Now, of course we can take the alarmist opinion that the corporations are doing their best to cover up the harmful aspects of their drugs and I cannot outright dispute that, but do we have any real and well reported evidence fin is a widespread problem with genuine repercussions? I continue to find it difficult to believe fin is having such problematic neurological effects. Who is paying for good trialling that discounts the safety of fin? In addition have these neurological side effects been accurately documented in humans? And why would it be that whilst one DHT blocker supposedly causes all sorts of problems a theoretically more potent DHT blocker (Saw Palmetto) is, in your opinion, safe?

For starters Saw Palmetto is commonly prescribed for BPH..In some cases is given as treatment for hair loss by main stream doctors. I think Saw Palmetto may be pretty well documented since that's case. Don't get me wrong I'm not a avid supporter of SP. I don't even use it. I think you can still get similar sides that arent as strong in the libido department..

 

 

Saw Palmetto does not decrease serum blood levels of DHT...Fin does. When DHT is cutoff this is what leads to neurological effects. DHT plays a important part in brain function.Fin inhibits production of neurosteroids by blocking everything down the 5-alpha reductase chain of hormone metabolites.

 

 

 

Finally, the insulin theories and treatments you have been citing - why have these not come into mainstream popularity and dermatologists/trichologists keen to take these ideas and treatments on board? I find it difficult to believe that insulin has been discovered as one of the major 'smoking guns' of hairloss with good treatments and lifestyle-based ways of solving the problem, but that professionals generally haven't it on board. This of course could be a genuine case of the mainstream being slow to take on the avant garde but something strikes me as being odd that I have heard of very few reputable doctors talking seriously about these theories and these treatments.

Its possible that a lot of them haven't read the studies. The theory itself however is realtively new. In the broad spectrum of things only a small handful of people would have even heard about this. The information is out there but people have failed to put it all together and do the math. If you look at it this way we have been led to believe that DHT is the problem without question. Not to say that its a conspiracy cause a lot of the doctors still do believe that

 

But maybe some doctors do know the underlying causes but play it safe and go mainstream.

 

 

 

And, as an aside, do you have any photo evidence that the regimens and supplements you're suggesting are truly beneficial? The theories do have an air of plausability, but I could say that about many theories that end up being bogus or ultimately ineffective. A good range of visual evidence would, I imagine, be available if this insulin reduction is taking off and proving to be useful.

I personally don't have any photos to mark my progress. All I can tell you is that i've been on it since Jan and my shedding as gone down. I'm also very, very slowly getting regrowth in my temples that I'm constantly monitering. However, I'm not fully taking everything I need to be yet. I figured I would implement slowly. I still have to change my diet which is a big part. But my life gets a little hectic and sometimes fast food is more convenient than make a healthy meal.

This is a little longer so I'll post a link at the end

 

 

 

Towards a "free radical theory of graying": melanocyte apoptosis in the aging human hair follicle is an indicator of oxidative stress induced tissue damage

 

Petra Clara Arck,1, Rupert Overall*,1, Katharina Spatz*, Christiane Liezman*, Bori Handjiski, Burghard F. Klapp, Mark A. Birch-Machin and Eva Milena Johanne Peters*,1 * Cutaneous Neuroimmunology, Biomedical Research Center, University Medicine Charit?, Virchow and Mitte Campus;

 

Psychoneuroimmunology, Biomedical Research Center, University Medicine Charit?, Virchow Campus; and

 

Internal Medicine, Psychosomatics, University Medicine Charit?, Mitte Campus, Humboldt-University of Berlin, Berlin, Germany; and

 

Dermatology, Medical School, University of Newcastle, UK

 

1Correspondence: Biomedical Research Center, Rm. Nr. 2.0549, University Medicine Charit?, Virchow Campus, Humboldt University of Berlin, Augustenburger Platz 1, Berlin 13353, Germany. E-mail: eva.peters@charite.de or frl_peters@yahoo.com

ABSTRACT

Oxidative stress is generated by a multitude of environmental and endogenous challenges such as radiation, inflammation, or psychoemotional stress. It also speeds the aging process. Graying is a prominent but little understood feature of aging. Intriguingly, the continuous melanin synthesis in the growing (anagen) hair follicle generates high oxidative stress. We therefore hypothesize that hair bulb melanocytes are especially susceptible to free radical-induced aging. To test this hypothesis, we subjected human scalp skin anagen hair follicles from graying individuals to macroscopic and immunohistomorphometric analysis and organ culture. We found evidence of melanocyte apoptosis and increased oxidative stress in the pigmentary unit of graying hair follicles. The "common" deletion, a marker mitochondrial DNA-deletion for accumulating oxidative stress damage, occurred most prominently in graying hair follicles. Cultured unpigmented hair follicles grew better than pigmented follicles of the same donors. Finally, cultured pigmented hair follicles exposed to exogenous oxidative stress (hydroquinone) showed increased melanocyte apoptosis in the hair bulb. We conclude that oxidative stress is high in hair follicle melanocytes and leads to their selective premature aging and apoptosis. The graying hair follicle, therefore, offers a unique model system to study oxidative stress and aging and to test antiaging therapeutics in their ability to slow down or even stop this process.—Arck, P. C., Overall, R., Spatz, K., Liezman, C., Handjiski, B., Klapp, B. F., Birch-Machin, M. A., Peters, E. M. J. Towards a "free radical theory of graying": melanocyte apoptosis in the aging human hair follicle is an indicator of oxidative stress induced tissue damage.melanocyte apoptosis in the aging human hair follicle is an indicator of oxidative stress induced tissue damage -- Arck et al. 20 (9): 1567 -- The FASEB JournalTowards a "free radical theory of graying":

Some more interesting studies

 

 

Vertex balding, plasma insulin-like growth factor 1, and insulin-like growth factor binding protein 3.

 

Platz EA, Pollak MN, Willett WC, Giovannucci E.

 

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA.

Abstract

 

BACKGROUND: A recent report suggested that men with vertex balding have higher levels of plasma insulin-like growth factor 1 (IGF-1). The association of its major carrier protein, insulin-like growth factor binding protein 3 (IGFBP-3), with male pattern hair loss has not been examined.

 

OBJECTIVE: We evaluated the relations of plasma concentrations of IGF-1 and IGFBP-3 with vertex balding in middle-aged and elderly men.

 

METHODS: Participants were 431 male members of the Health Professionals Follow-up Study who responded to a question in 1992 on their hair pattern at 45 years of age and who were 47 to 81 years old when they provided a blood specimen in 1993-1994. Odds ratios (ORs) of vertex balding associated with IGF-1 and IGFBP-3 were estimated from logistic regression models mutually adjusting for each other and controlling for age at blood draw.

 

RESULTS: Of the 431 men, 128 had vertex balding at age 45. Compared with men who were not balding, for a 1 standard deviation increase in plasma IGF-1 level (72.4 ng/mL), the OR for vertex balding was 1. 31 (95% CI, 0.95-1.81). For a 1 standard deviation increase in plasma IGFBP-3 (957 ng/mL), the OR for vertex balding was 0.62 (95% CI, 0.44-0.88).

 

CONCLUSION: Older men with vertex balding have lower circulating levels of IGFBP-3 and higher levels of IGF-1 when controlling for IGFBP-3 level.

Hormones and hair patterning in men: a role for insulin-like growth factor 1?

 

Signorello LB, Wuu J, Hsieh C, Tzonou A, Trichopoulos D, Mantzoros CS.

 

Department of Epidemiology and Harvard Center for Cancer Prevention, Harvard School of Public Health, Boston, Massachusetts 02115, USA.

Abstract

 

BACKGROUND: Androgens are important in hair growth and patterning, whereas growth hormone substitution enhances their effect in growth hormone-deficient men. No previous study has jointly evaluated the function of sex steroids, sex hormone-binding globulin (SHBG), and insulin-like growth factor (IGF-1) in determining hair patterning in men.

 

OBJECTIVE: We assessed the relationship between circulating hormone measurements and both head and chest hair patterning in a sample of elderly men.

 

METHODS: Fifty-one apparently healthy men older than 65 years of age were studied cross-sectionally. Head and chest hair patterning was assessed by a trained interviewer. Morning blood samples from all subjects were used for measurements of testosterone, estradiol, dehydroepiandrosterone sulfate, SHBG, and IGF-1.

 

RESULTS: Results were obtained from logistic regression models, adjusting simultaneously for all the measured hormones and age. Men with higher levels of testosterone were more likely to have vertex baldness (odds ratio [OR] = 2.5, 95% confidence interval [CI: 0.9 to 7.8] per 194 ng/dL increment of testosterone). In addition, for each 59 ng/mL increase in IGF-1, the odds of having vertex baldness doubled (95% CI [1.0 to 4.6]). Those who were found to have higher circulating levels of SHBG were less likely to have dense hair on their chest (OR = 0.4, 95% CI [0.1 to 0.9] per 24 nmol/L increment in SHBG]).

 

CONCLUSION: Testosterone, SHBG, and IGF-1 may be important in determining hair patterning in men.

When we eat, our blood sugar is suppose to rise, yet when we eat foods that are high glycemic, more insulin is needed to convert sugar into fat (Triglycerides). Higher and higher blood sugar levels, due to chronic ingestion of high glycemic foods could lead to insulin resistance. A few very notable studies have shown correlations between insulin resistance and balding, as well as heart disease, which is also "positively" associated with insulin resistance.

 

The higher our triglyceride count is, the more of a fatty build-up occurs in the liver, hence the more of a prevalence of high triglycerides in the blood. High density lipoprotein (HDL), also known as the "good" cholesterol carrys triglycerides in the blood to the liver. If it exhibits this action frequently, your HDL levels will be low as a result. One of the functions of the liver is to remove insulin from the bloodstream. However the more triglycerides carried to the liver via HDL (leading up to a fatty liver) the less efficient the liver is at removing the insulin from the blood stream.

 

As a result, the pancreas has to release more insulin to lower the blood sugar, hence triglyceride levels go up, the livers fatty deposits build up, more insulin is needed, which acts on the fat cells (called adipocyte differentiation) and the brain as a feedback loop to make you crave more insulin producing foods.

 

Chronically elevated glucose levels lead to increased cortisol release and a cascade of inflammatory cytokines, a rise in Reactive Oxygen Species (ROS) which has been shown to be elevated in balding dermal papilla cells.

 

Hair follicle regeneration are dependent upon a complex series of cross-talks involving cytokines from dermal papilla cells via paracrine and autocrine mechanisms. These are mitogenic substances influenced by way of hormonal signaling.

 

 

=

I see nothing whatsoever that suggests that a clinical effect on hair loss prevention or regrowth was shown in those studies. I don't even see that they were looking for that.

 

Perhaps I missed it. Would you cut and paste or put a link in so that I can see that it was shown to effect hair?

 

Thanks

 

Dr. L

There are plenty of studies that show the top supplements I listed reduce scalp inflammation, decalcification, lower free radicals, and help with insulin. All of these things contribute to genetic hair loss. Obviously if these issues are addressed it benefits hair loss. Its called putting the pieces together.

 

 

Example. High blood pressure is strongly associated with androgenetic hair loss

 

Abstract

 

Androgenetic alopecia is considered to be associated with coronary heart disease but the explanation of this association remains unknown. Hypertension is highly prevalent in patients with coronary heart disease. Essential hypertension is linked to hyperaldosteronism and spironolactone, an antihypertensive drug which is a mineralocorticoid receptor antagonist, has been used for a long time in the treatment of androgenic alopecia. We recently observed in a double transgenic mouse model that overexpression of a mineralocorticoid receptor targeted to the skin induced the development of alopecia. We prospectively studied the association of hypertension and androgenetic alopecia in Caucasian men. Two hundred and fifty Caucasian men aged 35-65 years were consecutively recruited by 5 general practitioners (50 per practitioner). Data collected included age, androgenetic alopecia score with a simplified Norwood's score (0-4), blood pressure or history of hypertension, smoking, history of diabetes mellitus or hyperlipidemia, familial history of androgenetic alopecia, and treatment. Chi-square, Fisher exact tests and linear regression model were used for statistical analysis. Hypertension was strongly associated to androgenetic alopecia (p < 0.001). Linear regression tests confirmed that this association was independent of age : odds ratio was 2.195 (95% CI : 1.1-4.3). Familial history of androgenetic alopecia was also strongly associated with androgenetic alopecia : odds ratio was 10.870 (95% CI : 4.3-27.1). Other variables (diabetes mellitus, hyperlipidemia, smoking, treatment) were not associated with androgenetic alopecia. We were limited by a relatively small study sample but in this study androgenetic alopecia was strongly associated with hypertension. Association of androgenetic alopecia and hyperaldosteronism warrants additional studies. The use of specific mineralocorticoid receptor antagonists could be of interest in the treatment of androgenetic alopecia.

It might sound simple but If I take a supplement that helps lower my blood pressure I'm helping my hair loss.

 

 

These supplements are suggested based on there ability to go after the underlying causes of hair loss

 

# Reducing insulin producing foods or the impact of such foods on glucose and insulin.

# Controlling over expressed DHT

# Removing heavy metals

# Correcting metabolic conundrums

# Reducing oxidative stress

# Improving glucose metabolism

# Optimizing thyroid function

# Normalizing estrogen metabolism

# Balancing prostaglandins

# Curtailing inflammation

# Balancing intestinal microflora

Its not for the crown. That specific product was intended only for receding hairlines. So its just is specifically to prevent miniaturization in the front

Serum Testosterone “Lower” In Men With MPB

 

 

As we previously reported, an age related decline in the testosterone to estrogen ratio in favor of estrogen has been shown to disrupt immune synchronization and increase the overall incidence of hair loss, prostate enlargement, and abdominal fat accumulation creating what is clinically termed the “estrogen syndrome”. It is well known that men with enlarged prostates are much more likely to have androgenetic alopecia, or MPB.

 

While finasteride (Propecia/Proscar) decreases serum DHT, it also is thought to increase estrogen which suggests that men over 35 may want to consider using it in conjunction with a systemic aromatase inhibitor such as Chrysin/Piperine (Super Miraforte), Arimidex, or stinging nettle extract, to maximize its hair growth effects and minimize potential side effects (that are listed in the PDR) such as Gynocaemastia (breast enlargement in males), sexual side effects, and an increase in fat deposition. These compounds have been reliably shown to increase testosterone and reduce excess estrogen, resulting in a youthful hormone profile that optimizes immune function and to some degree, body composition

 

Those contemplating testosterone replacement therapy who are also concerned about hair loss would be advised to use testosterone only in conjunction with a 5-alpha-reductase inhibitor and, possibly and aromatase inhibitor as well.

 

 

Following are excerpts of abstracts after a basic review of the medical literature:

 

* At the Veterans Administration in Los Angeles? they proved in men that no matter how low they made the testosterone levels fall it did not inhibit the prostate cancer growth.

* At the Imperial Cancer Research Fund in London? doctors gave mice huge doses of testosterone and could not get their prostates to grow.

* At the Medical College of Virginia in Richmond? men were measured for serum testosterone levels and no difference could be found between prostate cancer patients and normals.

* At the Harbor General Hospital in California it was shown that testosterone itself competes for binding in the prostate against DHT. When testosterone levels fall more DHT successfully binds thus causing dysfunction and DHT accumulation. A similar process is thought to occur in androgenetic alopecia.

* At the Leeds Medical School in England human prostate BPH tissue was shown to be deficient in testosterone yet had excess DHT levels.

* At the University of Innsbruck in Austria doctors found the lower the testosterone as men aged the higher the BPH,MPB and cancer, and individually higher testosterone levels were unrelated to disease.

* Again at the Leeds Medical School in London the same doctors did another study and found men with individually higher androgen levels did not have higher rates of disease of the prostate. As men aged and their androgen levels fell BPH and cancer rates rose dramatically to parallel the change.

* At the Institute of Endocrinology in Russia doctors found test animals with prostatitis have low levels of blood testosterone and androstenedione.

* At the Bicetre Hospital in France researchers made the point in laboratory animals very clearly where testosterone supplementation kept the prostates small and youthful, while the untreated animals prostates grew with age.

* At the Granada Medical Facility in Spain 104 men with BPH had lower testosterone levels compared to healthy men. Studies like this should leave no doubt in your mind that testosterone is your friend and low levels of it are pathological.

* At the Tenous Cancer Research Institute in Wales researchers found low testosterone in prostate cancer patients using saliva testing.

* At the Moscow Medical Institute in Russia doctors studied the hormone levels of men over 60 and found those with prostate cancer have much lower testosterone levels and higher estrogen levels giving a very low testosterone to estrogen ratio.

* At the Landeskrankenanstalten Urology Clinic in Austria men with BPH or prostate cancer had no higher testosterone levels than healthy men.

* At the Institute of Cancer Research in Norway doctors found that supplementing aged rats with testosterone reduced 5-alpha reductase activity and increased prostate enzyme activity generally leading to healthier functioning and metabolism.

* At the Polish Urology Clinic in Bialystok15 doctors consistently found low testosterone in men with BPH and MPB.

* At the Principe Hospital in Spain men with prostate cancer had low testosterone levels compared to healthy men as verified by both serum and saliva testing. Again at the Principe Hospital another study confirmed these findings with another group of men.

* In China, 18 doctors studied men with BPH and MPB and found consistently low levels of testosterone generally.

* A most important study done at the famous Johns Hopkins University in Baltimore19 men with BPH and prostate cancer were compared to healthy men and it was found testosterone levels were unrelated to progress or severity of the disease. This study was done by some of the foremost doctors in the country and published in the most important of all medical journals regarding prostate illness appropriately enough titled "Prostate". This study in itself completely disproves the "testosterone is bad for you" theory.

* At the Karolinska Institute in Sweden20 another landmark study was done but this time with 2,400! men. The doctors found men with prostate cancer generally had lower testosterone levels than healthy men. Yet today doctors are still cutting off men's testicles and giving them toxic drugs to stop their testosterone production knowing this treatment never works.

* At the University of Southern California in Los Angeles21 doctors studied 1,127 aged men from four distinct racial groups. They found the Asian men with the highest testosterone levels had the lowest levels of prostate illness while Caucasians with the lowest testosterone levels had the highest rates of BPH and cancer.

* At the Ben May Cancer Research Institute22 in Chicago some very brilliant doctors studied human androgen dependent cancer cells in vitro and found that testosterone actually prevented tumor growth. They said androgen deprivation is clearly wrong and we should be studying androgen supplementation for treatment. Doctors like these are going to be responsible for putting reality into medicine instead of the current insanity of stopping testosterone production.

* And yet another landmark study was done at the University of Utah in Salt Lake23 where doctors found the lower the testosterone level in men the larger the prostate volume as men age. Men with higher than normal testosterone levels did not suffer more BPH.

* To show the value of testosterone supplementation generally researchers at the University of New Orleans24 found that 62 aged men given testosterone supplements had increased sexual interest, more sexual arousal, and better sexual enjoyment as well as improved mood. Studies are going to show more and more that men over 50 who retain youthful testosterone levels are going to be healthier and live longer and better lives.

* At the University Medical Center in Norway25 239 men were tested for serum testosterone levels and they discovered higher levels had no relation at all to BPH or cancer of the prostate.

* It is never talked about but it is important to raise androstenedione levels per se as well as testosterone. At Gumna University in Japan 26 androstenedione was found to be a strong 5-alpha reductase inhibitor.

* At Leeds University in England5 human prostate tissue with BPH was found to be deficient in androstenedione.

* At the University of Edinburgh in Scotland27 doctors demonstrated androstenedione was a powerful inhibitor of 5-alpha reductase activity in the human prostate and had clinical therapeutic potential.

* At the University of Rochester in New York28 doctors found an analog of androstenedione called 5-androstenediol (commonly sold over-the-counter) had potential anti-cancer activity in human prostate cells. They concluded that the current theory of androgen blockage needs to be changed.

 

1. J. Urol. 99 (1968) p. 788-92 2. Gerontol. 14 (1968) p. 133-41 3. J. Lab. Clin. Med. 76 (1970) p. 530-6 4. J. Ster. Bio. 6 (1975), p. 1373-9 5. J. Endoc. 69 (1976) p. 15P 6. Prog. Clin. Biol. Res. 6 (1975) p. 143-58 7. J. Endoc. 71 (1976) p. 99-107 8. Probl. Endokrinol. 23 (1977) p. 111-4 9. Cancer Res. 38 (1978) p. 4126-34 10. Experientia 35 (1979) p. 844-5 11. J. Endoc. 83 (1979) p. 31P 12. Vestn. Akad. Med. Nauk USSR 3 (1980) p. 72-7 13. Klin. Exper. Urol. 4 (1982) p. 1930 14. J. Ster. Bio. 22 (1985) p. 521-8 15. Rocz. Akad. Med. Supl. 42 (1984) p. 177 16. Rev. Esp. Fisiol. 46 (1990) p. 63-8 17. Rev. Esp. Fisiol. 47 (1991) p. 161-6 18. Zhonghua Yixue Zazhi 73 (1993) p. 489-90 19. Prostate 27 (1995) p. 25-31 20. Brit. J. Urol. 77 (1996) p. 433-40 21. Cancer Epidem. Bio. Prev. 4 (1995) p. 735-41 22. Proc. Nat. Acad. Sci. 93 (1996) p. 11802-7 23. J. Clin. Endoc. Metab. 82 (1997) p. 571-5 24. Hormone Behav. 31 (1997) p. 110-19 25. Cancer Epidem. Bio. Prev. 6 1997) p. 967-9 26. Endoc. Japan 19 (1972) p. 97-106 27. Steroids 52 (1988) p. 237-47 28. Proc. Nat. Acad. Sci. 95 (1998) p. 11083-8

 

Hair loss and Serum Testosterone

I've only been using it for a month but, I'm already getting darker pigment in the miniaturized hairs. Also, seeing some regrowthiat the threshold of my temples that was just vellus hair

I've been using something called Juveline by elsoms research . Seems to be doing the job

I have also seen that spammer over the web.

 

I will oblige...is there coconut oil in the shampoo? I am trying to find out because I have heard different reviews and people have said that it is good/bad for the hair we have left.

 

Does anyone have any experience with coconut oil shampoo?

 

lotioncrafters sells it in powder form. I guess you can add to your own shampoo or customization

 

Coconut Endosperm

 

Coconut Endosperm is coconut water, the liquid endosperm of green coconuts (Cocos nucifera). It has been freeze dried to a free-flowing powder form using a patented lyophilization process which produces a stable composition retaining the inherent biological activity of its nutrients and growth factors.

Coconut Endosperm is not to be confused with coconut milk, the latter being harvested from the flesh of fully developed coconuts. Coconut Endosperm is the liquid reservoir of nutrients that nourishes the young coconut for a year of more of its life, delivering vital nutrients for sustained development of the solid endosperm (coconut meat) found inside the fruit. Rich in proteins, amino acids, sugars, vitamins, minerals and growth factors, it plays a pivotal role in supporting tissue growth.

RNA plays an important role in amino acid transport and respiratory metabolism in living cells. RNA-phosphorus (RNA-P) content is found to particularly high in young, green coconuts and Coconut Endosperm is harvested at an optimal stage of maturity to ensure a high content of RNA and growth factors, including shikimic acid, quinic acid and indole-3-acetic acid.

Since coconut water solids can support cell growth, coconut water may be used in products to support the growth of human tissues such as hair follicles, as validated in preclinical trials. Coconut water can therefore be used in revitalizing preparations for the care of skin, hair and nails. 100 g of Coconut Endosperm provides 324 mg of Calcium, 3050 mg of potassium, 206 mg of Magnesium, 4.3 mg of iron, 6.4 mg of vitamin C, and about 4.6 g of protein, in addition to natural sugars and fatty acids.

Coconut Endosperm easily disperses in water, blending seamlessly with cosmetic formulations, making it a versitile nutrient pool for use in topical formulations. Given its GRAS status, Coconut Endosperm can be used in lip care products to support hydration and tissue health.

 

Appearance: Cream colored crystalline powder

Solubility: Water soluble

Shelf Life: 18-24 months from date of purchase (stored in an air tight container in a cool, dark place).

Usage Rate: 1 - 5%

 

INCI: Cocos Nucifera (Coconut) Fruit Juice

 

Hi Swimmy

 

Thanks for taking the time to respond to our questions..I asked my homeopathic doctor about the ingredients and she said that there are a number of plants and other herbs that go in the solution..she did not give me the names but i trust her since she has given me effective medicine for some of the other problems i have had..If you want i will probe her in more detail when i go to india next month..

 

all the supplements that you mentioned, where can one buy them..Do they have any side effects. I wanted to ask you Saw Palmetto in more detail. If SP also inhibits DHT(in fact both kinds of DHT), and Fin reduced only one, then why would i not get sides with SP..

 

By alternate medicine, i meant what ever except Fin..i have had such a terrible time with Fin that i dont want to go anywhere near it...That would include either topicals or pills..i am using rogaine currently

 

 

 

I usually buy them at Iherb and sometimes swanson. Sometimes swanson has the same brand for slightly cheaper. Its a lot cheaper overall than going to a vitamin store.

 

You can possibly get sides from Saw. They just wont be as powerful as those you got from fin. So don't expect the same. Fin also effects more than one outlet. It effects the neurosteroids as well. It completely messes with your hormonal conversion. Some theorize that saw doesn't effect serum DHT levels. But the androgen receptors

 

 

Alternatives to fin? Do you mean solely DHT blockers? Or the new cutting edge stuff being explored like growth factors?

Association of androgenetic alopecia and hypertension.

 

Ahouansou S, Le Toumelin P, Crickx B, Descamps V.

Department of Public Health, Avicenne Hospital, Assistance Publique-H?pitaux de Paris, Bobigny Cedex. France.

Abstract

 

Androgenetic alopecia is considered to be associated with coronary heart disease but the explanation of this association remains unknown. Hypertension is highly prevalent in patients with coronary heart disease. Essential hypertension is linked to hyperaldosteronism and spironolactone, an antihypertensive drug which is a mineralocorticoid receptor antagonist, has been used for a long time in the treatment of androgenic alopecia. We recently observed in a double transgenic mouse model that overexpression of a mineralocorticoid receptor targeted to the skin induced the development of alopecia. We prospectively studied the association of hypertension and androgenetic alopecia in Caucasian men. Two hundred and fifty Caucasian men aged 35-65 years were consecutively recruited by 5 general practitioners (50 per practitioner). Data collected included age, androgenetic alopecia score with a simplified Norwood's score (0-4), blood pressure or history of hypertension, smoking, history of diabetes mellitus or hyperlipidemia, familial history of androgenetic alopecia, and treatment. Chi-square, Fisher exact tests and linear regression model were used for statistical analysis. Hypertension was strongly associated to androgenetic alopecia (p < 0.001). Linear regression tests confirmed that this association was independent of age : odds ratio was 2.195 (95% CI : 1.1-4.3). Familial history of androgenetic alopecia was also strongly associated with androgenetic alopecia : odds ratio was 10.870 (95% CI : 4.3-27.1). Other variables (diabetes mellitus, hyperlipidemia, smoking, treatment) were not associated with androgenetic alopecia. We were limited by a relatively small study sample but in this study androgenetic alopecia was strongly associated with hypertension. Association of androgenetic alopecia and hyperaldosteronism warrants additional studies. The use of specific mineralocorticoid receptor antagonists could be of interest in the treatment of androgenetic alopecia.

 

 

Some more info

At the risk of getting slammed by a lot of you all out there I'll throw my 2 cents in. Note that it is free advice....and you get what you pay for.

 

There are lots of anecdotal reports of supplements, shampoos, lasers....out there that do wonders for hair and most anything else. Before you spend significant money, try to find ONE, more if you want, but I bet you will have trouble finding even one: controlled study published in a peer reviewed (meaning other doctors have examined the study techniques and agree its not likely a scam) journal published in a real medical journal in the US...or even Europe (who may be a bit more progressive on this than us in the US) showing whatever you are interested in actually has a CLINICAL effect in human beings.

 

IF you can find even one study, then I'd say its likely worth a try. IF you can't ask yourself why. ALL doctors want to show how great their results are. IF a doctor finds something that works, I guarantee you that he wants to be the first to publish it!

 

Now I'll pipe down. I can completely understand folks wanting to try things they hear about and avoid or augment meds and surgery. All I'm saying is know what you are spending your hard earned money on.

 

Dr. Lindsey McLean VA

 

 

 

From the OP. Everything can be supported here with studies.

 

http://www.ncbi.nlm.nih.gov/

 

 

The inhibitory effects of eckol and dieckol from E... [biol Pharm Bull. 2006] - PubMed result

The importance of dual 5a-reductase inhibition in the treatment of male pattern hair loss.

Olsen E. et. al.

SUMMARY

In the study, 416 men with male pattern hair loss (MPHL) ages 21 to 45 years old, were randomized to receive dutasteride 0.05, 0.1, 0.5 or 2.5 mg, finasteride 5 mg, or placebo daily for 24 weeks. The results of the study showed that dutasteride increased hair counts in a dose-dependent fashion and dutasteride 2.5 mg was superior to finasteride 5mg at 12 and 24 weeks.

Although testosterone is the major circulating androgen, to be maximally active in scalp hair follicles it must first be converted to dihydrotestosterone (DHT) by the enzyme 5?-reductase. The importance of DHT as a causative factor in male pattern hair loss is shown by the absence of this MPHL in men with a congenital deficiency of the type 2 5?-reductase enzyme. A type 1 5?-reductase, which also metabolizes testosterone to DHT, differs in its location and amount in different tissues. In the skin, type 1 5?-reductase is the principal isoenzyme in sebaceous and sweat glands. There is no recognized genetic deficiency of type 1 5?-reductase in humans to assess its role in MPHL.

Dutasteride (Avodart) inhibits both type 1 and type 2 5?-reductase and is approved at the 0.5-mg dose for treatment of symptomatic benign prostatic hyperplasia (BPH). It is about 3 times as potent as finasteride at inhibiting type 2 5?-reductase and more than 100 times as potent at inhibiting the type 1 5?-reductase enzyme.

Dutasteride caused scalp and serum dihydrotestosterone levels to decrease and testosterone levels to increase in a dose-dependent fashion. Whereas 5-mg finasteride decreases serum DHT by about 70%, dutasteride can decrease serum DHT by more than 90%.

Results

In this phase II, dose-ranging study, 2.5-mg dutasteride was superior to 5-mg finasteride in improving scalp hair growth in men between ages 21 and 45 years with MPHL as judged by target area hair counts, expert panel assessment, and investigator assessment at 12 and 24 weeks.

In a test area at 24 weeks, results showed:

Placebo -32.3 hairs Finasteride 5mg 75.6 hairs Dutasteride 0.1 mg 78.5 hairs Dutasteride 0.5 mg 94.6 hairs Dutasteride 2.5 mg 109.6 hairs Dutasteride 2.5mg vs. 0.5mg

The 2.5-mg dutasteride dose was consistently superior to 0.5-mg dutasteride in promoting scalp hair growth. The 2.5-mg dose was also better than the 0.5-mg dose at suppressing scalp DHT (79% vs. 51%), whereas it was only marginally better at suppressing serum DHT (96% vs. 92%). This difference in the dose-response of serum and scalp DHT to inhibition with dutasteride is likely to be due to the greater contribution of type 1 5?-reductase to scalp DHT concentrations.

Finasteride 5mg vs. Dutasteride 0.1mg

5 mg finasteride suppressed scalp DHT to a similar degree as 0.1 mg dutasteride group (41% and 32%, respectively). Many of the clinical effects (hair count changes, global panel assessment, and investigator assessment) were also similar in these two groups, supporting the similarity in scalp suppression between 5-mg finasteride and 0.1-mg dutasteride.

Adverse Effects

Both dutasteride and finasteride were well tolerated in this phase II study, and no new safety concerns have arisen in any of the phase II and phase III studies of dutasteride given at doses up to 5 mg daily (the 5-mg dose was used in a phase II study for BPH).

There were no significant differences in side effects, serious adverse events, or withdrawals due to adverse events among any of the treatment groups, including placebo. In total, 11 subjects withdrew because of adverse events: 3 were in the placebo group (irritable bowel syndrome and impotency), 7 in the dutasteride 0.1 mg group (decreased libido, malaise and fatigue, mood disorders, skin disorders, injuries caused by trauma, and gastrointestinal- and neurology-related complaints) and 1 in the dutasteride 0.5 mg group (gastrointestinal discomfort and pain).

Decreased libido was noted in:

 

 

• 2 subjects in the placebo group

• 2 subjects in each of the 0.05-mg and 0.1-mg dutasteride groups

• 1 subject in the 0.5-mg dutasteride group

• 9 subjects in the 2.5 mg dutasteride group

• 3 subjects in the finasteride group

 

Of the 9 subjects with decreased libido in the 2.5-mg dutasteride group:

 

 

• 4 resolved while receiving therapy

• 1 resolved within 3 weeks

• 1 resolved within 8 weeks of stopping drug therapy

• 1 subject, decreased libido continued after therapy had been stopped and was presumed by the subject to be unrelated to the trial or drug therapy

 

Concerning possible sexual adverse events, there was no evidence in the present study that either dutasteride or finasteride was associated with impotence. However, 9 men in the 2.5-mg dutasteride group complained of decreased libido, compared with 1 man in the 0.5-mg dutasteride group and 3 men in the finasteride group. As with previous studies with finasteride, this adverse event was characterized as either mild or moderate in severity and often resolved with continuation of the medication. In the 4-year follow-up of the phase III trials in BPH, dutasteride (0.5 mg) was well tolerated and the incidence of the most common sexual adverse events was low and tended to decrease over time.

The only subject to develop gynecomastia was in the placebo group.

Duration of Effects

The serum half-life of finasteride is 6 to 8 hours. Dutasteride has a serum half-life of approximately 4 weeks, and this long half-life was evident in the persistent suppression of DHT with the 0.5-mg and 2.5-mg doses after dutasteride treatment was stopped. Because of this long half-life, men being treated with dutasteride should not donate blood until at least 6 months past their last dose to prevent administration to a pregnant female transfusion recipient.

 

 

Crazy

I've noticed that Swimmy is pretty knowledgeable about hair supplements, which vitamins to take, etc. What are the top ones to help hair growth?

 

Well the most powerful "known" supplement for hair loss is Fibroboost. The research on it is amazing.

 

Ecklonia Cava is also known as a phlorotannin and is 40% fat soluble, this means it acts as both a water and fat soluble anti-oxidant. Ecklonia cava is by far the most versatile supplement I've ever discovered to treat hair loss. Besides it potent inhibition of MMP-9, it effects a whole array of systems.

The polyphenols of Ecklonia cava can last up to 12 hours in human metabolism, while compared to most plant-based tannins have a half-life of just 30 minutes. Ecklonia cava's oxygen radical absorbance capacity (ORAC) value, the score for anti-oxidation potential is 8,300, is much higher than most land-based polyphenols.

 

Ecklonia Cava is one of the most powerful and versatile plant tannins in existence. It's been found to regulate cortisol, lower blood pressure, increase growth hormone levels, lower triglycerides, provides anti-inflammatory effects by a variety of mechanisms, such as inhibition of the NF-kB inflammatory pathway which also serves to normalize blood glucose levels.

 

The benefits do not end there, besides its ability to penetrate the blood-brain-barrier, offering protection against oxidative stress, it also offers a significant increase in trans-cranial blood flow giving powerful release in alpha brain waves and parasympathetic nerve response. This creates a heightened sense of relaxation and mental alertness. Animal research shows positive increases in gamma-aminobutyric acid (GABA), noripenepherine and serotonin levels. A large number of human users report improved sleep

 

In addition, this phlorotannin posesses a potent anti-plasmin inhibition activity, which results in thinner blood viscosity. Generally, the thinner our blood, the longer we live. Ecklonia cava helps maintain normal blood pressure and has been comparable to the ACE inhibitor drug, enalapril.

 

Recently, it was found that high blood pressure is strongly associated with androgenetic hair loss.

 

 

 

 

Stabilized R-lipoic Acid in combo with acetly L carnitine (biotin necessary)

 

The value of Lipoic Acid.

 

Lipoic acid, also known as Alpha Lipoic acid is a lipid (fat) and water soluble anti-oxidant. Lipoic acid boosts the body's endogenous anti-oxidants like Superoxide Dismutase (SOD) & Glutathione, it also increases the bioavailability of exogenous (outside the body) anti-oxidants like vitamins C & E. Lipoic acid recycles and acts as a carrier or transport for anti-oxidant protection into the mitochondria (cell factory engine).

 

Lipoic acid offers strong protection against oxidative stress, and not only reactivates vitamins C & E, but regenerates Co-enzyme Q10. Besides these benefits of anti-oxidant protection on multiplicity of actions, the main benefit of Lipoic acid is its effect on glucose metabolism.

 

 

The role elevated glucose levels play in the body is highly detrimental to health and hair loss. Lipoic acid boosts mitochondrial production of Superoxide Dismutase (SOD) and serves as a protectant against decreased microvascular profusion, which would otherwise deprive oxygen transport along tiny endothelial passages.

Lipoic acid acts as an insulin mimic, increases glucose transport through muscle cells and reduces glycation. The combination of Lipoic acid and Acetyl L-Carnitine has been shown to reverse neurogenerative deficits in aged rats back to near normalcy. The list of attributes is seemingly endless.

 

 

 

 

Iodine. For thyroid Since 90% of the population is deficient in it.(if take Selenium- methylselenocysteine later in the day)

 

Thyroid problems, both hypothyroid and hyperthyroid are epidemically undiagnosed. This is because the standard thyroid test, known as thyroid stimulating hormone (TSH) is not a reliable indication of thyroid status, except in advanced cases. The reason is due to thyroid hormone resistance, in which tissues are insensitive to thyroid hormone.

 

Under performing thyroid is strongly correlated with elevated Lipoprotein(a) which is not only linked with androgenetic alopecia, but appears to be linked with Dickkopf-related protein 1 (DKK-1), a gene that is significantly upregulated in balding scalps.

 

Both insufficient and excess levels of thyroid hormones T3 and/or T4 can result in hair loss. For example, T4 prolongs the duration of the hair growth phase (anagen) possibly due to the down-regulation of TGF-beta2.

 

 

These are also beneficial for hair. Its a little late so I won't be able to get into all of this with a lot of detail. But to finish the list off

 

 

Curcumim and Resveratrol together synergistically.

 

Vitamin D3 with K2-MK7

 

Krill Oil

 

Magnesium

 

 

 

Supplements you should avoid are.. Iron and Calcium. Unless you have a serious deficiency. But its unlikely a Young male should be deficient in any of these

 

 

If you have a any questions. I'll get back. But the one thing is there is isn't just one single vitamin that will cure your hair loss. Usually with a healthy diet and all the top mentioned above together should halt hair loss. There are also plenty of other supplements out there with known benefits for hair Such as Green Tea, brewers yeast, etc. But as with anybody everyone is different and some may respond to certain things better than others. Usually finding the right right vitamins to fight hair loss can be a trial and error. But generally its best to start with the top and go from there.

 

 

 

 

 

 

 

 

 

Yes RCwest. I absolutely agree with you. It would be really helpful if Swimmy can list down some valuable information here.

 

Question for Swimmy - I have tried propecia off and on...recently, i had major side effects which included brain fog, depression, anxiety (to a point i could not get up in the morning) and ofcourse ED..I could live with the ED part of it but it was the other stuff that got me scared. I have never felt like this before and i am 33..i stopped taking it 3 weeks back and i feel better now...I am taking homeopathic medicine from India currently but live in the US..What do you think about homeopathic medicine...In addition i am taking Zinc 50mg, Biotion 5000 mg, Rogaine 5% liquid...One of the doctors told me to get on MSM..What do you think about MSM? The same doctor also told me to get on Saw palmetto. but i am hesistant..the reason is because it blocks DHT as well, then why would i not get any side effects from SP? I would really appreciate your response to my post and maybe you can list down some alternative medicine as well..Thanks

 

 

I'm not sure on the homeopathic medicine. What is it you are doing? There are reports of it helping MPB though.

 

 

MSM is good for thickening and growing out your hair faster. It won't do much in the way of regrowth. It may slow down hair loss slightly. But Its even better if taking with a proper vitamin C supplement. They work well together.

 

 

Saw Palmetto is similar to fin. But it probably wont be as powerful as Fin is. So you may not experience the same side effects. Or at the least no where near what you experienced in the past. The best thing to do is start on a very low does and work your way up slowly to higher doses. Then stop and back down to the previous dosage when you start to feel symptoms.

 

 

By alternative medicines. You mean topicals or internals?

Where can one find more information about this product? Do they have a web site? Almost sound to good to be true.

 

Ingredients

IHT 9 is a natural shampoo made with natural ingredients. It is best natural baldness cure shampoo. Effective as natural herbal shampoo for thinning hair, IHT 9 contains all natural ingredients. Each 200ml pack contains:

 

Trigonella foenum-graecum

Commonly known as Fenugreek, Trigonella foenum-graecum has beneficial effects on hair growth, lustre and health. Fenugreek is thought to work by increasing the dilation of blood vessels to the scalp, thereby improving blood circulation and nutrient supply to this area.

 

Emblica Officinalis

Emblica Officinalis or Indian Goosaberry enriches hair growth and hair pigmentation. It strengthens roots of hair , maintains color and luster. Eating fresh fruit or applying its paste on hair roots improves hair growth and color.

 

Eclipta Alba

Bhringraj (as it is commonly known in India) is an ancient herb used for health of hair and other parts of body. Eclipta alba is also used externally to treat athlete foot, eczema & dermatitis, on the scalp to address hair loss.

 

Acacia Concinna

Acacia Concinna or Shikakai is used to control dandruff, promoting hair growth and strengthening hair roots. It is popularly referred as "fruit for the hair" as it has a naturally mild pH, that gently cleans the hair without stripping it of natural oils. It is a common, prickly, scandent shrub, which grows in tropical jungles throughout India.

 

Sapindus Mukorossi

Reetha or Sapindus Mukorossi is an excellent hair tonic and used as a natural cleanser for washing hair, and forms a rich, natural lather. It is still being used as a naturally produced shampoo by the rural folks in India for washing their hair.

 

Azadirachta Indica

Azadirachta Indica (Common Indian Name - Neem) is used to remove dandruff and has a detangling effect on the hair. It possesses antidandruff, antibacterial, anti viral and fungicidal properties.

 

Lawsonia Inermis

Popularly known as Henna, Lawsonia Inermis can actually enrich, color and enhance your hair. It is a powerful and natural hair conditioner that can help heal the hair shaft by repairing and sealing the cuticle, protecting hair against breakage and loss of shine. Henna is excellent for the maintenance of healthy hair.

 

Barbadensis Miller

Aloe Vera is common name of Barbadensis Miller. Aloe Vera is considered to be one of the best treatments for hair loss. It has anti-inflammatory properties that prevent hair loss and are even beneficial for curing Alopecia. Moreover, the herb is very effective for hair growth.

 

Citrus Limon

A natural rich source of Vitamin C, Citrus Limon or Jambri Nimbu prevents oxidative skin damage and used for clearing greasy skin and hair and its ability to combat many scalp infections

Sorry Trying to give you some more information so you can see where its going. This is the author of the site a small piece.

Ultimately, I believe hair loss is determined by the thyroid, and insulin resistance can be consequence of it, or can be

exacerbated by foods in the diet that were not intended for the ancestry.

 

Getting even more to the root, is mitochondrial decay and/or poor oxygenation within the cell, which are both driven by insulin resistance and/or low thyroid function.

 

Both causes of thyroid dysfunction as well as the dysfunction itself can be cause this impairment.

 

DHT is harmless without free radicals. In non-balding scalps there is very little gene upregulation in DKK-1. Upon the ingestion of high glycemic foods, in balding susceptible individuals, this gene is significantly upregulated, and while insulin itself promotes more DHT (due to a hormone resistant compensation), the said upregulation of DKK-1 will insure hair follicle degradation.

 

Anything that adversely affects the thyroid alters the regulation of TGF-beta and its effects on hair cycling and apoptosis.

 

The health of hair not only relates to the thyroid but of teeth and gum health. The process of acquiring cavities is a systemic disease, whereby phosphate levels are depressed below 3.5 upon the ingestion of fruits and other high insulin producing foods in peoples originating from colder climates, this also causes rapid calcification in soft tissue, a factor in MPB.

 

Regarding the cavities (this might be difficult to swallow for some), however, this was proved using stomach tube feeding in mice, which have identical teeth physiology to humans. Regardless of how the sugar was fed (through the mouth or stomach tube), all acquired cavities.

 

Metals that accumulate are a source of oxidation and in insulin resistance, this is a large factor. The antioxidants used help ameliorate this condition by neutralizing free radicals, which in turn attenuate inflammation that is initially signaled by DHT.

 

Balancing the thyroid will go a way towards fighting inflammation, because in a sub-clinical hypothyroid state, which is epidemic world-wide, (thanks to an improper "gold standard" in thyroid testing), because a low thyroid means there is absolute inflammation in the body.

 

Eating the right food for the ancestral type, eliminating metals (teeth), and within organs and bones using natural chelators and antioxidants can ultimately achieve success in a battle otherwise lost in aggressive cases.

 

Believe me they aren't pulling this stuff out of their arse. The Author of the site sources all of his information. Just do a search at the forum and you will find loads of information on Insulin and its effect on hair loss

 

 

 

I'll try and provide some more quick knowledge on Insulin.

 

While early male pattern baldness or premature, androgenetic hair loss is often cited as "genetic," studies show that men who experience advanced balding under the age of 35 tend to have high blood insulin levels. Additionally, there is a strong prevalence of insulin resistance with androgenetic alopecia. (Lancet. 2000 Sep 30;356(9236):1165-6.)

It is widely accepted that male pattern baldness progresses with advancing age, and with that brings on a breakdown of many of our body's antioxidant defenses. This means tissue is more subject to free radicals, which can impair circulation and create inflammation.

Insulin resistance or high blood insulin levels is brought on by high levels of free radicals, known as reactive oxygen species (ROS). Using an array of potent, natural, free radical fighters can decrease insulin resistance significantly. (Nature. 2006 Apr 13;440(7086):944-8.)

It is also known that those who suffer from male pattern baldness have higher levels of free radicals in their scalp sebaceous glands. (J Invest Dermatol. 1996 Aug;107(2):154-8.)

Diet certainly plays a role, as processed foods encourage the influx of free radical formation in our bodies.

This is especially the case with refined vegetable oils and processed, grains and sugars. Refined vegetable oils not only increase free radicals, they also increase levels of the enzyme 5-alpha reductase, which helps the body make DHT. Levels of DHT are also increased when insulin in the blood is rising. Simple, refined carbohydrate easily breaks down to glucose, raising blood insulin levels. (Reprod Biol. 2002 Nov;2(3):277-93.)

Managing to balance blood glucose and insulin levels is an important to step to help halt the progress of hair loss. Some species of plant extracts offer very powerful antioxidant protection, far greater than what is found in ordinary fruits and vegetables. Additionally, there are inexpensive dietary supplements that help increase your body's own antioxidant defenses.

The organ system involved with hair growth is extremely complex. Ensuring that each and every factor contributing to your hair loss must be adequately resolved before significant hair regrowth can occur.

There's some interesting information in the articles you've posted Swimmy, but in my opinion there are some big issues in those presentations too.

 

 

Firstly, I don't really see how Saw Palmetto could be a 'safe' DHT inhibitor. It has to border on common sense that if finasteride causes side effects it's the lowering of DHT itself which is the problem? The major difference between finasteride and Saw Palmetto is that SP decreases two types of DHT - including one found in the brain (it's exact usage is unknown but it's commonly concluded it must have a use if it's in the brain). To that extent Saw Palmetto would seem the riskier option to me - especially when combined with the knowledge that extensive testing has not been done on it.

 

 

 

You assume there are no studies on it . The link below contains many Including saw palmetto. So far there seems to be very little risk in its use compared to Fin. There are some studies on the risks. But basically any DHT blocker is gonna have issues.

 

National Center for Biotechnology Information

 

 

 

I also feel there are some problems with the studies you provided. Although they are interesting and I don't doubt there may be some validity in them, there are problems in the studies themselves. For example the study related to insulin looked at just fifty one men, all over the age of 65. That is nowhere near a big enough cross section to prove or disprove anything.

 

 

 

I provided only one study. It doesn't mean its the only one.

 

The supposed link between MPB and insulin seems unlikely in my opinion. Although I admit I have not looked at the trials you posted in a lot of detail I fail to see a major link between insulin and MPB. I mean, for a start, surely diabetics with low insulin levels would fare better in the hair department? I know you say insulin isn't the only factor but if it was that important surely we would see a more obvious link.

 

 

You wouldn't see a obvious link Because the medical industry keeps pointing at DHT as the main culprit when it really isn't. The mainstream is too focused on blocking DHT and not addressing the underlying problems. Just like most medicines do. Treat the symptoms but not the cause.. Now its not just insulin that plays a role in hair loss. There are many factors.

 

 

As I say, I do find these reports interesting but they don't really convince me. I have no doubt eating properly and good vitamin supplementation will help keep your hair healthy and possibly keep more of it but it strikes me as odd that some people are happy taking half a ton of herbs, oils, vitamins and turning their diet upside down but won't consider using finasteride. I know plenty of people who eat terribly, have awful skin and are greasy but have a thick head of hair and are in their 30's or 40's. I don't think the answer lies in that direction, personally.

 

 

Its not just the benefits of keeping your hair by turning your diet upside down and take supplements. But living a overall healther, longer and more energetic lifestyle as a bonus. Also, the people who have gone full out on the regimen find that they have little use for Fin..Since they are addressing the underlying cause..But not all the answers are known. Its trial and error and where the site is today took a group effort of information and research find what works and what doesn't and giving their experiences.

 

You are also forgetting the genetic factor. What makes some more vulnerable to hair loss than others. So someone with low insulin doesn't correlate to anything factual but a broad generalization. A greasy, fat, 30 year old can have a full head of hair because of their genetics.

ya i'll let you guys know. I put an order in a few days ago using a debit card via paypal, from the czech site galleon.com or something..... google RENOKIN and then look for the 60mg solution on whatever site looks like galleon or galliun... i dont know. It cost me a little over $200 for 2 bottles i believe.

 

)

 

Google Translate

 

 

Hmm well here it is way cheaper. If it is the same product?

 

Or might the price conversion be off or something. All I know is people are gonna have a hell of a time ordering this stuff

 

But I heard they are getting a distributor in NYC

One last piece for now

 

 

 

Hair loss is not just rooted in DHT. DHT stimulates TGF-B1, which stimulates collagen enzymes, which further stimulate apoptosis. Cytokines such as Tumor Necrosis Factor alpha, ROS (Reactive Oxygen Species), Superoxide, Prostaglandin imbalances and stress hormones, prolactin, HTPA and other factors play an important role as well. Moreover, diet plays a strong role in how much additional DHT and the above mentioned factors will be allowed wreak havoc on your hair. Much of this is due to the inflammatory nature of adulterated and/or processed foods.

If you doubt the veracity of my statement concerning diet, try eating packaged, convenience foods day after day, especially those loaded with hydrogenated oils, sugar, fructose, corn syrup, enriched, bleached flour-based ingredients. What you may find is that in as little as days, a strong prevalence of newly formed acne can result, and some notice of disturbance of the skin on the scalp.

Refined starches and sugars, processed oils, margarines, trans-fatty acids throw a wrench into healthy prostaglandins, enzymes related to skin and hair, liver health, hormonal balance, and various metabolic functions critical to health. Also, due to commonly over prescribed anti-biotics (Greek for anti-life), yeast overgrowths produce acetylides and other toxic substances, which result in Candida overgrowth. An imbalance in intestinal microflora gives rise to hormone imbalances. Please visit the physiology page for more information on Candida overgrowth, since this factor alone can prevent any benefit from the regimen from working.

A protein upregulated in balding scalps called DKK-1 is also triggered by DHT. Some research suggests that DKK-1 levels can be buffered by lowering Lp(a) levels. The most effective way to do this is to insure that thyroid hormone is balanced. I hypothesize that male pattern baldness is actually a result of thyroid hormone imbalance. Both insufficient and excess levels of thyroid hormones T3 and/or T4 can result in hair loss. For example, T4 (thyroxine) prolongs the anagen phase possibily due to the downregulation of TGF-beta2.

 

While thyroid problems are largely undiagnosed, even if they are a large proportion of these patients only receive synthetic T4, which can cause hair loss. However patients do much better when taking natural T4 and T3 (Triiodothyronine). It is estimated that as many as 70% of the world (perhaps more) have less than optimal levels of iodine. Note that iodine is required for proper conversion of T3 from T4. Complicating matters, since most patients only receive synthetic T4, this can inhibit iodine levels further. If you're willing to experiment, I would suggest taking 50 milligrams of lugol's solution daily. The easiest way to acheive this is by adding 8 drops of 5% Lugol's solution to your daily water intake.

To manage most factors critical to staving off hair loss, covering the following areas are most important:

 

 

• Reducing insulin producing foods or the impact of such foods on glucose and insulin.
  
• Controlling over expressed DHT
  
• Removing heavy metals
  
  
• Correcting metabolic conundrums
  
  
• Reducing oxidative stress
  
• Improving glucose metabolism
  
• Optimizing thyroid function
  
• Normalizing estrogen metabolism
  
• Balancing prostaglandins
  
• Curtailing inflammation
  
• Balancing intestinal microflora
  

 

Taking Curcumin to reduce TGF-B1 andEcklonia Cava to combat MMP-9 (Matrix Metalloproteinase), also referred to as Gelatinase B) stimulation is very important. Both Curcumin & Ecklonia Cava do so much more and will radically reduce inflammation. Stabilized R-Lipoic Acid (with Biotin will increase the body's antioxidant defense system and improve glucose and insulin regulation).

Balancing out prostaglandins is just as crucial as reducing oxidative stress. Krill oil is a very convenient way to supplement the diet to achieve optimal essential fatty acids to improve prostaglandin balance.

Other sources of essential fatty acids include Fish oil, Cod liver oil, Borage Oil, and Black Currant Oil. Note: The only cod liver oil worth purchasing as of this writing is Blue Ice Fermented Cod Liver Oil. The reason is due to "modern" distillation methods which have removed the natural balance of Vitamins once contained in it.

Managing stress can be difficult, and what follows stress can be neurogenic inflammation. This maybe the most rapid way to lose one's hair. Adding resveratrol along with curcumin can help combat this type of inflammation.

Acetyl L-Carnitine is very helpful in reducing stress and the associated rise in cortisol. Keeping a lid on this hormone will help preserve hair, as cortisol levels are increased due to stress, hair follicle levels of CRH (Corticotropin releasing hormone) which is a hypothalamic hormone that is responsible for secretion of Adrenocorticotropic hormone (ACTH) can spell disaster if it's not controlled. A very useful aid in controlling cortisol isAshwagandha as Sensoril, a patented form that helps balance out copper levels as well; a potentially critical contributor to hair regrowth.

But here's what his regimen is like and what I'm currently on as well

 

 

Ecklonia cava extract, one 400 milligram capsule morning and evening

Caution: Avoid other brands, must be from Nutricology only!

One capsule of Curcumin 95 taken with largest meal only

Take a thousand milligrams of Krill Oil once or twice per day

100 milligrams per meal Bio-Enhanced Na-RALA*

see notes below.

1000 milligrams per meal; target three times dailyAcetyl L-Carnitine

Update* Vitamin D3 (5,000 IU) + Vitamin 90 mcg K2 as MK-7, take once per day,

take less frequently if season and latitude apply

5,000 (5 milligrams) of Biotin (essential if Lipoic Acid is used)

 

Ancillary/Supplemental

 

200 milligrams once per day trans-Resveratrolworks as an adjunct to Curcumin

to neutalize neurotrophins

Update* Selenium with Sulforaphane once daily

 

Brewer's Yeast (food based B-vitamins) take a few per meal

Jarrow EPS Probiotic

1000 milligrams of Magnesium (mixed forms) daily

 

Green Tea Phytosome, one 250 milligram capsule per day

Update* Several drops of Iosol per day in water daily

Formerly taking 400 milligrams of Chasteberry per day.

225 milligrams daily of Sensoril, Patented Ahwagandha extract