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Swimmy

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Posts posted by Swimmy

  1.  

    Out of interest the people that you know who have stopped their hairloss without fin or minox; would you mind sharing what you know about the techniques and products they used? I'm always interested in hearing alternative regimes and have an open mind about the possibility that there are other effective treatments out there so I'm interested to know more.

     

    Before I post what they take. I'll post some of the science behind MPB. What the real Causes are that trigger DHT to attack hair follicles and the mechanisms.This is back by Science research. So its pseudo nonesense. If you want to check the links. I wont post all of it cause theirs a lot. As said I'll link you then.

     

     

     

    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.

    Chronic elevations of insulin result in increased circulating levels of Insulin Growth Factor-1 (IGF-1) and lower levels of Insulin like growth factor binding protein 3 (IGFBP-3).

     

    J Am Acad Dermatol. 2000 Jun;42(6):1003-7.

     

     

    J Am Acad Dermatol. 1999 Feb;40(2 Pt 1):200-3.

     

     

    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.

     

     

    British Journal of Dermatology Volume 154 Page 609 - April 2006

     

     

     

     

    Live longer and grow your hair by reducing your insulin levels.

     

     

     

    Lowering your insulin isn't everything, yet it is fundamental for everything else you do. Insulin, as a matter of speaking is the "hormone of death." A study on mice revealed an interesting finding. Genetically altered mice rendered in a manner that allowed their fat cells to be unresponsive to insulin, ate as much food as they desired. Despite that, they remained thin. While they actually consumed 55 percent more food than the control mice, they had 70 percent less body fat than the control group. Additionally, the genetically altered mice lived 18 percent longer than the control mice. This study shows control of insulin is probably why calorie restriction helps with life extension. However, it is the insulin control that is important, not necessarily the the amount of food consumed. Insulin release is stimulated in response to grain, starch and sugar consumption.

    Extended Longevity in Mice Lacking the Insulin Receptor in Adipose Tissue

    Science 299 (5606): 572-574

     

     

     

    While insulin resistance is a driving force of male pattern baldness, the underlying cause maybe thyroid problems, and or hypothyroidism.

    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.

    J Clin Endocrinol Metab. 2008 Nov;93(11):4381-8.

  2. Regarding the 'studies' that say finasteride can increase chances of cancer or bring about neuro-degenerative problems I would be very dubious. These allegations may of course be true, but who is conducting these tests? Who is paying large amounts of money to conduct proper, full investigations into the negative aspects of finasteride?
    I think you misread. It decreases prostate cancer. But increases the SEVERITY of the cancer, if you get it.

     

     

    As for depression and neuro degenerative problems

     

    "Animal studies suggested that finasteride could alter 5alpha-reductase activity in some regions of the brain, and lead to behavioral and mood changes. It has been shown that finasteride is able to inhibit 5alpha-reductase in medial basal hypothalamus in pregnant rats, and induce behavioral changes [13]. Significant inhibition of hypothalamic and pituitary 5alpha-reductase is also noticed in adult male rats [14]. In addition to animal studies, although there are some case reports suggesting finasteride induction of depressive symptoms and anxiety in humans, [15] but no prospective study has been carried out, in order to investigate finasteride behavioral effects. In the present study, we have investigated any depressive symptoms or anxiety induced by finasteride administration, in the patients with diagnosis of androgenetic alopecia."

     

    5alpha-reductase is a critical enzyme in the conversion of several steroids such as testosterone, progesterone, aldosterone and corticosterone in the brain. This enzyme converts testosterone to the most natural potent androgen DHT, and also it acts an important role in conversion of progesterone to dihhydroprogesterone (DHP). DHP is further converted to allopregnanolone (5alpha, 3alpha-tetrahydroprogesterone) by 3alpha-HSD [9,21]. Allopregnanolone is a modulator of gamma amino butyric acid type A receptor (GABA-A), and increases chloride conductance. This neurosteroid has been found to exert anti-convulsant, anesthetic and anxiolytic effects [22-24]. Moreover, change in the levels of allopregnanolone is found to be associated with depressive disorders. [25,26]

     

    Our results are in agreement with the past published reports [15], and indicate that finasteride might induce depressive symptoms. The 95% confidence interval, for the difference in the means of the BDI scores, was ranging from 0.34 to 1.04. This shows that the overall change induced by finasteride is minimal, but statistically significant. Anxiety scores were also increased, but the difference was not significant.

     

    A decline in serum DHT level occurs after finasteride administration [27]. This may contribute to finasteride induced depression. Some studies have been shown that serum DHT level, which is in equilibrium with the brain [28], is inversely associated with depression. A study by Barrett-Connor E. et al. showed that BDI scores were inversely associated with bioavailable testosterone and DHT level [29]. Furthermore, it was found that DHT had anti-depressant effects on behavior of male rats and its replacement in castrated rats was able to partially decrease the immobility behavior, which is indicative of depression [30].

     

    Finasteride induced psychiatric dysfunction can also be attributed to its inhibitory effect on androgen and steroid 5alpha-reduction in the brain. Animal studies suggest that finasteride has inhibitory effects on 5alpha-reduction of testosterone and progesterone in the brain and inhibits the formation of allopregnanolone [31,32]. Allopregnanolone has an important role in depressive disorders [26]. In 1998 Romeo E. et al, revealed that episodes of unipolar major depressive disorder in men is associated with a decline in the plasma concentrations of allopregnanolone [25]. Furthermore, a study carried out by Uzunova V. et al. showed that CSF levels of allopregnanolone were significantly lower in depressed patients, and there was negative correlation between allopregnanolone levels in CSF and HAM-D scores. [33].

     

    Since finasteride is a potent 5AR type2 inhibitor and the predominant isoform of the enzyme in human brain is 5AR type1 [34,35], some points should be noted concerning finasteride inhibitory effect on brain steroid metabolism. (i) Although finasteride is a potent 5AR type2 inhibitor, but it has also some inhibitory effects on 5AR type1 [36]. (ii) Finasteride administration in humans has been reported to be associated with some behavioral and mental disorders related to low levels of allopregnanolone in the brain [37]. This may also improve the concept of brain allopregnanolone suppression by finasteride in humans.

    This is why I don't trust the Merck study. How could 5 years of studies miss such a obvious symptom and inbalance? I believe the Merck Study has down played a lot of the symptoms associated with Fin.

     

     

     

     

    My main concern with the dismissal of finasteride is really the alternatives people go for instead. I see people who dismiss finasteride as poison but go taking ridiculous amounts of saw palmetto, spiro and lord knows what else; dosing themselves up with herbs and oils. Anything 'natural' can be just as dangerous and unpredictable as anything produced by pharmaceutical companies and the true effects and reliability of these alternative therapies have not been studied or documented thoroughly. I think it's fine to dislike or dismiss finasteride but not at the expense of pumping yourself with a lot of "natural" remedies that could be doing just as much or more harm.

     

    Saw Palmetto is a effective treatment. Its safe and works similar to Fin.

    As the studied quoted

     

    BARCELONA—A new study performed by Euromed and published online ahead of print in Advances in Therapy journal found a novel saw palmetto extract (SPE), SPET-085, is as effective as finasteride, the standard prescription drug therapy, in blocking the critical enzyme that leads to benign prostatic hyperplasia (BPH), a condition that involves symptoms such as urinary hesitancy, weak urine stream, nocturia, incontinence, and recurrent urinary tract infections.

    There are two types of 5α-reductase, the enzymes that irreversibly catalyses the conversion of testosterone to the most potent androgen, 5α-dihydrotestosterone (DHT). The focus of the current study was on type II 5α-reductase, which is found in human prostate tissue. Researchers compared the ability of SPET-085 and finasteride to inhibit 5α-reductase isoenzyme type II in vitro.

    SPET-085 inhibited this enzyme at a lower dose than commonly used hexane extracts of saw palmetto. Further, SPET-085 was determined to have bioactivity similar to that of finasteride, the most commonly prescribed medicine for the treatment of BPH; side effects of this drug include decreased sex drive, impotence, or decreased ejaculate amount.

    “The results of this study verify the high activity of our novel saw palmetto extract, SPET-085, to help maintain healthy prostate function,” said Joe Veilleux, General Manager, Euromed USA. “Euromed is committed to ongoing clinical research to provide scientific evidence which will differentiate SPET-085 from other saw palmetto extracts.”

    "I look forward to seeing if these interesting results in the laboratory translate into better patient outcomes in the National Institutes of Health-funded CAMUS study, an ongoing 18 month clinical trial comparing this saw palmetto supplement against a placebo for urinary symptoms attributed to benign prostatic enlargement," said Michael J. Barry, M.D., Professor of Medicine, Harvard Medical School.

     

    As for herbs and such. They are underrated in the fight against hair loss. Its possible just by adjusting your diet and getting the right supplements you can completely halt your hair loss. Again I know people who've done this. I've been to forums where people go this route against MPB and its a purely internal regimen.

     

     

     

    If you want all the information you can get on Fin go to this site. Its loaded with studies and feedback and is very informative. I'm not sure if we are

     

    PROPECIAHELP: Unresolved Finasteride Propecia Proscar side effects info & forum

     

    There should be a lot of useful information at their forum to

     

    As for the last part I'll reply in a new post

  3. That is a spelling error" Estrogenic"

     

    To put it simple. When a male is young his body is Testosterone dominant. As one gets older the spectrum shifts and a male becomes estrogenic. Fin is not good in this circumstance since it can cause a total dominance of estrogen. High estrogen will then result in possible BPH which a lot older men coincidentally experience.

    A study conducted by a University of Southern California (USC) medical team found 8 out of 27 high-risk men taking the drug Proscar developed tumors within one year, despite having 67% lower DHT levels. I propose the real problem is not DHT; it is high estrogen levels in the prostate. Proscar lowers the DHT too much and can cause impotency, whereas the beta sistosterol in saw palmetto proved to be twice as effective in restoring urine flow in men with enlarged prostate, without the side effects of impotency. This is because beta sistosterol inhibits androgen receptor binding, while finasteride (Proscar) only reduces 5 alpha reductase. Even though Proscar reduces DHT concentration in the prostate by 80%, it only decreases the prostate size by 18%. Over 63% of men experience no improvement in symptoms using Proscar, even after being on the drug for a year, and over 5% of Proscar users suffer decreased libido, impotence, and ejaculatory disorders

     

     

    However, MPB is not that simple. Firstly there are lots of factors contributing to hairloss. There's two types of DHT, for a start, and the probability of numerous other hormonal and genetic issues that create hairloss. Lowering DHT does a great job of helping your hair but it doesn't stop balding.

    Yes I know the causes and symptoms. Fin is not a permanent solution it only attacks the symptoms. That's exactly what DHT is, a symptom in the grand scheme of things. Not the cause. I know plenty of people who've completely stopped their hair loss without Minox or Fin . I have part of the answer its just gonna take a lot of discipline to follow through.

     

     

     

     

     

    Secondly, whilst of people have reported problems on finasteride, some extreme, we have no proof of long term of permanent problems strictly due to finasteride. In addition to this the percentage of people experiencing side effects in the real world is, frankly, unknowable. Think of it this way; if just 4 million people on this planet are using fin for hairloss (the figure, I imagine, is a lot higher) and the number of people experiencing side effects was just 2% (the rate Merck suggests) that would mean there would be 80,000 people with side effects. If just 20% of them voiced their concerns on the net (and I imagine the chances are it would be higher) that would be 16,000 people on the net with problematic sexual or other side effects. If you can find me 16,000 individual people complaining about finasteride on the net I'd be very surprised.

     

    First off when a company does a study on its own product or a unbias source I'd consider it unreliable. It amazes me that some actually accept the Merk studies without question. I know I wouldn't. Their job is to make money. If there's one thing I know its that the medical companies out there are very corrupt and have pushed products on the market before that were dangerous only to be recalled..As if they didn't know the effects to begin with. It happens all the time. ....But yes most people I've met on hair loss forums other than this have told of the horrors of being on Fin. I've found the other forums to be a better indicator of people experiencing sides effects than some study fueled by a companies own interests. But if you aren't experiencing sides on this (whomever) then good for you.

     

     

    That's not to say you're wrong, I'm just trying to bring some balance to the argument. Almost every reputable HT doctor on this planet is very happy (and indeed, insistent) to provide finasteride. People aren't dying because of it, or we're not seeing mass cases of infertility, ED or cancer (where you got the cancer idea from I don't know, the only connection between fin and cancer I have ever seen is that it lowers your risk of prostate cancer). I can't speak for the overall effectiveness or risk of using fin, but it is not "poison".

    I don't have the site, But you can take my word for it until I can actually find the site again. Research does show that Fin decreases Prostate cancer. But studies have also shown a increase in severity of the cancer. So its sort of a trade off.

     

     

    Pharmacopsychiatry. 2010 May 18.

     

    Finasteride Treatment Inhibits Adult Hippocampal Neurogenesis in Male Mice.

    R?mer B, Pfeiffer N, Lewicka S, Ben-Abdallah N, Vogt MA, Deuschle M, Vollmayr B, Gass P.

     

    RG Behavioural Biology, Central Institute of Mental Health, Mannheim, University of Heidelberg, Germany.

     

    Abstract

    INTRODUCTION: The 5-alpha-reductase inhibitor finasteride is used for the treatment of androgenic alopecia, benign prostate hyperplasia and prostate cancer. Besides inhibiting the conversion of testosterone to the biologically more active 5alpha-dihydrotestosterone, it also inhibits the production of neurosteroids. Decreased neurosteroid levels are postulated to be involved in the pathophysiology of psychiatric disorders such as depression. As neurosteroids metabolized by 5-alpha-reductase influence neural plasticity, we investigated whether finasteride treatment alters adult hippocampal neurogenesis, implicated in the pathophysiology of depression. METHODS: Male C57BL/6N mice were treated subchronically (7 days) with finasteride or vehicle. Adult neurogenesis was assessed at two different time points after treatment (day 1; day 35) using immunohistochemistry. RESULTS: Finasteride treatment led to a significant decrease in brain 5alpha-dihydrotestosterone levels and induced a reversible reduction in the number of newborn cells and young neurons in the hippocampus. 35 days after the last finasteride injection, neurogenesis had returned to normal. DISCUSSION: These data indicate that inhibition of 5-alpha-reductase activity by finasteride treatment influences neuronal plasticity on a structural level. These changes might contribute to the pathophysiology of depressive episodes observed after finasteride treatment. © Georg Thieme Verlag KG Stuttgart · New York.

     

    Long term use of finasteride is potential neurodegenerative capabilities. Research has already shown that finasteride promotes a greater likelihood of anxiety and depression. Through the same mechanism, which is a reduction in the production of pregenolone & progesterone the propensity to acquire a neurodegenerative disease, such as early dementia is possible.

     

     

    "I'm not "pro" fin, either. I am going to have to start using it soon but am, like many, quite worried about possible side effects. My concern, however, is a lot of the 'fin haters' come up with all sorts of weird and wacky myths and ideas about how bad it is and most of the time people who dislike fin end up coming up with some unproven or untrue reason why its so bad. The sort of hysterical hatred I see for it usually weakens the argument that fin is risky, not strengthens it. I know that for every one scaremonger who wants to tell the world how bad fin is there are 50 men out there who take the drug, live a normal life, and don't even know about the controversy surrounding it.

     

     

     

    I don't think I said anything out of line. Or said anything untrue. I never said Fin could kill ya.

     

     

    But of you are gonna go on something like this. Its a good Idea to take DIM. It will block the bad estrogen and limit the sides.

  4. man, i had no idea that K was so bad. Thanks for your perspective, doc. I'm thankful for this.

     

    just trying to get all the information i can.

     

    K-2 isn't bad for you. If you actually believe that its misinformation. Your body needs it and is powerful at prevent osteoporosis and preventing calcification of the arteries...Along with the scalp. Stopping cardio vascular disease.Particularly MK-7.

     

    But if you want to believe k-2 is bad be my guest. The symptoms of deficient K-2 can lead to these Good symptoms as a result

     

     

    Anemia

     

    Heart disease

     

    Calcification of soft tissue

     

    easy bruising

     

    eye hemorrhage

     

    fractures

     

    gastrointestinal bleeding

     

    gum bleeding

     

    heavy menstrual bleeding

     

    hematuria

     

    Hypercalciuria

     

    osteopenia

     

    osteporosis

     

    Purpura

     

    Nosebleeds

     

     

    This doesn't include the numerous birth defects it can cause.

  5. There is no evidence that I have heard of that states it "wears off"....yes....over time, your more sensitive hair becomes affecting by the lower amounts of DHT in the body, but that does not mean that the fin is not lowering your DHT....most people (I believe) who start taking it at 30 will have much more hair at 50 then if they had not taken it...even if they do lose some....who is to say where they would be at if they hadn't....that is why twin studies are so great...

     

     

    It wears off as you age. As your body becomes more estrogenetic.

     

     

    Anyway...I do think that if you don;t want to take fin because in 10 years it will be less effective and you may start losing hair, then hair loss is not that important to you you and you should not worry about it... my 2 cents...

     

     

     

    So if someone doesn't take fin they aren't worried about their hair loss? Nice logic. I know plenty of people and other forums that people refuse to take fin. Actually most other hair loss forums refer to Fin as "poison" and yes the % of people experiencing side effects is greatly under exaggerated. There's a lot of people out there taking and doing other things to prevent hair loss other than Fin.

  6. The problem is you all are duped into believing that they don't work. That the only Lasers available are the likes of the laser comb or going to a clinic. All of it is ridiculously expensive and over priced. The problem isn't that they don't work. They aren't STRONG enough! They are selling you underpowered laser that's made out of cheap plastic. A ripoff

     

    The truth is LLLT is effective against hair loss. They reducing inflammation, help to replicate your mitochondria and increase ATP production. The only way to do this cheap and effectively compared to the alternative is build your own laser helmet which certain sites can instruct you on doing or may even build one for you. These homemade laser helmets are powerful enough to get results.

  7. Doing a quick searc h on Polysorbate 80, I found that it is really used as an emulsifier and does not appear to have any relationship with topical treatments.

     

    "Polysorbate 80 is frequently used for pharmaceutical formulations as an emulsifier, solubilizer and stabilizer. Improving its characteristics (color, odor, oxidation stability, cytotoxicity and hemolysis) by ultra-pure Polysorbate 80(HX)TM is very suitable for pharmaceutical application."

     

    More information can be found at Polysorbate 80 - Wikipedia, the free encyclopedia

     

     

    Um. Its actually being use in a lot of topical formulations for awhile now

  8. Some info

     

     

     

    Durk Pearson and Sandy Shaw popularized the use of polysorbate 80 for alopecia in their best-selling book, Life Extension: A Practical Scientific Approach. In their book, Pearson and Shaw report that use of polysorbate 80 in studies has resulted in an average of 60 percent hair regrowth after just six months of daily use.

     

    Although histamine is usually considered the culprit behind seasonal allergies, in actuality this substance is essential for cell growth and reproduction. In fact, since histamine is a growth factor, applying to the scalp a substance that triggers histamine release may also promote hair growth. In animals, administration of polysorbate 80 triggers the production of histamine in mast cells and plasma histamine concentrations rise after administration of polysorbate 80. In humans, the administration of polysorbate 80 causes effects in the body similar to the body’s response after histamine administration. One way polysorbate 80 may result in hair regrowth may be through its ability to trigger histamine release in the scalp, stimulating cell growth

     

     

    Polysorbate 80 may also remove dihydrotestosterone (DHT) from the scalp. Excessive levels of DHT are thought to cause hair loss. In addition, polysorbate 80 may

    affect genetic activities in the hair follicle cells due to its ability to reverse early tissue damage that occurs at the beginning of toxin-induced carcinogenesis.

  9. There's a lot of shampoos on the market and good conditioners. Its a trial and error to find what you really like

     

     

    However,

     

    My Shampoo recommendation would be Organix South Thera Neem Scalp Therape Shampoo. It contains beneficial ingredients for hair loss. Contains Natural anti DHT inhibitors and I believe is Anti Fungal as well. Its only 12 dollars and maybe cheaper at other sources.

     

    Ingredients

    Aqueous Extracts of Azadirachta Indica (Neem) Leaf*, Mentha Piperita (Peppermint)*, Rosmarinus Officinalis* and Melissa Officinalis (Lemon Balm)*, Aloe Barbadensis Leaf Juice*, Cetearyl Alcohol, Glyceryl Stearate, Butyrospermum Parkii (Shea Butter) Fruit, Azadirachta Indica (Neem) Oil*, Panthenol, Stearalkonium Chloride, Hydrolyzed Rice Protein, Essential Oils of Citrus Medica Limonum (Lemon) Peel, Mentha Piperita (Peppermint) and Lavandula Angustifolia (Lavender), Guar Hydroxypropyltrimonium Chloride, Simmondsia Chinensis (Jojoba) Seed Oil*, Phenoxyethanol, Tocopherol (Natural Vitamin E), Ethylhexyl Glycerin. * Certified Organic

     

     

     

    As for the conditioner one of the very best is Luxe Conditioner. Yeah its 22 dollars but with shorter hair it should go along way and it wont clog your follicles like most conditioners do. It also contains a lot of natural anti hair loss ingredients

     

    Ingredients: water, behentrimonium methosulfate, cetearyl alcohol, *cetyl babassuate, *babassu oil, **emu oil, wheat amino acids, soy amino acids, arginine, serine, threonine, acetamide MEA, hydrolyzed hair keratin, panthenol, sorbitol, sodium cocoyl, collagen amino acids, cocoyl sarcosine, wheat germ acid, wheat germ oil, linolenic acid, linoleic acid, sulfur, polysorbate 80, oleth-10, *jojoba oil, ***organic rosemary essential oil, organic lavender essential oil, organic thyme essential oil, organic cedarwood essential oil, ***organic orange essential oil, tocopheryl acetate, hydrolyzed glycosaminoglycans, dehydroacetic acid, benzyl alcohol.

  10. I've been paying about $35 for mine for the last 2 years -- no complaints !!

     

    What really pisses me off is when I think back about how expensive and hard to get it was 10 years ago!! I had to order from a canadian pharmacy and they needed a new prescription every time. Because it was like this I allowed myself to miss several months out of every year !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

     

    Even though I was only an early NW4 pre-HT this year I can't help but wonder how much better off I would be had I 1) always had a consistent supply and 2) been able to start it at age 22 instead of age 30 !!

     

    I am almost certain had I started it at age 22 that my genetics were good enough to keep me at a strong NW3 with no crown loss. This is why when I see these young early MPB bucks today saying they'd rather not take fin it makes me laugh at how stupid some of them are. They have it so good compared to what us older guys had to go thru !!

     

     

     

    I wouldn't call someone who refused to use Fin stupid. There are a lot of side effects. Some of them can be irreversible or required heavy treatment. Or the fact that it can increase severity of cancer. Androgen sensitive hair. That over time it does wear off and you are screwed later on.

  11. Masturbation does increase hair loss. The evidence is very valid.

     

    It increases prolactin in the body thus increasing DHT and scalp inflammation.

     

     

    Biol Psychol. 2006 Mar;71(3):312-5. Epub 2005 Aug 10.Related Articles, Links

     

    The post-orgasmic prolactin increase following intercourse is greater than following masturbation and suggests greater satiety.

     

    Division of Psychology, School of Social Sciences, University of Paisley, Scotland, UK. stuartbrody@hotmail.com

     

    Research indicates that prolactin increases following orgasm are involved in a feedback loop that serves to decrease arousal through inhibitory central dopaminergic and probably peripheral processes. The magnitude of post-orgasmic prolactin increase is thus a neurohormonal index of sexual satiety. Using data from three studies of men and women engaging in masturbation or penile-vaginal intercourse to orgasm in the laboratory, we report that for both sexes (adjusted for prolactin changes in a non-sexual control condition), the magnitude of prolactin increase following intercourse is 400% greater than that following masturbation. The results are interpreted as an indication of intercourse being more physiologically satisfying than masturbation, and discussed in light of prior research reporting greater physiological and psychological benefits associated with coitus than with any other sexual activities.

     

     

     

    Interestingly enough sex doesn't have the same side effect

     

     

     

     

    "This current study examined the effect of a 3-week period of sexual abstinence on the neuroendocrine response to masturbation-induced orgasm. Hormonal and cardiovascular parameters were examined in ten healthy adult men during sexual arousal and masturbation-induced orgasm. Blood was drawn continuously and cardiovascular parameters were constantly monitored. This procedure was conducted for each participant twice, both before and after a 3-week period of sexual abstinence. Plasma was subsequently analysed for concentrations of adrenaline, noradrenaline, cortisol, prolactin, luteinizing hormone and testosterone concentrations. Orgasm increased blood pressure, heart rate, plasma catecholamines and prolactin. These effects were observed both before and after sexual abstinence. In contrast, although plasma testosterone was unaltered by orgasm, higher testosterone concentrations were observed following the period of abstinence. These data demonstrate that acute abstinence does not change the neuroendocrine response to orgasm but does produce elevated levels of testosterone in males."

    Endocrine response to masturbation-induced orgasm ... [World J Urol. 2001] - PubMed result

     

  12.  

    • Anti depressant & Stimulant: The components of Bergamot Oil, like Alpha Pinene and Limonene, are anti depressant and stimulant in nature. They give a feeling of freshness, joy and energy in cases of sadness and depression by improving circulation. They also stimulate hormone secretion and thus help maintaining proper rates of metabolism. This stimulating effect increases secretion of digestive juices, bile and insulin, thereby aiding digestion, proper absorption of nutrients, assimilation and decomposition of sugar and t
    • he resultant lowering of blood sugar level.
    • Relaxant & Sedative: The Flavonoids present in Bergamot oil are very good relaxants too. They soothe nerves and reduce nervous tension, anxiety, stress etc. and hence help cure ailments associated with stress such as sleeplessness, high blood pressure etc.
    • Anti Biotic & Disinfectant: Certain components of the essential oil of Bergamot are anti biotic and disinfectant in nature. They inhibit growth of germs, virus and fungi. They also effectively prohibit infections, such as those of skin. If regularly used with bathing water or in soaps (this is already used extensively in skin-care soaps), the skin and hair remains protected from infections and become shiny. It also cures infections of colon, intestines, urinary tract and kidneys.
    • Anti Septic & Vulnerary: The same disinfectant and anti biotic properties of Bergamot Oil make it a good anti septic and vulnerary agent. It not only helps fast healing up of wounds, cracks on skin and heels, ulcers, eczema, itches etc. but also protects wounds from being septic and developing tetanus.
    Febrifuge: Febrifuge is a substance or an agent that reduces fever and lowers body temperature. Bergamot is a good febrifuge due to many reasons. First, being an anti biotic, it fights infections from virus, bacteria and protozoa which cause fever, such as influenza (virus), malaria (protozoa) and typhoid (typhus bacteria), and thus helps curing fever. Second, it stimulates the metabolic system and secretions, thereby giving a feeling of warmth and resulting in more secretion (perspiration or sweat) from the Eccrine glands (sweat glands) and sebaceous (sebum) glands, thus reducing body temperature.
    Analgesic: It reduces the feeling of pain in the body. Actually it stimulates secretion of certain hormones which lessen sensitivity of nerves to pain. Thus it is very helpful in case of headache, sprains etc. all those symptoms which require heavy dosage of analgesic pills.
    Digestive: As discussed above, it activates and increases secretions of the digestive acids, enzymes and bile and facilitates digestion. It also synchronizes or regulates the peristaltic motion of the intestines and this way too, help in digestion.
    Cicatrisant: This property of Bergamot oil is the reason behind its extensive use in cosmetics, skin-care products such as beauty soaps, creams, lotions etc. Cicatrisant is a property or an agent which helps the scar and other marks on the skin to disappear. It also makes the distribution of pigments and melanin even and uniform, resulting in the fading away of marks.
    Deodorant: No doubt, this property of bergamot oil is going to attract the teenagers who are after every new deodorant in the market and desperately want something really refreshing and natural. This is an excellent deodorant. Its own refreshing aroma (fragrance) and disinfectant properties (which inhibit growth of germs causing body-odor) make it a really effective and attractive package as a deodorant.
    Anti Spasmodic: It relaxes nerves and muscles and thus gives quick relief in cramps, convulsions, painful muscle contractions etc.
    Vermifuge: It kills worms. Thus it is going to be a very fragrant choice for children who have worms. It can also be applied on the affected tooth or used as a mouthwash to kill oral germs and protect teeth from cavities.

     

    It does cover a lot of aspects of hair loss, theoretically. It might be worth a try

  13. Acetyl L Carnitine should always be taken synergistically with Alpha Lipoic Acid. Preferrably the stabilized version. Don't take L carnitine by itself. Through its generation of ATP through the mitochondria, it can increase free radicals without Lipoic acid. But together they are a very powerful antioxidant and will help your hair. Also you'll need to supplement with biotin then to. Since Lipoic Acid will drain biotin from your body.

     

     

    The combo is effective. Anyone looking to prevent hair loss internally, this is part of the equation

  14. There are a lot of high quality herbal shampoos out there on the market. Try to avoid Shampoo that uses chemicals. Particularly SLS. If you go to Iherb. Its a distribution site for VItamins, shampoo etc. They usually carry some good shampoos.

     

    I've recently been using Aubrey Organics Ginseng Biotin. Its not a miracle shampoo but its nice. My advice would just experiment.

     

     

    I took a plunge and bought Bicolin Phydrium advance shampoo. For a whopping 40 dollars this stuff better be good.

  15. My regimen to keep my hair is working for me..But my temples are transparent and the only way around this is if I get lucky and get Lots and lots of regrowth there (unlikely). My hair is medium length so the transparent temples becomes a problem. At times on a good hair day I can get around it. But most times not so much. I would go shorter but I do not look good at all. It does nothing to compliment my features but only showcases the worst..Also I have a mole in the upper right corner on my temple that would be noticeable if I got it short.

     

    It seems that my hair wouldn't look too bad and would be bearable in public if I just had my temples filled to provide adequate coverage on the sides. Not to mention a whole other reason just to cover that mole up..Of course I'm 24 but would I be turned down by a good HT doctor for such minor work?

  16. Ann Dermatol Venereol. 2007 Apr;134(4 Pt 1):347-51.

    [Lithium gluconate 8% in the treatment of seborrheic dermatitis]

     

     

    Dr?no B, Blouin E, Moyse D.

     

    D?partement de Dermatologie, CHU de Nantes, 44035 Nantes Cedex. bdreno@wanadoo.fr

     

     

    Seborrheic dermatitis is a chronic from of inflammatory dermatitis characterized by erythema and desquamation with predominant localization on the face (nasolabial folds, eyebrows, hair-line and ears). It appears to be caused by proliferation of Malassezia yeasts. Lithium gluconate 8% gel (Lithioderm 8% gel) is the only drug containing topical lithium salt commercially available in France for the treatment of seborrheic dermatitis. The mechanism of action of topical lithium is not well known; it may act through anti-inflammatory and antifungal action. Efficacy and safety were assessed in 2 clinical studies, one versus placebo and the other versus ketoconazole 2% foaming gel using the same principal criterion defined as the rate of patients showing complete remission after 2 months of treatment (complete disappearance of both erythema and desquamation). Lithium gluconate 8% was significantly more effective than placebo and than ketoconazole 2% foaming gel and was well tolerated. Adverse events observed were cutaneous (burning sensation, erythema and pruritus), for the most part of mild severity. No cutaneous side effects contributed to those reported with the use of systemic lithium in psychiatric disorders were noted. Pharmacokinetic studies have shown that systemic absorption after topical application is low. Lithioderm 8% gel is applied twice daily over a recommended period of 2 months. It constitutes a new alternative in the treatment of facial seborrheic dermatitis, regardless of severity.

     

     

     

    Br J Dermatol. 2003 Jun;148(6):1230-6.

    Lithium gluconate 8% vs ketoconazole 2% in the treatment of seborrhoeic dermatitis: a multicentre, randomized study.

    Dreno B, Chosidow O, Revuz J, Moyse D; STUDY INVESTIGATOR GROUP.

     

    Clinique Dermatologique, CHU Nantes, H?tel Dieu, BP 1005, 44305 Nantes cedex, France. bdreno@wanadoo.fr

    Abstract

     

    BACKGROUND: Lithium significantly improved seborrhoeic dermatitis symptoms in comparison with placebo. Objectives This randomized controlled trial was designed to show a non-inferiority of 15% (primary end-point) of lithium gluconate 8% ointment compared with ketoconazole 2% emulsion. METHODS: The study population comprised out-patients who had facial seborrhoeic dermatitis for at least 2 months, with moderate to severe erythema and desquamation at inclusion. The primary end-point was complete remission, defined as the disappearance of both erythema and desquamation. The non-inferiority of lithium was assessed on the 95% confidence interval (CI) of the difference between treatments. RESULTS: The intent-to-treat analysis (ITT) involved 288 patients and the per protocol (PP) analysis 269 patients. Treatment groups were comparable at baseline on age, sex, disease duration and symptoms. For the main criterion, the success rate was 52.0% (lithium) vs. 30.1% (ketoconazole) in the ITT population and 53.2% (lithium) vs. 30.7% (ketoconazole) in the PP population. The non-inferiority of lithium was demonstrated with differences of 21.9% (95% CI 10.0-33.7%) and 22.5% (95% CI 10.2-34.8%), respectively, in the ITT and PP population. As the lower limit of the 95% CI was > 0, the superiority of lithium was shown. Lithium also showed better results on other symptoms: burning and dryness. Adverse events were reported by 26.3% (lithium) and 25% (ketoconazole) of patients. CONCLUSIONS: Lithium was 22% more effective than ketoconazole in giving complete remission of seborrhoeic dermatitis, with comparable safety.

     

     

    Proc Natl Acad Sci U S A. 2003 May 13;100(10):5834-9.

    A Wnt- and beta -catenin-dependent pathway for mammalian cardiac myogenesis.

    Nakamura T, Sano M, Songyang Z, Schneider MD.

     

    Center for Cardiovascular Development and Department of Biochemistry, Baylor College of Medicine, Houston, TX 77030, USA.

    Abstract

     

    Acquisition of a cardiac fate by embryonic mesodermal cells is a fundamental step in heart formation. Heart development in frogs and avians requires positive signals from adjacent endoderm, including bone morphogenic proteins, and is antagonized by a second secreted signal, Wnt proteins, from neural tube. By contrast, mechanisms of mesodermal commitment to create heart muscle in mammals are largely unknown. In addition, Wnt-dependent signals can involve either a canonical beta-catenin pathway or other, alternative mediators. Here, we tested the involvement of Wnts and beta-catenin in mammalian cardiac myogenesis by using a pluripotent mouse cell line (P19CL6) that recapitulates early steps for cardiac specification. In this system, early and late cardiac genes are up-regulated by 1% DMSO, and spontaneous beating occurs. Notably, Wnt3A and Wnt8A were induced days before even the earliest cardiogenic transcription factors. DMSO induced biochemical mediators of Wnt signaling (decreased phosphorylation and increased levels of beta-catenin), which were suppressed by Frizzled-8Fc, a soluble Wnt antagonist. DMSO provoked T cell factor-dependent transcriptional activity; thus, induction of Wnt proteins by DMSO was functionally coupled. Frizzled-8Fc inhibited the induction of cardiogenic transcription factors, cardiogenic growth factors, and sarcomeric myosin heavy chains. Likewise, differentiation was blocked by constitutively active glycogen synthase kinase 3beta, an intracellular inhibitor of the Wntbeta-catenin pathway. Conversely, lithium chloride, which inhibits glycogen synthase kinase 3beta, and Wnt3A-conditioned medium up-regulated early cardiac markers and the proportion of differentiated cells. Thus, Wntbeta-catenin signaling is activated at the inception of mammalian cardiac myogenesis and is indispensable for cardiac differentiation, at least in this pluripotent model system.

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