AAS and Hair Loss

Luscious Lei

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Following my post on RU 58841, a few members expressed their interest for an extensive post on the hair loss topic, I therefore took a few minutes of my times to put this together and hopefully inform and answer pretty much all the questions a member, juicer or not, might have on the subject.

1. The Hair

The knowledge of the hair composition is, in itself, of little help or interest when it comes to hair loss and its prevention, so I won’t detail the subject extensively. To cut it short, it is a filamentous biomaterial mainly made of keratin and produced by the hair follicle. There are two types of hair, vellus hair, very fine hair present all over the body, and the thick terminal hair, found on particular body areas (scalp, pubis, etc…).
The visible hair is actually made of “dead” tissues, the “living” part of it being at the follicle level. So long for all the commercials bombing us with the “life” of our hair.

2. The hair follicle

This is the part that interests us since this is where the hair is, or isn’t, produced. It has a fairly complex structure: papilla, matrix, root sheath, bulge and of course the hair itself (hair fiber). On top of these, other structures are associated to the follicle: arrector pili muscles, sebaceous glands and apocrine sweat glands.
The hair follicle activity is divided in 3 distinct phases: anagen, catagen and telogen
The anagen phase is the “hair production” phase: the root of the hair is dividing rapidly, creating hair fiber at an average rate of 1cm/month. The length of this cycle is genetically determined and set the hair length, the longer the cycle, the longer the hair. Scalp hair follicles have a cycle length of 2 to 7 years, body hair 4 to 7 months. That’s why you need a haircut here and there but can’t grow a ZZTop beard on your chest.

The catagen phase is a short transition stage signaling the end of the hair growth phase. The hair is cut from its blood supply, the phase lasts a couple of week.

The telogen phase is the resting period of the hair follicle. Cut from its blood supply during the catagen phase, the hair turn into a club hair, a “dead” fully keratinized hair, which ends up falling. In scalp this phase lasts around 3 months, and is an interesting phase since some forms of alopecia are related to a sudden and massive telogen phase for a higher than normal amount of hair. Normally, 50 to 100 club hair are shed from the scalp, but in the condition called telogen effluvium a higher percentage (up to 70%) of hair get into telogen phase causing massive and sudden hairloss. This condition can be provoked by extreme stress and is very different, in term of mechanism, from the form of hair loss we are interested in.

3. Hair loss

There are numerous types of hair loss, or alopecia. Their symptoms are various, from the local alopecia areata that affect partial areas of the scalp to alopecia universalis which leads to the loss of all hair, body hair included. Their causes are numerous too, ranging from simple nutritional deficiencies to autoimmune reactions. Actually, every human being, men and women, are subject to alopecia. It is known as involutional alopecia and is the result of the progressive increase of hair going to anagen to telogen phase, therefore the question is not “will I go bald?” but “how long will it take for me to go bald?”.

It is a very wide subject so we will jump straight to the form of hair loss that interest us, and that is also the most common form of alopecia: alopecia androgenica, or Male Pattern Baldness (MPB).

MPB is surprisingly both extremely common and relatively poorly understood. We could expect such a widespread affliction to be studied more thoroughly but the reality is that men go bald since the dawn of time without any other issues than aesthetic ones and that medical science is focused on more important matter. None of the drugs efficient at reducing / preventing / reverting MPB have been developed primarily to treat it.
Here I will push the laziness button and simply paste/copy the Wikipedia description of MPB, since it is both concise and accurate:

More than 95% of hair thinning in men is male pattern hair loss (also known as androgenic alopecia). Male pattern hair loss is characterized by hair receding from the lateral sides of the forehead (known as a "receding hairline") and/or a thinning crown (balding to the area known as the ‘vertex’). Both become more pronounced until they eventually meet, leaving a horseshoe-shaped ring of hair around the back of the head.
The incidence of pattern baldness varies from population to population and is based on genetic background. Environmental factors do not seem to affect this type of baldness greatly. One large scale study in Maryborough, Victoria, Australia showed the prevalence of mid-frontal baldness increases with age and affects 73.5 percent of men and 57 percent of women aged 80 and over. A rough rule of thumb is that the incidence of baldness in males corresponds to chronological age. For example, according to Medem Medical Library's website, male pattern baldness (MPB) affects roughly 40 million men in the United States. Approximately 25 percent of men begin balding by age 30; two-thirds begin balding by age 60.
There is a 4 in 7 chance of receiving the baldness gene. Onset of hair loss sometimes begins as early as the end of puberty, and is mostly genetically determined. It was previously believed that baldness was inherited from the maternal grandfather. While there is some basis for this belief, both parents contribute to their offspring's likelihood of hair loss. Most likely, inheritance involves many genes with variable penetrance.
The trigger for this type of baldness is dihydrotestosterone, a more-potent form of testosterone often referred to by its acronym DHT. DHT is an androgenic hormone, body- and facial-hair growth promoter that can adversely affect the prostate as well as the hair located on the head. The mechanism by which DHT accomplishes this is not yet fully understood. In genetically prone scalps (i.e., those experiencing male or female pattern baldness), DHT initiates a process of follicular miniaturization, in which the hair follicle begins to deteriorate. As a consequence, the hair’s growth phase (anagen) is shortened, and young, unpigmented vellus hair is prevented from growing and maturing into the deeply rooted and pigmentedterminal hair that makes up 90 percent of the hair on the head. In time, hair becomes thinner, and its overall volume is reduced so that it resembles fragile vellus hair or "peach fuzz" until, finally, the follicle goes dormant and ceases producing hair completely.


It is interesting to note that follicles don’t “die” but go dormant and therefore that hair regrowth is always theoretically possible, although practically it is rather rare.

Another important aspect of MPB is that its correlation with age seems to be “programmed”. An individual prone to MPB following a treatment stopping the evolution of his hair loss for 20 years will not see his condition progressively evolve once the treatment is discontinued, but will quickly reach the level where he would have been if he had never taken any drug. Eunuchs receiving exogenous testosterone in their 20s develop slight and progressive MPB, while subjects following the same regimen in their 50s-60 rapidly develop strong MPB and lose their hair at a very high rate. It means that the prevention / treatment for the individual subject to MPB is pretty much a life-long treatment.

MPB being closely related to androgenic hormones in general and DHT in particular, the use of AAS has the potential to have a very substantial impact on it. DHT being the main actor in follicular miniaturization, injecting large amount of exogenous testosterone, and therefore dramatically increasing the DHT levels, or injecting DHT derivatives will obviously kick start or speed up the thinning process.

That’s where MPB and AAS can be a bitch cocktail. For people with pre-existing condition, it is possible to predict the effect that a particular compound will have, but brutal change in hormone levels can also trigger a MPB that would have otherwise started years or decades later. I’ve recently been in touch with a juicer in his late 30s who had done a dozen of test-mast-tren cycles without losing a hair and who brutally starting to shed at a very high rate a few weeks into a test-mast cycle. No one can be 100% sure that he will never be affected by this condition.
Another tricky aspect of MPB is that individuals will react differently to a particular hormone, some might be relatively DHT-proof but will shed with DHT derivative when others can be in an opposite situation. Typically, I don’t shed under test at 750/w but had hair thinning during a light test250/Eq500 cycle, which makes me guess that I’m particularly sensitive to dihydroboldenone.

4. Steroids

The potential aggravating / triggering effect of steroids on MPB depends on how androgenic and how close to DHT the compound is, with the former being the most important. For example, Oxandrolone is a DHT derivative but has the reputation to be one of the safest AAS when it comes to hairloss when Tren isn’t but is a potential hair murderer due to being highly androgenic.
The list below is non-exhaustive and I hope my fellow members will chime in to give their inputs. Also, as stated above, MPB and AAS are a highly unpredictable combination, I know juicers who shed on DHT derivative as “safe” as var or primo but who do fine on heavy tren cycles, so don’t take anything as granted but rather like rough guidelines.

Orals

Oxandrolone (Anavar, “var”)

Although it is a DHT derivative, var is famous for being one of the safer, if not the safest, oral steroid regarding hair loss, even at high dose.

Turinabol (“Tbol”)

Although its structure is very close to Dbol, Tbol has the reputation to be very safe on the hairline, probably because it is virtually not androgenic at all.

Methandrostenolone (Dianabol, “Dbol”)

Being very androgenic, Dbol is supposedly not a safe compound, although topical prevention should be able to minimize / prevent hair loss.

Oxymetholone (Anadrol, “drol”, “Abombs”)

Anadrol has a terrible reputation regarding MPB, being very highly androgenic and converting to DHT at a very high rate, and will very likely aggravate the situation of users with pre-existing condition.

Stanozolol (Winstrol, Stromba,“winny”)

Winny is a DHT derivative and although it doesn’t have a high androgenic rating, it is famous for being the ultimate oral hair murderer. Not only topical ancillaries won’t be enough to protect the scalp but even people without MPB might experience hair loss with it.

Injectables

Nandrolone (Deca Durabolin, “Deca”, NPP)

Nandrolone is probably the safest injectable compound, with a high anabolic rating but a very low androgenic one. However it should, like all AAS, be used with a Test base and it is not recommended to use nandrolone in conjunction with 5AR inhibitors like Finasteride or Dutasteride. Preventing its conversion will turn nand into a much more androgenic compound and will make it 150% more androgenic. That being said, some users argue that being very lightly androgenic to begin with, it is still a safe compound after this 150% increase of its androgenic properties. I got no experience with nand so I hope members will give their feedback on this topic.

Methenolone (Primobolan, “primo”)

The safety of primo, hair loss wise, is a tricky subject. Being very mildly androgenic it is generally considered a very safe option but it is also a DHT derivative and DHT sensitive users might experience serious shedding on it. Another delicate subject is the dose, being mildly anabolic as well, users often take it at high doses, 1g/w and over, and at this level MPB is a worrisome matter. That being said it is generally considered one of the most “hair friendly” injectable.

Testoterone

Since testosterone converts to DHT, it is responsible for existing MPB and therefore increasing its level will obviously have an impact. However test is a fairly safe compound since its effects are easily predictable, and when used with Finasteride / Dutasteride it actually becomes one of the safest AAS.

Boldenone (Equipoise, “Eq”)

Boldenone is a safe compound, generally considered safer than testosterone, however, just like primo it is often ran at fairly high dose to make it up for its low anabolic properties. It might then be harsh on the hairline since a part of boldenone is converted into dihydroboldenone, a very androgenic hormone with the potential to hit the follicles harder than DHT.

Trenbolone (Parabolan, “tren”, “fina”)

Being very highly androgenic, trenbolone is harsh on the hairline, with some users experiencing hair thinning although they are not prone to MPB (even if in that case hair will thicken back to normal once the cycle is discontinued). Reactions between individuals are highly variable, with sensitive people doing fine under low to moderate dose while and others will see their hair literally slaughtered. To be used with caution.

Dihydroboldenone (1-Test cyp)

Dihydroboldenone cypionate is a derivative from the rather mildly androgenic boldenone, but DHB is a lot more potent than boldenone and actually is a very androgenic compound despite its relatively low rating of 100 on the androgenic / anabolic scale, therefore aggravated MPB condition is definitively a serious concern.

Drostanolone (Masteron)

With some fairly elevated androgenic properties and a structure very close to DHT, masteron has a terrible reputation when it comes to hair loss and is often considered as the worst of all injectables and should be totally avoided by users prone to MPB.

5. Ancillaries

As explained at the beginning of this thread, MPB is not the world’s medical research top priority and very few options are to be considered, none of them being an ideal solution. DHT or other similar androgens being the culprit, the idea is to lower it or to prevent its binding to the follicles receptors.

Systemic

Finasteride / Dutasteride

Finasteride (Proscar, Procepia, etc…) and Dutasteride (Avodart) are, by far, the most effective available compound to lower DHT levels. Both of them have been primarily designed to fight prostate enlargement (Benign Prostatic Hyperplasia, or BPH) by preventing testosterone conversion to DHT.Testosterone in males is produced primarily in the testicles, but also in the adrenal glands. The majority of testosterone in the body is bound to sex hormone-binding globulin(SHBG), a protein produced in the liver that transports testosterone through the bloodstream, prevents its metabolism, and prolongs its half-life. Once it becomes unbound from SHBG, free testosterone can enter cells throughout the body. In certain tissues, notably the scalp, skin, and prostate, testosterone is converted into 5α-dihydrotestosterone (DHT) by the enzyme 5α-reductase. DHT is a more powerful androgen than testosterone (as it has approximately 3-10 times the potency at the androgen receptor, the site of action of the androgen hormones), so 5α-reductase can be thought to amplify the androgenic effect of testosterone in the tissues in which it's found.

Finasteride and Dutasteride work by acting as a potent and specific, competitive inhibitor of the subtypes of 5α-reductase, the type II isoenzyme for Finasteride and I and II typea for Finasteride. In other words, they bind to the enzyme and prevents endogenous substrates such as testosterone from being metabolized. 5α-reductase type I and type II are responsible for approximately one-third and two-thirds of systemic DHT production, respectively.
Usual dose for Finasteride are 1mg/day for BPH treatment and 0.5mg/day for MPB. There’s no substantial difference in scalp DHT levels between 0.5 and 1mg.

Dutasteride is FDA approved for BPH only, but usual dose for MPB is set around 0.5mg/day, which is the same dose than for BPH. It generally comes in soft gel caps, making the dose split difficult but its longer half life allows for EOD or E3D intake schedules.
Since Dutasteride work on 2 of the 3 isoenzyme types, it is more efficient than Finasteride at lowering DHT. However its half-life is also much longer than Finasteride, we are talking about hours for Fina and weeks for Duta. In a study measuring DHT blood levels 12 weeks after discontinuation of the treatment, Finasteride users had recovered normal DHT levels but those under Dutasteride still had lower than normal levels.
It should be noted that the overall DHT decrease is higher at a global level than at the scalp level: 1mg of Finasteride will decrease DHT blood concentration by 73% but scalp DHT by 32% only.

Fina/Duta present two main issues. The first is that, since they prevent test conversion to DHT, they will be effective on testosterone only. They won’t any effect on any other AAS than test. The second is that DHT is an androgenic anabolic hormone that play an important role in libido. Lowering DHT levels in the scalp is great for the hair, but lowering them elsewhere doesn’t go without potential side effects. Fina/Duta are often described as miracle drugs, which they are to a certain extent, and as evil libido killers. Personally, I would take them as a last resort option but I will try to stay as neutral as possible and will simply list a few facts:

- Finasteride and Dutasteride are the sole an only compounds that have been clinically proven efficient at stopping and often reverting MPB. Numerous clinical studies have been carried and are easy to find on the web.
- The potential side effects, as listed on the drug leaflets, are: impotence, loss/decrease of libido, reduction of semen volume (frequent) – Breast puffiness (uncommon) – palpitations, liver malfunction, testicular pain (rare) – lactation (very rare)
- Clinical studies repeatedly reported substantial decrease in sperm count among Fina/Duta users
- Some cases of permanent side effects have been reported.
The debate between the safety / danger of these drugs is virtually endless, so I won’t develop further and invite the persons contemplating to use them to do their homework before blindly popping pills.

Topical

Minoxidil (Rogaine, generic minoxidil)

Minoxidil is neither a DHT blocker nor a DHT killer. It is an antihypertensive vasodilator, primary developed to treat high blood pressure. Regarding MPB, it acts as a growth stimulator, although the mechanism by which it promotes hair growth is not clearly understood. Hypothetically, its vasodilator properties allow more oxygen, blood and nutrients to the follicle. People respond differently to it, with results ranging from very substantial regrowth to no result at all. Some even use it to add density to facial hair with success. Results seem to be dose dependent, with some users not experiencing any improvement with 2% lotion once a day but obtaining strong regrowth with 5% lotion twice daily. Users getting substantial regrowth generally experience a strong shedding at the beginning of the treatment, this shedding should therefore be taken positively and the treatment continued since regrowth of existing and new hair generally follows. It generally comes in standardized 2% or 5% solution, those looking for higher concentration can simply multiply the applications.

Ketoconazole (Nizoral shampoo)

Ketoconazole is a synthetic imidazole antifungal medication primarily used to treat fungal infection, systematically and topically, although its systemic use is getting progressively banned due to a bad efficiency / potential side effects (liver strain) ratio. Topically it is used to treat a variety of skin fungal infections as well as seborrheic dermatitis, including dandruff. It also has antiandrogenic properties and that’s where it is a compound of interest for MPB, by inhibiting the activity of some enzymes involved in the conversion of cholesterol to testosterone, by blocking the DHT synthesis and by acting as an androgen receptors antagonist. It comes in cream and shampoo forms at 1% and 2% concentration. It is often said that it is bad for the hair if used daily but it is because it can dry the scalp excessively, in the case of an athlete on cycle, with the commonly more than usual oily skin, daily usage is not an issue.

Spironolactone (Spiro)

Spiro is a synthetic steroidal antimineralocorticoid and antiandrogen primarily used as diuretic and antihypertensive but also as an androgen activity suppressor. It is both an androgen receptor antagonist and an inhibitor of androgen production and is used off label to treat various androgen-related conditions like hirsutism, acne, seborrhea and MPB. Although it is far to be the most potent androgen receptor antagonist it is pretty effective at doing so and is used in HRT in transgender men. Therefore its use for MPB is topical only since even low systemic doses would generate feminization side effects. Its efficacy as a topical is limited by its poor ability to cross the transdermal barrier and its short half-life. It generally comes in 5% solutions.

Azelaic acid

Azelaic acid is saturated dicarboxylic acid, and is not medically used to treat MPB, it is primarily used to treat acne by killing the bacteria responsible for skin pores infections. However, it is supposed to “break” DHT and has been added to various cosmetic lotions used to treat MPB. Although only one debatable study has proven its “DHT killing” properties, it seems that the minoxidil+azelaic acid are more efficient than minoxidil alone. Unfortunately this addition to topical lotions has been banned by the US FDA and now it must be purchased as a separate compound. Being primarily aimed at acne, it generally comes in cream form, at concentration around 20%. This cream form makes its scalp topical use a bit annoying.

RU 58841

Originally studied by Roussel-Uclaf, hence the “RU”, it is one of the very few compound primarily developed for the treatment of MPB. It is one of the most potent and effective antiandrogen known at the moment, displaying a very high affinity and selectivity to the androgen receptors. It acts as Spironolactone but much more aggressively, binding to both types of DHT receptors, and is therefore theorically efficient at protecting the follicles from any AAS. The drawback of the compound is that it readily pass the transdermal barrier and is quite hardy, therefore the RU that doesn’t bind to the scalp androgen receptors will continue its journey and ultimately binds to other organs receptors. It can therefore generates the usual side effects associated with antiandrogen, but at a lower level than systemic compounds. Another issue is its relatively short shelf life, it is sensible to oxygen and temperature and should be kept in the freezer. Also, since the development of the drug has been stopped (although it has been sold for a short period of time in Europe and Japan), it is available in raw form only. For the reasons mentioned above, batches of 5 to 10 applications should be prepared at a time, since the final product will quickly lose its potency.

CB 03 01

CB is currently under development by Cosmo and has finished the final clinical studies phase for the 1% concentration. This concentration is too low to be helpful for MBP, but the 5% version is in Phase II. It displays the same antiandrogen properties than RU 58841, but is more stable, drastically extending its shelf life, and is much cheaper. But its most interesting property is its rapid degradation into a neutral compound once it has passed the transdermal barrier. Therefore, there is not risk of antiandrogen associated side effects since the CB that doesn’t bind to the hair follicles receptors will degrade before reaching other organs. Like RU, it can be bought in raw form but is pretty useless since there’s no DIY readily available carrier to make an efficient scalp lotion in a “bathroom lab”, it is preferable to wait for the final product release, which should come relatively soon.

6. Vitamins, Minerals and supplements

No vits or supps will make a drastic difference with you hair health and growth, especially since the rich diet followed by most gymrats already covers most daily intakes and there are very few chance that you are deficient in any of them. Iron is important but excessive Iron levels are very unhealthy, if not dangerous, so there’s no reason to supplement unless you’re deficient, which should be assessed by blood works. Vitamin D is important but once again, you should be fine unless you’re living in an area with limited sunlight. Zinc also plays an important part in hair health but you’re probably already supplementing with it. Vitamins B, especially B7 (Biotin), B3 (Niacin) and B12 (Cobalamin) also display hair strengthening properties but once again you probably already got plenty of them thank to your diet.

7. Hair transplantation

Surgery is a bit off topic, but since we try to cover the subject extensively let’s talk about it. There are 3 methods, all based on the same principle, which is to surgically extract hair follicles from the lateral humps and to relocate them on the baldness affected area generally the crown, midscalp, central forelock and temporal angles. The advantage of this operation is that the hair follicles in the lateral humps are not genetically DHT sensitive, it is therefore a theoretically definitive solution.

The Follicular Unit Transplantation (FUT) method

Also known as “strip method”, it is based on the harvesting of one or several “strips” of scalp from an area with good growth (generally the back of the head). While closing the resulting wounds, assistant surgeons dissect the harvested strips into individual follicles. Those are then grafted one by one on the balding areas. The drawback of this method is the severity of the harvested area scars. They can be pretty bad although the latest method, called trichophytic closure, leaves much finer scars. The scars are covered by the hair, but is the transplants fail, which is rare but possible, and the patient decide to give up and to shave his head, they will become very visible.

The Follicular Unit Extraction (FUE) method

It is based on the same principle as the FUT method except than instead of long strips of scalp, tiny “patches” of 1 to 4 follicles are extracted. It is less invasive than the FUT method but is obviously a much more tedious and time consuming process. Waiting lists are substantially long, and patients are selected upon a “fox test”, consisting of a biopsy of few follicles to examine them and check how easy their removal is and how suitable they are for transplant. Being longer to perform, the operation is also more expensive than FUT.

Hair Stem Cell Transplantation (HST)

The name of the method is confusing and shouldn’t be mistaken for the real stem cell therapy which is still at an experimental stage. It has been developed by Dr Coen Gho and is therefore also known as “the Gho method”.
With this method, specifically designed tools harvest only parts of the hair follicles. Most of the harvested follicles heal after the harvesting and therefore keep producing hair. The grafts then develop into fully functional hair follicles. For this reason, the method is also called “hair multiplication” since there’s no real relocation. Very few clinics (6) perform these procedure and they are quite expensive, with a starting price of 10K+ USD for a basic 1600-1800 follicles transplant. The method is much less invasive than FUT and FUE and the results are as impressive as the bill is painful.

8. Stem Cell Therapy

As stated above, the use of Stem Cell Therapy to treat MPB is still at an experimental stage. Hair follicles also contain stem cells, and some researchers predict research on these follicle stem cells may lead to successes in treating baldness through an activation of the stem cells progenitor cells. This treatment is expected to work by activating already existing stem cells on the scalp. Later treatments may be able to simply signal follicle stem cells to give off chemical signals to nearby follicle cells which have shrunk during the aging process, which in turn respond to these signals by regenerating and once again making healthy hair. Most recently, Aeron Potter of the University of California has claimed that stem cell therapy led to a significant and visible improvement in follicular hair growth . Results from his experiments are under review by the journal Science (journal).

9. FAQs

Q: What is the most hair-friendly cycle?
A: The most hair friendly cycle is no cycle at all.

Q: My hair is fine, will my first cycle hurt them?
A: Nobody knows. You might do perfectly fine just like you could start shedding, even if you never displayed MBP.

Q: My hair starts to recede/thins, will my cycle make things worse?
A: Nobody knows. You might do well without ancillaries, just like the situation could worsen even with them.

Q: I haven’t shed during my previous cycle, can I be sure than I’m not prone to MPB and therefore safe whatever the gear I run?
A: No, as explained above MPB can start as early as puberty and as late as well into your 40s/50s, therefore nothing can guarantee that you’re genetically predisposed and that your next cycle won’t trigger hair loss.

Q: I have lost shitloads of hair during my previous cycle, will it regrow?
A: Nobody knows. If you never lost any during previous cycles with the same compounds, they might. If you had a pre-existing condition and your cycle made things worse, not likely.

Q: Is there any way to predict how I will react to a particular compound?
A: No, even if you had previous success with particular compounds nothing can guarantee that the situation won’t evolve.
 

NbleSavage

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Nice post. Sticky, please?
 

stonetag

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Do a lot of you guys have this problem? I get most all the sides from gear, in a not so bad sort of way, except hair loss. All the years I've cycled, no hair loss...weird.
 

SuperBane

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No mention of GH and the effects on hair?
 

ECKSRATED

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Deca always makes my hair thick and healthy as fukk. Tren I thin and shed a little but no balding

good post.
 

goodfella

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No mention of GH and the effects on hair?

Gh will help the hair line if anything. I think i've seen post of guys mentioning sum falling out but then growing back much thicker if any hairloss at all. Basically the GH getting rid of the bad hair and growing new grass/follicles. Surprisingly with superdrol being close to mast, I actually never noticed hair shedding for those who stay away from dbol.
 

widehips71

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I wanna hear from someone who has straight up went bald because of mast. Of compounds that would be new to me, it's the one I'm most interested in trying next. We don't have mpb on either side of my family so it's never been a concern for me before, but holy hell would my life take a turn for the worse if my luxurious mane started falling out.
 

Luscious Lei

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Superbane, I didn't mention GH because the potential side effects are minor and contradictory: in some studies IGF-1 have been associated with vertex balding, in others it has been shown to promote growth, results vary depending on the presence or absence of insulin, etc...It's a very grey zone. If any effect is noted it should be minor and more likely towards the "good" (anti-apoptotic properties of GH) than the "bad".

Goodfella, I never tried it but Superdrol has been repeatedly reported as very safe on the hair line, which is indeed surprising and shows that a very minor modification of a molecule can make the difference between a harsh and safe compound.

Widehips, if I were in your shoes I would start with Mast prop at low dose and work my way up from there. It should be noted that even with short esters, it takes weeks for the hair follicle to shrink / go dormant, and even longer for the process to revert, therefore even if you stop when you start shedding you will keep losing / thinning for a while before it stops / regrows.
 

AliCat

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A cautionary tale to the ladies here and for men with wives who lift. A year ago I upped my dose to about double what my gyno prescribed. Had great results, but at the same time we hit some financial problems and to save money I let my bc pills fall to the wayside. The result was that within six weeks, I lost 80% of my hair. I got back on the pills and within four days the shedding stopped, but here it is a year later and I have yet to successfully grow it more than four inches. It may never come back the same as before. In my case, I'm pretty happy with that because I look better in short hair. I don't want long hair again, but if I did, it would take three years and some bad do's to get there. Since then I am very careful to keep things in balance. For a year I went back to only prescribed levels. Now I am very, very careful.
 
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Very useful and well written article with great frequently ask questions with answers. But how much it will cost in India for hair transplantation with latest FUE treatment.
 

conan

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Excellent information. Thank you for this!
 

anewguy

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Even though this is an old post I am wondering if anyone can answer a question. Obviously AAS is hard on hairline, thinning, MPB, etc. Does it also contribute to grey hair?
 
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im bald as sh*t and i dont give a flying f*ck.... i got a fat ass wallet and thats all that matters haha
 
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man i just feel bad for the dudes that care too much about their hair, hair has nothing to do with what ur about, who u r, and what ur doing... and to be worried about it all the time is no way to live.... its like they become a prisoner of their own minds, just let it go... literally and metaphorically haha what it all comes down to is the ladies.... they care about money, body, and laughs in that order, unless u find a poor woman to fall in love with ur *ss than only the last one is relevant
 

anewguy

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man i just feel bad for the dudes that care too much about their hair, hair has nothing to do with what ur about, who u r, and what ur doing... and to be worried about it all the time is no way to live.... its like they become a prisoner of their own minds, just let it go... literally and metaphorically haha what it all comes down to is the ladies.... they care about money, body, and laughs in that order, unless u find a poor woman to fall in love with ur *ss than only the last one is relevant

I care about my hair like I care about my body. Call me crazy, but I'm tryin to be sexy over here.
 
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haha im just talking about us lucky few that r predestined to be bald....but nothing sexier than a sexy bank account
 

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