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*** Answers to Hairloss Questions Here ***
- Thread starter decem
- Start date
i just wanted to come back and update this thread a little..
i'm gonna cut and paste from another one of my thread's entitled Winny Hairloss Mechanisms + Finasteride after Deca
here goes:
Winny Hairloss Mechanisms + Finasteride after Deca
I have two hairloss questions that I haven't seen answers to yet... and I'm hoping to get some light shed on them.
1. WINNY - doesn't react with the 5-alphareductase enzyme (specificly 5AR II that is located in the scalp and the prostate) that converts testosterone and its derivitives to dihydrotestosterone (DHT - which is hard as hell on the scalp). right? ok... so if it's not turning into DHT, then how does Winny, purportedly one of the worst on the hairline second to halo/methyltest/test, have such an adverse effect on the hairline? what's the science behind it?
2. DECA - can't be used with finasteride because finasteride will block it's conversion from nandrolone to DHN.. DHN being easy on the scalp.. Nandrolone being harsh on the scalp.. so if it stays in its original form of nandrolone.. you're mr. clean in a few days. How long after taking Deca can one safely use finasteride to regrow the hair they lost while on a cycle which contained deca causing them to forgo the proper precautonary measures DURING the cycle. Obviously dosages would be a consideration here.. so let's take into account three different dosages of say 300mg, 500mg, and 800mg weekly for 10 weeks.
i'm hoping stew meat will respond to this.. as well as any of our resident chemists, and to make sure.. i will drop a few of them some pm's to request such attention to my thread. thanks ahead of time guys.
i also forwarded all of these replies to Dr. Lee and asked him what would be the best topical treatment to use while taking nandrolone to prevent the possibility of side effects from the whole nandrolone thing as well as to protect against hairloss..
he said to use the topical spirolactone...
i bought some.... it was $20 for the consultation and $20 for the stuff.. from www.minoxidil.com
i'm gonna cut and paste from another one of my thread's entitled Winny Hairloss Mechanisms + Finasteride after Deca
here goes:
Winny Hairloss Mechanisms + Finasteride after Deca
I have two hairloss questions that I haven't seen answers to yet... and I'm hoping to get some light shed on them.
1. WINNY - doesn't react with the 5-alphareductase enzyme (specificly 5AR II that is located in the scalp and the prostate) that converts testosterone and its derivitives to dihydrotestosterone (DHT - which is hard as hell on the scalp). right? ok... so if it's not turning into DHT, then how does Winny, purportedly one of the worst on the hairline second to halo/methyltest/test, have such an adverse effect on the hairline? what's the science behind it?
2. DECA - can't be used with finasteride because finasteride will block it's conversion from nandrolone to DHN.. DHN being easy on the scalp.. Nandrolone being harsh on the scalp.. so if it stays in its original form of nandrolone.. you're mr. clean in a few days. How long after taking Deca can one safely use finasteride to regrow the hair they lost while on a cycle which contained deca causing them to forgo the proper precautonary measures DURING the cycle. Obviously dosages would be a consideration here.. so let's take into account three different dosages of say 300mg, 500mg, and 800mg weekly for 10 weeks.
i'm hoping stew meat will respond to this.. as well as any of our resident chemists, and to make sure.. i will drop a few of them some pm's to request such attention to my thread. thanks ahead of time guys.
Andy13 said:
decem said:
decem said:
i also forwarded all of these replies to Dr. Lee and asked him what would be the best topical treatment to use while taking nandrolone to prevent the possibility of side effects from the whole nandrolone thing as well as to protect against hairloss..
he said to use the topical spirolactone...
i bought some.... it was $20 for the consultation and $20 for the stuff.. from www.minoxidil.com
Stew Meat said:
ANOTHER ARTICLE
SHEDDING AND HAIR LOSS
With its cycle of repetitive planned obsolescence and rebirth, hair is a unique organ system. It's of little wonder that with its complex and continuous recycling, there can be multiple clinical disorders based on cycling abnormalities. Although much is known about the organization and composition of the hairs themselves and of the follicles, we still have an incomplete and
rudimentary understanding of relevant pathways and mechanisms that regulate follicular function. In this article, we are addressing only entities that cause hair loss or shedding, rather than problems of hypertrichosis or overgrowth of hair.
The first hair follicles on the scalp form at approximately the 9th week of gestation. On the average, the human scalp will have 100,000 follicles and no further follicular neogenesis occurs after birth. You are born with as many hair follicles as you are ever going to have. The same follicles that produced lunago
(unpigmented ultra-fine) hair in the fetus and immediate postnatal life, eventually produce terminal hair. It is important to note that during one's lifetime, the same follicles can intermittently produce vellus or terminal hair.
A knowledge of the hair cycle is essential to understanding hair problems. Hair growth on the human scalp is an asynchronous regeneration of the hair follicle in repeated cycles, referred to as a mosaic pattern of follicular growth. The growth stage is the anagen phase. The duration and rate of growth of the anagen
phase normally varies at different body sites, in different individuals, and at various ages. Scalp hairs have a relatively long anagen phase typically ranging from 2 to 5 years, but has been documented to be as long as 10 years. The short-lived catagen period, usually 2 to 4 weeks in duration, is the transitional portion of the cycle. At this time, each terminal hair bulb moves
from its location in the dermis to a more superficial location by means of shrinkage and remolding of that portion below the bulge region where the arrector pilimuscle inserts. This muscle is not present on true vellus hair and allows terminal hairs to 'stand on end'. Once a hair has made the transition to the telogen phase, its existing hair shaft will not grow any longer. The hair
shaft during the telogen phase is no longer anchored securely in the dermis as it was in the anagen phase and can be easily dislodged with the gentle traction of brushing or shampooing or combing. Usually the shedding is unnoticed. Since the hair can accumulate in the shower drain or on soapy hands, patients can
erroneously associate washing the hair with causing hair loss. The telogen hair has a club shaped proximal end within the hair follicle and retains the club shape when it is shed. The new hair produced from the subsequent anagen phase does not "push out" the hair from the previous cycle and may on occasion be
found adjacent to the temporarily retained club hair within the follicular canal
------------------------------------------------------------------------------------------------------
NORMAL SCALP GROWTH OF TERMINAL HAIRS
Average number of brown/black scalp hairs: 100,000
10% more on blondes
10% less on redheads
Fastest Growth: between 15 and 30 years of age
Slow growth in infants and elderly
Average scalp hair growth: 0.35 mm/day or ~1 cm/month
Hair grows faster in summer than in winter
Month of greatest shed in the Northern Temperate zone: November
Anagen growth phase: 2 to 5 years
Percentage of hair in anagen phase: 85%-90%
Average daily numbers of hair shed: 50 to 100
Female hair grows faster than male hair
-----------------------------------------------------------------------------------------------------
Historically, alopecias have been classified as non-scarring or scarring. The scarring type is considered permanent because of the destruction of the follicle and the presence of fibrotic changes. The non-scarring alopecias don't destroy the follicle and there are little or no fibrotic changes around the follicle.
Therefore, regeneration of the follicle is theoretically possible. The division can be arbitrary and can often overlap. The transformation of a non-scarring to a scarring alopecia has been identified in some disorders.
NON-SCARRING ALOPECIAS
Alterations of hair growth
Telogen effluvium
Anagen effluvium
Miniaturization (i.e. Androgenetic Alopecia)
Congenital
Acquired
Follicular mucinosis
Chemical or physical agent
Trichodystrophies-alterations of hair
Congenital
Acquired
Trichotillomania-traction alopecia
Chemical or physical agents
Infectious agents
SCARRING ALOPECIAS
Inflammatory
Lupus erythematosus (chronic type)
Lichen planus pilaris
Planopilaris
Pseudopelade
Scleroderma
Bullous pemphigoid
Epidermolysis bullosa acquista
Folliculitis-secondary to infectious agents
Chemical and physical damage
Granulomatous inflammation
Noninflammatory
Nonscarring pseudopelade
Bullous pemphigoid
Neoplasms-benign and malignant
Many of the causes of alopecia listed above are rare and are not frequently encountered in any practice. A good dermatology textbook will describe the entities. However, it is important to understand that there are many causes for hair loss.
Although it may sound contradictory, shedding and hair loss is not synonymous. First, we must define our terms. Shedding refers to hair shafts that easily or spontaneously fall out of the scalp. There are multiple causes of shedding. Shedding normally occurs at the end of the telogen phase, but, in pathological
cases, can also occur during anagen. As a rule, shedding usually refers to a temporary event and suggests that the hair shaft will grow back again as thick as before, providing there is not an intervening pathological process.
In distinction, hair loss can refer to either the temporary or permanent loss of hair or a loss not in the number of hair shafts, but in the volume and texture of the hair shaft. For example, permanent hair loss can be caused by a scarring alopecia, such as occurs in third degree burns or radiation to the scalp.
Typical of a loss in the volume of hair, but not in the number of follicles, would be the miniaturization of the follicle due to male pattern baldness (MPB).
A complete medical history can almost always determine the cause of alopecia. If necessary, there are alternative ways for determining aberrations of scalp hair cycling. The first is the 'hair pull'. This simple technique involves gentle traction from the base to the terminal ends of a group of 25 to 50 hairs. Normally, only a few hairs are dislodged on six to eight such hair pulls.
Shedding of two to three hairs per pull is pathologic. If there is increased shedding, the proximal ends should be evaluated to determine if there is an intact hair shaft and bulb, which would indicate either an effluvium (Latin for "a flowing out") or hair breakage.
A biopsy of the scalp may or may not be helpful with the diagnosis of a particular hair disorder. The information it delivers about cycling aberrations is merely confirmatory to that obtained by other simpler, less expensive means, and the diagnosis of hair shaft abnormalities cannot be made by a scalp biopsy.
The real value of a scalp biopsy is in the insight it can offer into mechanisms of alopecia.
Since this article is being written primarily for the information of patients affected by pattern baldness, we'll limit the subject of shedding and hair loss due to physiologic processes, medications, telogen effluvium, anagen effluvium and male pattern baldness.
PHYSIOLOGIC SHEDDING
Since it would be normal to have 10 to 15% of all the hairs on the scalp in the telogen phase, we can expect that 50-100 of those hairs are at the end of the phase and will readily shed. The anagen phase is in proportion to the size of the follicle and can vary from months to years. Vellus hairs have an anagen period of a few months. However, regardless of the length of the growing period or of the size of the hair follicle, the length of the telogen phase remains fairly stable, i.e. approximately 100 days. As a consequence, the anagen/telogen ratio in an area affected by male pattern baldness is higher than in areas unaffected or less affected by male pattern baldness (MPB), so in any given time
period, there will be more shedding of hair from the areas affected by MPB than there will be in the remainder of the scalp.
At the end of the telogen phase, the follicle will re-enlarge and re-organize and begin producing a new hair shaft. To date, we do not have any medications that can be used safely to shorten the telogen phase.
SHEDDING DUE TO CHEMICAL AGENTS
Minoxidil
For the same reasons that minoxidil promotes hair growth, it can also cause shedding. Despite many years of research and use, the exact physiologic mechanisms whereby minoxidil stimulates hair growth is not known. The stimulatory effect of minoxidil on the hair follicle can cause hair that is in the telogen phase to shed before the end of the normal 100-day telogen period.
The effect of minoxidil on the hair follicles is dose dependent. The initial shedding was rarely reported during use of topical 2% minoxidil. With 5% topical minoxidil, it was usually not noticeable, but was infrequently reported. With the use of currently available minoxidil concentrations of 12.5%, the initial shedding is commonly reported. The shedding can be noted within weeks of initial use of topical minoxidil.
Since shedding due to the use of topical minoxidil only effects hair that is in the telogen phase, the increased shedding should not last longer than 100 days and should only effect those areas of the scalp where the topical minoxidil is being applied.
Finasteride
There have been multiple reports of excessive shedding several months after finasteride therapy. Typically, there is a good response to finasteride to prevent or reverse MPB. Then, around the 11th to 16th week, there can be sudden shedding, sometimes on a massive scale. The entire phenomenon fits the
description of a telogen effluvium. It is a common observation that post-partum women often suffer the same temporary hair loss. In the case of finasteride use, the telogen effluvium appears to be a reaction to the sudden change in the systemic levels of the sex hormone, DHT. Often the cause of a telogen effluvium
are obscure, but has been related to high fevers, stress, trauma, medications, etc.
The shedding is generally diffuse (global) and can affect areas of the scalp not usually affected by MPB. So, it would be common to note shedding from the sides and back of the head in addition to the crown, vertex and frontal areas. The shedding tends to be fairly symmetrical, but will be more noticeable in the areas affected by MPB, because there is a higher ratio of hairs in the telogen phase than in the other areas of the scalp.
The duration of a telogen effluvium is variable, but rarely lasts more than a few months and there is invariably complete restitution unless another pathologic process also occurs.
As a rule, treatment is not necessary because the hair will grow back. For most patients, there is no evidence of residual loss of hair within a year. However, there have been cases of patients taking finasteride and reporting repeated bouts of excessive shedding. In this situation, it would be advisable to discontinue use of finasteride in favor of alternative anti-androgens.
TELOGEN EFFLUVIUM
This is a common type of temporary hair loss and may occur at any age. The phenomenon represents a precipitous shift of a percentage of anagen hairs to telogen, typically 3 to 4 months after an inciting event. The reaction can be to a variety of physical or emotional stresses:
Etiologies of Telogen Effluvium
Endocrine
Post-partum
Post or peri-menopausal state
Hypo or hyperthyroidism
Nutritional
Caloric or protein deprivation
Zinc deficiency
Biotin deficiency
Iron deficiency
Drugs
Anticoagulants
Angiotensin-converting enzyme inhibitors
Chemotherapeutic agents
Beta blockers
Lithium
Oral contraceptives
Retinoids (e.g. Accutane)
Hypervitaminosis A
Physical stress
Anemia
Systemic illness
Surgery
High fevers
Psychological stress
In a significant number of patients, no obvious cause is found for the telogen effluvium. Telogen effluvium is always potentially completely reversible and does not lead to total scalp loss. Rarely does more than 50% of the hair become involved in a telogen effluvium. For more details on telogen effluvium, please
refer to the article found in the Journal Articles on this website.
ANAGEN EFFLUVIUM
The daily loss of some telogen hairs is entirely normal. It is always abnormal to shed anagen hairs. The term anagen effluvium, used to describe the pathologic loss of anagen hairs, is misleading, as the abnormal anagen hairs in this condition are usually broken off rather than shed. An anagen effluvium is an
acute, extreme alteration of growth of the majority of anagen follicles, resulting in acute loss of greater than 89-90% of the scalp hair. The hair is usually dystrophic because of the interruption of growth and break off at the level of the scalp. Unlike the shed telogen hair, the anagen effluvium hair lost
does not have an attached bulb. These sheds occur 1-2 weeks following the precipitating cause and result in an acute, extensive alopecia that can involve 80-90% of the scalp hair.
The classic and easily recognizable causes of anagen effluvium of the scalp are radiation therapy to the head and systemic chemotherapy, especially with alkylating agents. In addition, there are a large number of toxic chemicals known to cause anagen effluvium such as poisoning by thallium, mercury or
borates. Salts of lead, selenium and arsenic have also been incriminated.
Regrowth of hair can usually be anticipated if the precipitating agent is discontinued or removed. Regrowth after radiation therapy depends on type, depth and dose fractionation. The amount of regrowth is directly related to the amount of damage inflicted upon the hair follicles.
ALOPECIA ANDROGENETICA
The most common cause of shedding and hair loss is alopecia androgenetica, also called male pattern baldness, even though 20% of adult women also suffer from it. The onset is usually in the third to fourth decades, but the process can begin immediately after puberty in those most severely affected and may progress for decades. The basic etiologic factors in androgenetic alopecia are presumed to be the same in men and women, although phenotypic expression differs. Men commonly show bitemporal recession and vertex thinning, which may progress to an absolute baldness in the affected areas. On the other hand, women with MPB generally show preservation of the frontal hair line and a progressive thinning on the top of the scalp, but do not develop frank baldness.
It is well established that both genetic and hormonal factors play a role in MPB. The genetic factor is by far the more important. Perhaps, when the entire human genome is deciphered early in the third millennium, we will know exactly which gene or genes control MPB. Subsequently, there may be gene therapy for MPB. But for the present, we have only a partial and incomplete understanding of the pathogenesis of MPB.
The alopecia in MPB is caused by progressive miniaturization, rather than destruction of involved hair follicles. In affected follicles, the percentage of hairs in telogen is increased and the duration of anagen is decreased. As a consequence, there is relatively more shedding in areas affected by MPB. Since
vellus and intermediate hairs have a short anagen phase, they will shed frequently. There can be permanent hair loss because the replacement hair shaft is finer in texture and lacks the same volume.
The age of onset and the rate of progression of MPB are genetically controlled and cannot be predicted. There are times of remission and, alternately, times of acceleration. When there is a period of acceleration, it is often proceeded by a telogen effluvium. MPB can proceed with alarming speed and everyone is familiar with stories of men who went bald 'overnight'. Unfortunately (and understandably) the patient will blame whatever event or treatment coincided with the accelerated hair loss. It is the philosophical fallacy of post hoc, ergo propter hoc, i.e. "after this, therefore, because of this". Since the
dramatic miniaturization of the follicle occurs within one single hair growth cycle, these patients are poorly responsive to treatment and reversing the MPB is improbable.
The more usual course would be to notice gradual recession or thinning of the hair. Statistically, this group of patients responds better to treatment with minoxidil and an anti-androgen. Approximately 70% of patients using a 5% topical minoxidil with an effective anti-androgen will see a gradual reversal of MPB
with thicker hair growth in 4 to 6 months. An additional 13% report no improvement in the amount of hair, but the MPB will not have progressed. For the remaining 17%, the MPB progresses. However, it is very likely that the minoxidil/anti-androgen treatment is slowing the progress of MPB.
There is constant research into the understanding of hair physiology and pathology. For the present, we have only two classes of medications that are proven and safe for the treatment of MPB. Minoxidil is a non-specific promoter of hair growth. The anti-androgens can protect the follicles from miniaturizing
as a reaction to DHT. We are eagerly awaiting new medications and better understanding.
SHEDDING AND HAIR LOSS
With its cycle of repetitive planned obsolescence and rebirth, hair is a unique organ system. It's of little wonder that with its complex and continuous recycling, there can be multiple clinical disorders based on cycling abnormalities. Although much is known about the organization and composition of the hairs themselves and of the follicles, we still have an incomplete and
rudimentary understanding of relevant pathways and mechanisms that regulate follicular function. In this article, we are addressing only entities that cause hair loss or shedding, rather than problems of hypertrichosis or overgrowth of hair.
The first hair follicles on the scalp form at approximately the 9th week of gestation. On the average, the human scalp will have 100,000 follicles and no further follicular neogenesis occurs after birth. You are born with as many hair follicles as you are ever going to have. The same follicles that produced lunago
(unpigmented ultra-fine) hair in the fetus and immediate postnatal life, eventually produce terminal hair. It is important to note that during one's lifetime, the same follicles can intermittently produce vellus or terminal hair.
A knowledge of the hair cycle is essential to understanding hair problems. Hair growth on the human scalp is an asynchronous regeneration of the hair follicle in repeated cycles, referred to as a mosaic pattern of follicular growth. The growth stage is the anagen phase. The duration and rate of growth of the anagen
phase normally varies at different body sites, in different individuals, and at various ages. Scalp hairs have a relatively long anagen phase typically ranging from 2 to 5 years, but has been documented to be as long as 10 years. The short-lived catagen period, usually 2 to 4 weeks in duration, is the transitional portion of the cycle. At this time, each terminal hair bulb moves
from its location in the dermis to a more superficial location by means of shrinkage and remolding of that portion below the bulge region where the arrector pilimuscle inserts. This muscle is not present on true vellus hair and allows terminal hairs to 'stand on end'. Once a hair has made the transition to the telogen phase, its existing hair shaft will not grow any longer. The hair
shaft during the telogen phase is no longer anchored securely in the dermis as it was in the anagen phase and can be easily dislodged with the gentle traction of brushing or shampooing or combing. Usually the shedding is unnoticed. Since the hair can accumulate in the shower drain or on soapy hands, patients can
erroneously associate washing the hair with causing hair loss. The telogen hair has a club shaped proximal end within the hair follicle and retains the club shape when it is shed. The new hair produced from the subsequent anagen phase does not "push out" the hair from the previous cycle and may on occasion be
found adjacent to the temporarily retained club hair within the follicular canal
------------------------------------------------------------------------------------------------------
NORMAL SCALP GROWTH OF TERMINAL HAIRS
Average number of brown/black scalp hairs: 100,000
10% more on blondes
10% less on redheads
Fastest Growth: between 15 and 30 years of age
Slow growth in infants and elderly
Average scalp hair growth: 0.35 mm/day or ~1 cm/month
Hair grows faster in summer than in winter
Month of greatest shed in the Northern Temperate zone: November
Anagen growth phase: 2 to 5 years
Percentage of hair in anagen phase: 85%-90%
Average daily numbers of hair shed: 50 to 100
Female hair grows faster than male hair
-----------------------------------------------------------------------------------------------------
Historically, alopecias have been classified as non-scarring or scarring. The scarring type is considered permanent because of the destruction of the follicle and the presence of fibrotic changes. The non-scarring alopecias don't destroy the follicle and there are little or no fibrotic changes around the follicle.
Therefore, regeneration of the follicle is theoretically possible. The division can be arbitrary and can often overlap. The transformation of a non-scarring to a scarring alopecia has been identified in some disorders.
NON-SCARRING ALOPECIAS
Alterations of hair growth
Telogen effluvium
Anagen effluvium
Miniaturization (i.e. Androgenetic Alopecia)
Congenital
Acquired
Follicular mucinosis
Chemical or physical agent
Trichodystrophies-alterations of hair
Congenital
Acquired
Trichotillomania-traction alopecia
Chemical or physical agents
Infectious agents
SCARRING ALOPECIAS
Inflammatory
Lupus erythematosus (chronic type)
Lichen planus pilaris
Planopilaris
Pseudopelade
Scleroderma
Bullous pemphigoid
Epidermolysis bullosa acquista
Folliculitis-secondary to infectious agents
Chemical and physical damage
Granulomatous inflammation
Noninflammatory
Nonscarring pseudopelade
Bullous pemphigoid
Neoplasms-benign and malignant
Many of the causes of alopecia listed above are rare and are not frequently encountered in any practice. A good dermatology textbook will describe the entities. However, it is important to understand that there are many causes for hair loss.
Although it may sound contradictory, shedding and hair loss is not synonymous. First, we must define our terms. Shedding refers to hair shafts that easily or spontaneously fall out of the scalp. There are multiple causes of shedding. Shedding normally occurs at the end of the telogen phase, but, in pathological
cases, can also occur during anagen. As a rule, shedding usually refers to a temporary event and suggests that the hair shaft will grow back again as thick as before, providing there is not an intervening pathological process.
In distinction, hair loss can refer to either the temporary or permanent loss of hair or a loss not in the number of hair shafts, but in the volume and texture of the hair shaft. For example, permanent hair loss can be caused by a scarring alopecia, such as occurs in third degree burns or radiation to the scalp.
Typical of a loss in the volume of hair, but not in the number of follicles, would be the miniaturization of the follicle due to male pattern baldness (MPB).
A complete medical history can almost always determine the cause of alopecia. If necessary, there are alternative ways for determining aberrations of scalp hair cycling. The first is the 'hair pull'. This simple technique involves gentle traction from the base to the terminal ends of a group of 25 to 50 hairs. Normally, only a few hairs are dislodged on six to eight such hair pulls.
Shedding of two to three hairs per pull is pathologic. If there is increased shedding, the proximal ends should be evaluated to determine if there is an intact hair shaft and bulb, which would indicate either an effluvium (Latin for "a flowing out") or hair breakage.
A biopsy of the scalp may or may not be helpful with the diagnosis of a particular hair disorder. The information it delivers about cycling aberrations is merely confirmatory to that obtained by other simpler, less expensive means, and the diagnosis of hair shaft abnormalities cannot be made by a scalp biopsy.
The real value of a scalp biopsy is in the insight it can offer into mechanisms of alopecia.
Since this article is being written primarily for the information of patients affected by pattern baldness, we'll limit the subject of shedding and hair loss due to physiologic processes, medications, telogen effluvium, anagen effluvium and male pattern baldness.
PHYSIOLOGIC SHEDDING
Since it would be normal to have 10 to 15% of all the hairs on the scalp in the telogen phase, we can expect that 50-100 of those hairs are at the end of the phase and will readily shed. The anagen phase is in proportion to the size of the follicle and can vary from months to years. Vellus hairs have an anagen period of a few months. However, regardless of the length of the growing period or of the size of the hair follicle, the length of the telogen phase remains fairly stable, i.e. approximately 100 days. As a consequence, the anagen/telogen ratio in an area affected by male pattern baldness is higher than in areas unaffected or less affected by male pattern baldness (MPB), so in any given time
period, there will be more shedding of hair from the areas affected by MPB than there will be in the remainder of the scalp.
At the end of the telogen phase, the follicle will re-enlarge and re-organize and begin producing a new hair shaft. To date, we do not have any medications that can be used safely to shorten the telogen phase.
SHEDDING DUE TO CHEMICAL AGENTS
Minoxidil
For the same reasons that minoxidil promotes hair growth, it can also cause shedding. Despite many years of research and use, the exact physiologic mechanisms whereby minoxidil stimulates hair growth is not known. The stimulatory effect of minoxidil on the hair follicle can cause hair that is in the telogen phase to shed before the end of the normal 100-day telogen period.
The effect of minoxidil on the hair follicles is dose dependent. The initial shedding was rarely reported during use of topical 2% minoxidil. With 5% topical minoxidil, it was usually not noticeable, but was infrequently reported. With the use of currently available minoxidil concentrations of 12.5%, the initial shedding is commonly reported. The shedding can be noted within weeks of initial use of topical minoxidil.
Since shedding due to the use of topical minoxidil only effects hair that is in the telogen phase, the increased shedding should not last longer than 100 days and should only effect those areas of the scalp where the topical minoxidil is being applied.
Finasteride
There have been multiple reports of excessive shedding several months after finasteride therapy. Typically, there is a good response to finasteride to prevent or reverse MPB. Then, around the 11th to 16th week, there can be sudden shedding, sometimes on a massive scale. The entire phenomenon fits the
description of a telogen effluvium. It is a common observation that post-partum women often suffer the same temporary hair loss. In the case of finasteride use, the telogen effluvium appears to be a reaction to the sudden change in the systemic levels of the sex hormone, DHT. Often the cause of a telogen effluvium
are obscure, but has been related to high fevers, stress, trauma, medications, etc.
The shedding is generally diffuse (global) and can affect areas of the scalp not usually affected by MPB. So, it would be common to note shedding from the sides and back of the head in addition to the crown, vertex and frontal areas. The shedding tends to be fairly symmetrical, but will be more noticeable in the areas affected by MPB, because there is a higher ratio of hairs in the telogen phase than in the other areas of the scalp.
The duration of a telogen effluvium is variable, but rarely lasts more than a few months and there is invariably complete restitution unless another pathologic process also occurs.
As a rule, treatment is not necessary because the hair will grow back. For most patients, there is no evidence of residual loss of hair within a year. However, there have been cases of patients taking finasteride and reporting repeated bouts of excessive shedding. In this situation, it would be advisable to discontinue use of finasteride in favor of alternative anti-androgens.
TELOGEN EFFLUVIUM
This is a common type of temporary hair loss and may occur at any age. The phenomenon represents a precipitous shift of a percentage of anagen hairs to telogen, typically 3 to 4 months after an inciting event. The reaction can be to a variety of physical or emotional stresses:
Etiologies of Telogen Effluvium
Endocrine
Post-partum
Post or peri-menopausal state
Hypo or hyperthyroidism
Nutritional
Caloric or protein deprivation
Zinc deficiency
Biotin deficiency
Iron deficiency
Drugs
Anticoagulants
Angiotensin-converting enzyme inhibitors
Chemotherapeutic agents
Beta blockers
Lithium
Oral contraceptives
Retinoids (e.g. Accutane)
Hypervitaminosis A
Physical stress
Anemia
Systemic illness
Surgery
High fevers
Psychological stress
In a significant number of patients, no obvious cause is found for the telogen effluvium. Telogen effluvium is always potentially completely reversible and does not lead to total scalp loss. Rarely does more than 50% of the hair become involved in a telogen effluvium. For more details on telogen effluvium, please
refer to the article found in the Journal Articles on this website.
ANAGEN EFFLUVIUM
The daily loss of some telogen hairs is entirely normal. It is always abnormal to shed anagen hairs. The term anagen effluvium, used to describe the pathologic loss of anagen hairs, is misleading, as the abnormal anagen hairs in this condition are usually broken off rather than shed. An anagen effluvium is an
acute, extreme alteration of growth of the majority of anagen follicles, resulting in acute loss of greater than 89-90% of the scalp hair. The hair is usually dystrophic because of the interruption of growth and break off at the level of the scalp. Unlike the shed telogen hair, the anagen effluvium hair lost
does not have an attached bulb. These sheds occur 1-2 weeks following the precipitating cause and result in an acute, extensive alopecia that can involve 80-90% of the scalp hair.
The classic and easily recognizable causes of anagen effluvium of the scalp are radiation therapy to the head and systemic chemotherapy, especially with alkylating agents. In addition, there are a large number of toxic chemicals known to cause anagen effluvium such as poisoning by thallium, mercury or
borates. Salts of lead, selenium and arsenic have also been incriminated.
Regrowth of hair can usually be anticipated if the precipitating agent is discontinued or removed. Regrowth after radiation therapy depends on type, depth and dose fractionation. The amount of regrowth is directly related to the amount of damage inflicted upon the hair follicles.
ALOPECIA ANDROGENETICA
The most common cause of shedding and hair loss is alopecia androgenetica, also called male pattern baldness, even though 20% of adult women also suffer from it. The onset is usually in the third to fourth decades, but the process can begin immediately after puberty in those most severely affected and may progress for decades. The basic etiologic factors in androgenetic alopecia are presumed to be the same in men and women, although phenotypic expression differs. Men commonly show bitemporal recession and vertex thinning, which may progress to an absolute baldness in the affected areas. On the other hand, women with MPB generally show preservation of the frontal hair line and a progressive thinning on the top of the scalp, but do not develop frank baldness.
It is well established that both genetic and hormonal factors play a role in MPB. The genetic factor is by far the more important. Perhaps, when the entire human genome is deciphered early in the third millennium, we will know exactly which gene or genes control MPB. Subsequently, there may be gene therapy for MPB. But for the present, we have only a partial and incomplete understanding of the pathogenesis of MPB.
The alopecia in MPB is caused by progressive miniaturization, rather than destruction of involved hair follicles. In affected follicles, the percentage of hairs in telogen is increased and the duration of anagen is decreased. As a consequence, there is relatively more shedding in areas affected by MPB. Since
vellus and intermediate hairs have a short anagen phase, they will shed frequently. There can be permanent hair loss because the replacement hair shaft is finer in texture and lacks the same volume.
The age of onset and the rate of progression of MPB are genetically controlled and cannot be predicted. There are times of remission and, alternately, times of acceleration. When there is a period of acceleration, it is often proceeded by a telogen effluvium. MPB can proceed with alarming speed and everyone is familiar with stories of men who went bald 'overnight'. Unfortunately (and understandably) the patient will blame whatever event or treatment coincided with the accelerated hair loss. It is the philosophical fallacy of post hoc, ergo propter hoc, i.e. "after this, therefore, because of this". Since the
dramatic miniaturization of the follicle occurs within one single hair growth cycle, these patients are poorly responsive to treatment and reversing the MPB is improbable.
The more usual course would be to notice gradual recession or thinning of the hair. Statistically, this group of patients responds better to treatment with minoxidil and an anti-androgen. Approximately 70% of patients using a 5% topical minoxidil with an effective anti-androgen will see a gradual reversal of MPB
with thicker hair growth in 4 to 6 months. An additional 13% report no improvement in the amount of hair, but the MPB will not have progressed. For the remaining 17%, the MPB progresses. However, it is very likely that the minoxidil/anti-androgen treatment is slowing the progress of MPB.
There is constant research into the understanding of hair physiology and pathology. For the present, we have only two classes of medications that are proven and safe for the treatment of MPB. Minoxidil is a non-specific promoter of hair growth. The anti-androgens can protect the follicles from miniaturizing
as a reaction to DHT. We are eagerly awaiting new medications and better understanding.
Silent Method
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bump
PURE EXTRACT
New member
Bumping because I was losing my fucking hair....this was when I was offf cycle!!!!!!! shit
Underworld
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This thread should be a sticky - it would stop people asking 90% of hair questions!
Re: *** Answers to Hairloss Questions Here ***Please Help
Hi, I am new here and to steroids in general. I have read all your comments including the ones from the doc and have somewhat understood some of your conclusions. Anyhow.......
i am a little confused with this whole hair loss thing and how to prevent it on a cycle.+ taking deca. This is my dilema:
I am currently finishing a cycle of primoteston( test Enant) and six weeks into the cycle my hair started falling out....and now falling out without mercy. Genetically no one in the fam is bald...from both sides.
I am also took some deca in the last few weeks of the cycle to give me a bit more androgenic effect as primo on its own made me a bit flat. I took 2ml primo for six wks and 2 ml deca in the last two wks.
I went and seen the quack an he gave me minoxidil and said that it will re-grow my hair. and block DHT.....well it hasn't stoped falling out and i am about to start PCT....pregnyl and clomid. my quest are:
1) will minoxidil counter act with the deca as does all the other stuf like propecia and finast?
2) whats the best test / deca like cycles and dht blockers ( if posible) so that my hair won't fall out? or if taking deca is simply not advisable then what:
3) what Deca type stack can be taken...
at then end of the day i want to keep my hair whilst on a cycle
4) What is the best cycle with or without DHT blockers is what i am lookin for i guess.
i am not looking to be Arnie but looking for some good quality gains.
I hope someone can provide some good overall recomendations. Any feedback will be much appreciated.
Bruza005
Hi, I am new here and to steroids in general. I have read all your comments including the ones from the doc and have somewhat understood some of your conclusions. Anyhow.......
i am a little confused with this whole hair loss thing and how to prevent it on a cycle.+ taking deca. This is my dilema:
I am currently finishing a cycle of primoteston( test Enant) and six weeks into the cycle my hair started falling out....and now falling out without mercy. Genetically no one in the fam is bald...from both sides.
I am also took some deca in the last few weeks of the cycle to give me a bit more androgenic effect as primo on its own made me a bit flat. I took 2ml primo for six wks and 2 ml deca in the last two wks.
I went and seen the quack an he gave me minoxidil and said that it will re-grow my hair. and block DHT.....well it hasn't stoped falling out and i am about to start PCT....pregnyl and clomid. my quest are:
1) will minoxidil counter act with the deca as does all the other stuf like propecia and finast?
2) whats the best test / deca like cycles and dht blockers ( if posible) so that my hair won't fall out? or if taking deca is simply not advisable then what:
3) what Deca type stack can be taken...
at then end of the day i want to keep my hair whilst on a cycle
4) What is the best cycle with or without DHT blockers is what i am lookin for i guess.
i am not looking to be Arnie but looking for some good quality gains.
I hope someone can provide some good overall recomendations. Any feedback will be much appreciated.
Bruza005
Bumping this for some more answers...to anyone who takes any of the suggested medicines (minoxidil, propecia, proscar), can someone give an approximate cost? How much does this stuff run per month for you? I understand that proscar can be paid for by insurance, so that would just mean a copay? Thanks in advance...
ANIMAL STAK stopped my hair from falling. Still on it! Still no hair loss at all. My 2 cents
This is after deca, npp, winny, test trt dose. I suggest Animal Stak on the wait to nandrolone clearing up. Really helps in balancing hormones from my experience it works wonders. I say from experience that dht blockers and aromatase inhibtrs in animal stak must be g2g.
Too good to be true. 50€ and I'm covered... Who would have recommended it?
This is after deca, npp, winny, test trt dose. I suggest Animal Stak on the wait to nandrolone clearing up. Really helps in balancing hormones from my experience it works wonders. I say from experience that dht blockers and aromatase inhibtrs in animal stak must be g2g.
Too good to be true. 50€ and I'm covered... Who would have recommended it?
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