Testosterone

March 9, 2000

Hi, thanks for the interesting study below. However, the link that you

provided for the male hormone profile tests (as well as the female profile)

returns a " Not found (404) " message. Do you have a more current URL.?

Thanks, Jeff

Testosterone

Hi

All, I just wanted to pass this on.

Dale

- DOES TESTOSTERONE PROTECT AGAINST ALZHEIMER'S DISEASE?

==============

- THE POWERFUL IMPACT OF SEX HORMONES ON THE BRAIN

Testosterone - the popular image of this sex hormone is primarily as

a muscle-building machismo-inducing substance that " pumps men up. "

Yet clinical research is uncovering important roles for testosterone

in many other diverse areas of health and physiology, including the

brain. Now, new evidence suggests that testosterone may enhance

memory function and protect against the development of Alzheimer's

disease.

Neuroscientists from Rockefeller University and Weill Medical College

of Cornell University recently discovered that when neural cells from

the brains of rats are exposed to testosterone, the cells don't

produce as much Amyloid ß-peptide (Aß-peptide). The accumulation of

Aß-peptide can cause plaque deposits to form in the brain. These

deposits are believed to play a major role in the development of

Alzheimer's disease.

Past experimental research has shown that the female sex hormone

estrogen also slows the production of Aß-peptides. This may be why

postmenopausal women using estrogen replacement therapy have a

significantly lower risk of developing Alzheimer's, according to

recent studies.

Since testosterone appears to have the same protective effect against

the build-up of Aß-peptides as estrogen, researchers suggested that

this male sex hormone might be clinically useful for safeguarding

both men and women against Alzheimer's disease. In addition,

testosterone appears to improve certain cognitive abilities in men,

such as verbal and spatial memory function.

Levels of bioavailable testosterone are especially important, the

researchers emphasized, because these levels decline most rapidly as

men and women age, in conjunction with a progressive breakdown of

muscle and bone tissue and an increase in body fat.

Since high levels of testosterone have been linked with prostate

cancer in men and endometriosis in women, however, they urged caution

when using replacement therapy, carefully weighing the risks and

benefits for each patient.

Increasing levels of adrenal hormones such as cortisol, which rise in

response to stress and aging, may also play an important role in

Alzheimer's, the researchers pointed out. High levels of these

hormones can damage the hippocampus region in the brain, causing

learning impairment and memory loss. Testosterone, however, shows the

potential to reverse some of this damage.

NOTE: To evaluate the clinical need for sex hormone replacement

therapy in men, the Male Hormone Profile

(http://www.gsdl.com/services/malehormone.html) provides a circadian

analysis of bioavailable testosterone using timed salivary analysis.

Test results are crucial for making a more accurate risk-benefit

analysis for each patient and for shedding light on how hormonal

balance may be influencing musculoskeletal health, mood, sexual

drive, fat metabolism, cardiac function, and other important factors

in the aging process.

For women, the Menopause Profile

(http://www.gsdl.com/services/menopause.html) provides an evaluation

of estrogen, progesterone, and testosterone levels based on four

timed salivary samples, revealing the hormonal dynamics that can

profoundly affect the emotional, physiological, and cognitive health

of postmenopausal women.

The comprehensive versions of both of these profiles include assays

of melatonin, DHEA, and cortisol, for added insight into how levels

of these hormones may be influencing mechanisms of aging, chronic

symptoms, or potential degenerative conditions.

Source: Gouras GK, Xu H, Gross RS, Greenfield JP, Hai B, Wang R,

Greefard P. Testosterone reduces neuronal secretion of Alzheimers

ß-amyloid peptides. PNAS 2000;97(3):1202-05. PNAS

(http://www.pnas.org/) is one of several journals that now offer 24

hours of access to the full text and downloadable PDF files of

articles for a reasonable fee at their web sites. As of today, access

to full text of this article was free.

Call 800-522-4762 for more information or send your request for test

kits and educational materials to cs@...

------------------------------------------------------------------------

March 9, 2000

Sorry, go to endocronology in the by system block.

Fleeman wrote:

Hi, thanks for the interesting study below.

However, the link that you

provided for the male hormone profile tests (as well as the female

profile)

returns a "Not found (404)" message. Do you have a more

current URL.?

Thanks, Jeff

Testosterone

Hi

All, I just wanted to pass this on.

Dale

- DOES TESTOSTERONE PROTECT AGAINST ALZHEIMER'S DISEASE?

==============

- THE POWERFUL IMPACT OF SEX HORMONES ON THE BRAIN

Testosterone - the popular image of this sex hormone is primarily as

a muscle-building machismo-inducing substance that "pumps men up."

Yet clinical research is uncovering important roles for testosterone

in many other diverse areas of health and physiology, including the

brain. Now, new evidence suggests that testosterone may enhance

memory function and protect against the development of Alzheimer's

disease.

Neuroscientists from Rockefeller University and Weill Medical College

of Cornell University recently discovered that when neural cells from

the brains of rats are exposed to testosterone, the cells don't

produce as much Amyloid ß-peptide (Aß-peptide). The accumulation

of

Aß-peptide can cause plaque deposits to form in the brain. These

deposits are believed to play a major role in the development of

Alzheimer's disease.

Past experimental research has shown that the female sex hormone

estrogen also slows the production of Aß-peptides. This may be

why

postmenopausal women using estrogen replacement therapy have a

significantly lower risk of developing Alzheimer's, according to

recent studies.

Since testosterone appears to have the same protective effect against

the build-up of Aß-peptides as estrogen, researchers suggested

that

this male sex hormone might be clinically useful for safeguarding

both men and women against Alzheimer's disease. In addition,

testosterone appears to improve certain cognitive abilities in men,

such as verbal and spatial memory function.

Levels of bioavailable testosterone are especially important, the

researchers emphasized, because these levels decline most rapidly as

men and women age, in conjunction with a progressive breakdown of

muscle and bone tissue and an increase in body fat.

Since high levels of testosterone have been linked with prostate

cancer in men and endometriosis in women, however, they urged caution

when using replacement therapy, carefully weighing the risks and

benefits for each patient.

Increasing levels of adrenal hormones such as cortisol, which rise in

response to stress and aging, may also play an important role in

Alzheimer's, the researchers pointed out. High levels of these

hormones can damage the hippocampus region in the brain, causing

learning impairment and memory loss. Testosterone, however, shows the

potential to reverse some of this damage.

NOTE: To evaluate the clinical need for sex hormone replacement

therapy in men, the Male Hormone Profile

(http://www.gsdl.com/services/malehormone.html)

provides a circadian

analysis of bioavailable testosterone using timed salivary analysis.

Test results are crucial for making a more accurate risk-benefit

analysis for each patient and for shedding light on how hormonal

balance may be influencing musculoskeletal health, mood, sexual

drive, fat metabolism, cardiac function, and other important factors

in the aging process.

For women, the Menopause Profile

(http://www.gsdl.com/services/menopause.html)

provides an evaluation

of estrogen, progesterone, and testosterone levels based on four

timed salivary samples, revealing the hormonal dynamics that can

profoundly affect the emotional, physiological, and cognitive health

of postmenopausal women.

The comprehensive versions of both of these profiles include assays

of melatonin, DHEA, and cortisol, for added insight into how levels

of these hormones may be influencing mechanisms of aging, chronic

symptoms, or potential degenerative conditions.

Source: Gouras GK, Xu H, Gross RS, Greenfield JP, Hai B, Wang R,

Greefard P. Testosterone reduces neuronal secretion of Alzheimers

ß-amyloid peptides. PNAS 2000;97(3):1202-05. PNAS

(http://www.pnas.org/) is

one of several journals that now offer 24

hours of access to the full text and downloadable PDF files of

articles for a reasonable fee at their web sites. As of today, access

to full text of this article was free.

Call 800-522-4762 for more information or send your request for test

kits and educational materials to cs@...

------------------------------------------------------------------------

March 9, 2000

I have been using Testosterone for years and I know for a fact that my mind

becomes clearer and more focused,and the degree of my abiliy to concentrate

is definately increased.I become more decisisive,and less depressed..I

personally feel that it would definately be becificial,but that would be

contingent on what the subjects current level of Testosterone is.I't is also

my belief that testosterone treatment would be benificial in the treatment

of alcholics and certain drug addictions,but I have no idea if any studies

have been done on that aspect of it's use,and most of these statements are

my opinions,based on personal experience and not scientific research.

Rick-

Testosterone

> Hi

>

> All, I just wanted to pass this on.

>

> Dale

>

> - DOES TESTOSTERONE PROTECT AGAINST ALZHEIMER'S DISEASE?

>

> ==============

>

> - THE POWERFUL IMPACT OF SEX HORMONES ON THE BRAIN

>

> Testosterone - the popular image of this sex hormone is primarily as

> a muscle-building machismo-inducing substance that " pumps men up. "

> Yet clinical research is uncovering important roles for testosterone

> in many other diverse areas of health and physiology, including the

> brain. Now, new evidence suggests that testosterone may enhance

> memory function and protect against the development of Alzheimer's

> disease.

>

> Neuroscientists from Rockefeller University and Weill Medical College

> of Cornell University recently discovered that when neural cells from

> the brains of rats are exposed to testosterone, the cells don't

> produce as much Amyloid ß-peptide (Aß-peptide). The accumulation of

> Aß-peptide can cause plaque deposits to form in the brain. These

> deposits are believed to play a major role in the development of

> Alzheimer's disease.

>

> Past experimental research has shown that the female sex hormone

> estrogen also slows the production of Aß-peptides. This may be why

> postmenopausal women using estrogen replacement therapy have a

> significantly lower risk of developing Alzheimer's, according to

> recent studies.

>

> Since testosterone appears to have the same protective effect against

> the build-up of Aß-peptides as estrogen, researchers suggested that

> this male sex hormone might be clinically useful for safeguarding

> both men and women against Alzheimer's disease. In addition,

> testosterone appears to improve certain cognitive abilities in men,

> such as verbal and spatial memory function.

>

> Levels of bioavailable testosterone are especially important, the

> researchers emphasized, because these levels decline most rapidly as

> men and women age, in conjunction with a progressive breakdown of

> muscle and bone tissue and an increase in body fat.

>

> Since high levels of testosterone have been linked with prostate

> cancer in men and endometriosis in women, however, they urged caution

> when using replacement therapy, carefully weighing the risks and

> benefits for each patient.

>

> Increasing levels of adrenal hormones such as cortisol, which rise in

> response to stress and aging, may also play an important role in

> Alzheimer's, the researchers pointed out. High levels of these

> hormones can damage the hippocampus region in the brain, causing

> learning impairment and memory loss. Testosterone, however, shows the

> potential to reverse some of this damage.

>

> NOTE: To evaluate the clinical need for sex hormone replacement

> therapy in men, the Male Hormone Profile

> (http://www.gsdl.com/services/malehormone.html) provides a circadian

> analysis of bioavailable testosterone using timed salivary analysis.

> Test results are crucial for making a more accurate risk-benefit

> analysis for each patient and for shedding light on how hormonal

> balance may be influencing musculoskeletal health, mood, sexual

> drive, fat metabolism, cardiac function, and other important factors

> in the aging process.

>

> For women, the Menopause Profile

> (http://www.gsdl.com/services/menopause.html) provides an evaluation

> of estrogen, progesterone, and testosterone levels based on four

> timed salivary samples, revealing the hormonal dynamics that can

> profoundly affect the emotional, physiological, and cognitive health

> of postmenopausal women.

>

> The comprehensive versions of both of these profiles include assays

> of melatonin, DHEA, and cortisol, for added insight into how levels

> of these hormones may be influencing mechanisms of aging, chronic

> symptoms, or potential degenerative conditions.

>

> Source: Gouras GK, Xu H, Gross RS, Greenfield JP, Hai B, Wang R,

> Greefard P. Testosterone reduces neuronal secretion of Alzheimers

> ß-amyloid peptides. PNAS 2000;97(3):1202-05. PNAS

> (http://www.pnas.org/) is one of several journals that now offer 24

> hours of access to the full text and downloadable PDF files of

> articles for a reasonable fee at their web sites. As of today, access

> to full text of this article was free.

>

> Call 800-522-4762 for more information or send your request for test

> kits and educational materials to cs@...

>

> ------------------------------------------------------------------------

>

February 10, 2001

> From: Brad Schoenfeld<highnrg123@...>

>

> : FYI, studies by Joubert show that testosterone does indeed cause

the

> profileration of satellite cells (1,2,3). More evidence that the

> anabolic effects of testosterone are on par with that of IGF-1.

>

I am not doubting the anabolic effects of testosterone, and I am not

doubting it is important component if one is interested in obtaining

*optimal* or *maximal* hypertrophy. My point was that it is not *critical*

to hypertrophy, i.e., if you take testosterone away, hypertrophy can still

occur. But if you take IGF-I away, hypertrophy cannot occur. Thus, again,

I am stating that IGF-I is the critical growth factor to hypertrophy. No

other hormone appears to be critical. They definitely make big

contributions, but they are not critical.

Krieger

Graduate student, exercise science

Washington State University

February 10, 2001

> From: Brad Schoenfeld<highnrg123@...>

>

> : FYI, studies by Joubert show that testosterone does indeed cause

the

> profileration of satellite cells (1,2,3). More evidence that the

> anabolic effects of testosterone are on par with that of IGF-1.

>

I am not doubting the anabolic effects of testosterone, and I am not

doubting it is important component if one is interested in obtaining

*optimal* or *maximal* hypertrophy. My point was that it is not *critical*

to hypertrophy, i.e., if you take testosterone away, hypertrophy can still

occur. But if you take IGF-I away, hypertrophy cannot occur. Thus, again,

I am stating that IGF-I is the critical growth factor to hypertrophy. No

other hormone appears to be critical. They definitely make big

contributions, but they are not critical.

Krieger

Graduate student, exercise science

Washington State University

February 11, 2001

> > From: Brad Schoenfeld<highnrg123@a...>

> >

> > : FYI, studies by Joubert show that testosterone does indeed

cause

> the

> > profileration of satellite cells (1,2,3). More evidence that the

> > anabolic effects of testosterone are on par with that of IGF-1.

> >

>

> I am not doubting the anabolic effects of testosterone, and I am not

> doubting it is important component if one is interested in obtaining

> *optimal* or *maximal* hypertrophy. My point was that it is not

*critical*

> to hypertrophy, i.e., if you take testosterone away, hypertrophy

can still

> occur. But if you take IGF-I away, hypertrophy cannot occur.

Thus, again,

> I am stating that IGF-I is the critical growth factor to

hypertrophy. No

> other hormone appears to be critical. They definitely make big

> contributions, but they are not critical.

Let me approach this from a slightly different angle...

I will grant that there is some research to indicate that hypertrophy

can occur in the absence of testosterone (i.e. Golberg, et al, 1975).

But given that testosterone elicits the proliferation of satellite

cells as well as increasing protein synthesis (which I believe we

both agree are the primary factors in muscle hypertrophy), then why

wouldn't some degree of hypertrophy occur in the absence of IGF-1? In

other words, provided testosterone is available for the muscle, why

would IGF-1 be critically important to induce a hypertrophic

response? Any ideas?

Brad Schoenfeld, CSCS

February 12, 2001

> From: highnrg123@...

>

> I will grant that there is some research to indicate that hypertrophy

> can occur in the absence of testosterone (i.e. Golberg, et al, 1975).

> But given that testosterone elicits the proliferation of satellite

> cells as well as increasing protein synthesis (which I believe we

> both agree are the primary factors in muscle hypertrophy), then why

> wouldn't some degree of hypertrophy occur in the absence of IGF-1? In

> other words, provided testosterone is available for the muscle, why

> would IGF-1 be critically important to induce a hypertrophic

> response? Any ideas?

I do not know. The papers you cited earlier, did the testosterone directly

exert its effects on the cells, or was the effect indirect by stimulating

local production of IGF-I?

Krieger

Graduate Student, Exercise Science

Washington State University

February 13, 2001

" Krieger " <jkrieger@w...> wrote:

From: highnrg123@a...

> > I will grant that there is some research to indicate that

> > hypertrophy can occur in the absence of testosterone (i.e. Golberg, et al,

> > 1975). But given that testosterone elicits the proliferation of satellite

> > cells as well as increasing protein synthesis (which I believe we

> > both agree are the primary factors in muscle hypertrophy), then

> > why wouldn't some degree of hypertrophy occur in the absence of IGF-

> > 1? In other words, provided testosterone is available for the muscle,

> > why would IGF-1 be critically important to induce a hypertrophic

> > response? Any ideas?

> I do not know. The papers you cited earlier, did the testosterone

> directly exert its effects on the cells, or was the effect indirect by

> stimulating local production of IGF-I?

-----------------

:

The studies by Joubert didn't address whether IGF played a role in

satellite cell proliferation. This piqued my interest and I did a

little research. I must say that after looking at some of the data,

the results seem to be very ambiguous. Here's what I was able to come

up with:

1) In support of your theory, Urban found that testosterone increased

IGF-1 m-RNA levels in muscle. This would indicate that testosterone

does indeed act as a precursor to IGF-1 production. Studies by Arnold

and Saggese also seemed to support this conclusion, showing positive

correlation between testosterone and IGF-1 levels (2, 3).

2) What's more, suggested that satellite cell recruitment might

be mediated in part by IGF-1 (4). He linked this mediation to an IGF-

induced expression of myogenin, a myogenic regulatory factor (MRF)

that is important to stem cell differentiation.

3) On the other hand, a more recent study by Sheffield- showed

no increase in IGF-1 m-RNA as a result of testosterone

supplementation. Any increases in protein synthesis were attributed

to increased AR expression (5).

4) In what would seem to be a more definitive study with respect to

satellite cells, Doumit concluded that that satellite cells are

direct targets for androgen action, and testosterone *did not* alter

the subsequent responsiveness of cells to growth factors

(6). Thus, according to this study, it appears that testosterone

functions independently from IGF on satellite cells.

5) Testosterone also has other indirect anabolic effects which need

to be considered. Blanco showed that testosterone significantly

increased the levels of choline acetyltransferase (ChAT), the enzyme

responsible for synthesis of acetylcholine (7). Theoretically,

increased ChAT levels could allow for a greater amount of

acetylcholine to be available, which in turn could help to sustain

muscular contractions and thereby increase hypertrophy.

6) Gelber reported that IGF-1 has direct effects on testosterone

production (8). Some of the articles I reviewed also alluded to an

IGF-1 induced upregulation of AR receptors in muscle after IGF-1

treatment. Thus, the relationship between IGF-1 and testosterone

seems to be reciprocal.

7) Interestingly, it appears that insulin is critical to the

hypertrophic effects of IGF-1. found that, in a hypoinsulemic

environment, IGF-1 had little effect on protein synthesis. However,

when insulin was infused, there was a significant increase in protein

synthesis (9). Thus, irrespective of testosterone, to say that IGF-1

is " critical " might be misguided.

In sum, the evidence is far from clear as to a " critical " importance

of any anabolic hormone, including IGF-1. The interplay between IGF,

testosterone and even insulin are extremely complex and seem to be

interwined. There is definitely a synergism between the hormones and,

based on what I've been able to ascertain, they're all vitally

important in the growth process.

1) Urban RJ, et al, Testosterone administration to elderly men

increases skeletal muscle strength and protein synthesis. Am J

Physiol, 269(5 Pt 1):E820-6 1995 Nov

2) Arnold, A. M., Peralta, J. M., & Thonney, M. L. (1996). Ontogeny

of growth hormone, insulin-like growth factor-I, estradiol, and

cortisol in the growing lamb: Effect of testosterone. Journal of

Endocrinoloqy, 150(3), 391-399.

3) Saggese G, et al, Testosterone-induced increase of insulin-like

growth factor I levels depends upon normal levels of growth hormone.

Eur J Endocrinol, 135(2):211-5 1996 Aug

4) , C. K., Janney, M. J., & , R. E. (1994). Temporal

expression of myogenic regulatory genes during activation,

proliferation, and differentiation of rat skeletal muscle satellite

cells. Journal of Cellular Physiology, 159, 370-385.

5) Sheffield- M, et al, Short-term oxandrolone administration

stimulates net muscle protein synthesis in young men. J Clin

Endocrinol Metab, 84(8):2705-11 1999 Aug

6) Doumit ME, et al, Testosterone up-regulates androgen receptors and

decreases differentiation of porcine myogenic satellite cells in

vitro. Endocrinology, 137(4):1385-94 1996 Apr

7) Blanco CE, et al, Anabolic-androgenic steroid induced alterations

in choline acetyltransferase messenger RNA levels of spinal cord

motoneurons in the male rat. Neuroscience, 78(3):873-82 1997 Jun

8) Gelber SJ, Effects of insulin-like growth factor-I on androgen

production by highly purified pubertal and adult rat Leydig cells. J

Androl, 13(2):125-30 1992 Mar-Apr

9) , R., Hu, X., Niederstock, D., Hasan, S., McNulty, P. H.,

Sherwin, R. S., & Young, L. H. (1996). IGF-1 stimulation of muscle

protein synthesis in the awake rat: Permissive role of insulin and

amino acids. American Journal of Physiology, 270, E60-E66

------------

Brad Schoenfeld, CSCS

February 14, 2001

From: Brad Schoenfeld<highnrg123@...>

> 7) Interestingly, it appears that insulin is critical to the

> hypertrophic effects of IGF-1. found that, in a hypoinsulemic

> environment, IGF-1 had little effect on protein synthesis. However,

> when insulin was infused, there was a significant increase in protein

> synthesis (9). Thus, irrespective of testosterone, to say that IGF-1

> is " critical " might be misguided.

This would seem to contradict the results of a recent study by Farrell

of Penn. St. University, where he does research on diabetic rats and muscle

hypertrophy. If I recall the results of this paper correctly (I may be

wrong here because I'm relying on memory and I'm being too lazy right now to

go look the study up), diabetic rats subjected to a resistance training

program experienced the same magnitude of hypertrophy as non-diabetic rats.

But what they found was that the muscle of the diabetic rats compensated for

the lack of circulating insulin by increasing local production of IGF-I.

Despite all of these complex relationships between these growth factors and

hormones, there is one simple thing to remember. Muscle cells can produce

their own IGF-I, but they can't produce their own testosterone, so if we

take testosterone away, muscle cells can still adapt. However, if we take

IGF-I away, and don't have any testosterone around to compensate, then it

appears that hypertrophy is much more difficult to come by.

Ultimately, muscle plasticity implicates many redundant regulatory mechanisms

such that, in the absence of some important factor to the hypertrophic

process, another important factor simply takes its place. Which is why the

search for some critical, be-all end-all signal for hypertrophy is futile,

because it is likely that there are multiple signals for hypertrophy at both

the cellular and molecular level.

Krieger

Graduate Student, Exercise Science

Washington State University

February 15, 2001

Kreiger:

<Ultimately, muscle plasticity implicates many redundant regulatory mechanisms

such that, in the absence of some important factor to the hypertrophic process,

another important factor simply takes its place. Which is why the search for

some critical, be-all end-all signal for hypertrophy is futile, because it is

likely that there are multiple signals for hypertrophy at both the cellular

and molecular level.>

Just wanted to add some casual obervations that I have been making from my

work:

IGF-1 levels in individuals (mostly men) with larges amounts of muscle mass

tend to decrease as additional hypertrophy occurs. This makes me suspect

that there is some negative feedback inhibition taking place. These guys

are not taking anything (as far as steroids, insulin, GH, or growth

factors). Could this be a possible reason why gains decrease in more

experienced trainees? Could this also be why guys taking drugs such as

insulin, steroids, GH and growth factors get so much larger, (ie they

override normal feedbakc mechanisms)?

While I agree that both T and IGF-1 make it easier to gain muscle when

administered exogenously, I haven't seen any mechanistic data that shows the

exercised induced hormonal responses are directly responsible for muscle

growth, everything so far has been correlated, yet often interpreted as

causative. One abtracts I recall reading years ago from Pete Lemon's lab

indicated no correlation between anabolic hormone release and the time

course of skeletal muscle protein synthesis. I haven't seen the asbtract

published, but if the results are correct it may force us to change the way

we view or think about using some of these values to predict future muscle

growth.

Also I am not so sure that I agree entirely with ' statement above.

From what I interpret when reading through the various papers on

intracellular signaling pathways is that a variety of surface and cytosolic

receptors activate many of the same intracellular components. Perhaps if we

could figure out the best way of activating this intracelluar sequence of

events, we could make it easire to prevent muscle wasting diseases, add lean

body weight, etc.

Just some thoughts.

Tom

Incledon

Human Performance Specialists, Inc.

Plantation, FL

954-577-0689

hpsinc@...

Incledon

Human Performance Specialists, Inc.

Plantation, FL

954-577-0689

hpsinc@...

July 13, 2001

On Fri, 13 Jul 2001 15:44:10 -0000

jfleeman@... wrote:

> 1. Why isn't there more discussion / use of natural

> testosterone

> which is easily available (with a prescription) from

> compounding

> pharmacies in a transdermal gel or cream formulation? I

> presume that

> this causes also causes downregulation of endogenous

> production but

> presumably you are getting all the benefits of the

> complete hormone.

Transdermal testosterone is a good product but has

limitations:

1. Physicians will not prescribe it for patients whose

endogenous prodution is within the normal range for their

age group. Those who seek a level representative of a

younger group must seek other sources.

2. The rate of transdermal absorption depends on surface

area and skin thickness. This limits the functional dosage

regardless of the amount applied. Oral products can achieve

higher total dosages while intranasal or sublingual products

can higher peak levels faster.

There are prohormones that convert to chemically identical T

so effectively that there is no reason to be concerned about

" the complete hormone " . T also side effects that can be

avoided by the designer prohormones.

There are prohormones which resist 5AR or convert to DHT

variants which have less androgenic effect (for those

concerned about hair loss or prostate enlargement). There

are some which don't aromatize into estrogens and thus avoid

the risk of breast enlargement, water retention, fat

deposition or the risk of hormone dependant cancers. There

are some which are much more effective than T for muscle

growth.

> 2. Does HCG cause downregulation? A poster to the

> AntiAging group

> uses 500 mg. daily and claims that it cannot effect

> natural

> testosterone production.

Neither claim is true. HCG is commonly used to restore

natural production after long-term downregulation has taken

place. It can upregulate natural production although that

effect is limited by other feedback loops.

Those who do use it for long-term upregulation or who

consume it prophilactically to prevent downregulation may

well downregulate the HCG receptors themselves and not have

HCG's therapeutic function available when they need it.

Bob Cruder

July 13, 2001

> On Fri, 13 Jul 2001 15:44:10 -0000

> jfleeman@... wrote:

> > 1. Why isn't there more discussion / use of natural

> > testosterone

> > which is easily available (with a prescription) from

> > compounding

> > pharmacies in a transdermal gel or cream formulation? I

> > presume that

> > this causes also causes downregulation of endogenous

> > production but

> > presumably you are getting all the benefits of the

> > complete hormone.

>

Why not use a good progesterone creme transdermally, which converts into

testosterone in the body? Not many men are aware that progesterone is not

just for menopausal women, but can benefit them as well?

July 13, 2001

Bravo !! I'm sure your no. 1 question is on

everybody's mind - nobody wants to inject testostorone

! we need some information !!

--- jfleeman@... wrote:

> These are questions for Bob (or anyone else who

> feels that they have

> pertinent info):

>

> 1. Why isn't there more discussion / use of natural

> testosterone

> which is easily available (with a prescription) from

> compounding

> pharmacies in a transdermal gel or cream

> formulation? I presume that

> this causes also causes downregulation of endogenous

> production but

> presumably you are getting all the benefits of the

> complete hormone.

>

> 2. Does HCG cause downregulation? A poster to the

> AntiAging group

> uses 500 mg. daily and claims that it cannot effect

> natural

> testosterone production.

>

> Thanks,

>

> JGF

>

__________________________________________________

July 14, 2001

Bob,

Thank you for your well researched, well reasoned and

informative posts. Could you identify the specific

prohormones you are refering to below and identify

which exhibit the qualities mentioned?

Thank you

Monty Knight

--- bcruder@... wrote:

> There are prohormones that convert to chemically

> identical T

> so effectively that there is no reason to be

> concerned about

> " the complete hormone " . T also side effects that can

> be

> avoided by the designer prohormones.

>

> There are prohormones which resist 5AR or convert to

> DHT

> variants which have less androgenic effect (for

> those

> concerned about hair loss or prostate enlargement).

> There

> are some which don't aromatize into estrogens and

> thus avoid

> the risk of breast enlargement, water retention, fat

> deposition or the risk of hormone dependant cancers.

> There

> are some which are much more effective than T for

> muscle

> growth.

>

__________________________________________________

August 11, 2005

My daughter had her testosterone checked last year by endo. Their interpretation is "nice level...looks good, if she were a he." be sure you request a lab which has pediatric ranges.(we supposedly can only use one particular lab through our insurance-and I try to make them pay for everything possible, obviously-but this lab has a seperate division for pediatric labs) after this crappy interpretation was given to me, I inquired about the WHAT NOW factor--she has SO much going on medically that we can barely keep our heads above water. I know Lupron has been used to lower testosterone levels...anyone with experience??? My guess is the girls will show "nice levels...if they were boys"...

And how about our girls....are they dainty and sweet and petite little flowers? Or are they a little un-feminine looking? My daughter looks like a girl, don't get me wrong, she just seems so unfeminine--not like my friends girls who are unaffected. Or does she seem unfeminine due to the social issue and the behavior???

Cris

On Thu, 11 Aug 2005 16:32:36 -0000 "Debi" <fightingautism@...> writes:

If I remember correctly, he also thinks that it might be possiblegirls start making more testosterone to try and bind the mercury inthe body, and that the girls with high testosterone often start makingtoo much estrogen to try and counteract the imbalance, throwing theminto precocious puberty.I've got allie's testosterone labs waiting for my viewing pleasure...Debi> Dr. Mark Geier's theory is that tetestorone (sp?) enhances thedamaging effects of mercury, and that estrogen can protect against thedamaging effects of mercury. Some females have more testestorone intheir bodies than most so maybe that is why some girls are autistic. If he is right, and I think he is, then IT IS THE VACCINES that causeautism.> >

August 12, 2005

Dr. Geier now has a testosterone study going on, I think it's Lupron

injections every 45 days? until age 12, while chelating with DMPS-TD.

there's some other stuff, too, he's got I think 8 kids in the study,

we're working on getting all the stuff out of the way for allie Kat to

participate, last I knew he had no girls.

Debi

> > Dr. Mark Geier's theory is that tetestorone (sp?) enhances the

> damaging effects of mercury, and that estrogen can protect against the

> damaging effects of mercury. Some females have more testestorone in

> their bodies than most so maybe that is why some girls are autistic.

> If he is right, and I think he is, then IT IS THE VACCINES that cause

> autism.

> >

August 16, 2006

Hi:

I went off testosterone and hgh for 8 months and measured my baseline

levels. Although my level for total was a reasonable 451 ng/dL, my

free test was low, at 12.4 pg/mL. (This indicates that I hadn't shut

down my natural testosterone production, despite all the

warnings) During that period, I was lifting a bag of concrete from a

pickup truck for a project at my house and I slipped and I tore the

ligaments - giving me " tennis elbow " - im both arms. After trying a

number of supplements, including homeopathic, (I didn't try 1/2 cup

of MSM per day, but perhaps should have) I went to a mainstream

allopathic doctor and he said that although there were a number of

treatments, there was really little that could be done in his

experience to reduce the time to heal to less than about 2 years. I

reasoned that testosterone would help. I began taking testosterone

again, 1 mL depot per week with 250 mg per mL, with the blessings of

an alternative doctor and within 3 months, the tendons were

healed. They began healing dramatically fairly

quickly. Testosterone has amazing healing powers. It lowers the

risk of heart disease and cancer and speeds the recovery from

injuries. Of course the trick is often getting the free testosterone

up to a reasonable level, because that is the only testosterone you

can really use. Tonkat Ali, in the form of LJ-100, a 100 X

concentrate, is considered good for that. Does anyone have

experience with anything else that raises free testosterone?

At 07:40 AM 8/15/2006, you wrote:

>Thought that this was an interesting report from Life Extension

><mailto:lifeextension%40lefbc.com>lifeextension@...

>

>Low testosterone levels in older men increase the risk of death during

>4 year average follow-up

>

>A report published in the August 14/28, 2006 issue of American Medical

>Association journal Archives of Internal Medicine, revealed a

>correlation between reduced levels of the male hormone testosterone

>and an increased risk of mortality during up to 8 years of follow-up.

>Testosterone levels in men decrease by approximately 1.5 percent per

>year after age 30, which can eventually result in muscle mass and bone

>density reduction, diminished energy and libido, and depression and

>irritability.

>

>Molly M. Shores, MD, and colleagues at the Veterans Administration

>Puget Sound Health Care System and University of Washington, Seattle,

>analyzed the association between testosterone levels and death in 858

>male veterans over the age of 40. The participants' testosterone

>levels were measured at least twice between 1994 and 1999. Subjects

>were followed through 2002, and any deaths among the group were noted.

>

>Nineteen percent of the participants were found to have a low total

>testosterone level of less than 250 nanograms per deciliter, or a free

>testosterone level of less than 0.75 nanograms per deciliter.

>Fifty-three percent had normal testosterone levels and 28 percent had

>tests that measured an equal number of low and normal levels. While

>only 20 percent of the men with normal testosterone died during

>follow-up, deaths occurred among 24.6 of those with equivocal levels

>and 35 percent of those with low levels. After adjustment for age,

>illness and other factors, men whose testosterone levels were

>classified as low experienced an 88 percent adjusted increased risk of

>dying over the course of the follow-up compared to those with normal

>levels. To reduce the effect of acute illness on the finding, the

>researchers reanalyzed the data excluding men who died within the

>first year of follow-up, yet they still found an increase of 68

>percent in the risk of dying among men with low testosterone.

>

> " The persistence of elevated mortality risk after excluding early

>deaths suggests that the association between low testosterone and

>mortality is not simply due to acute illness, " the authors conclude.

> " Large prospective studies are needed to clarify the association

>between low testosterone levels and mortality. "

>

August 16, 2006