Looking at most guys post, it seems like docs start you out on testosterone with or without hcg, then add in arimidex based on follow up labs. IS it not smart to use something like an E blocker right from the get go??
Not smart. Why use more drugs if it might not be necessary?
I haven't met ONE guy using Androgel who needs an AI.
I have had some guys take the T+hCG+AI protocol to there docs and get the whole kit from the get go. This is rare, but proves that some docs can think outside of the HMO box.
It is rare that hCG or AI are not needed. My experiences with guys here is totally contradictory to Brick's experiences.
We do have Androgel guys who are non absorbers who have low T levels and LH then does not zero out. Those have to be regarded at therapeutic failures. I have been in the habit of stating that lack of LH/FSH shutdown was a definition of ineffective T delivery. If transdermals are dosed to product the same serum levels of T as injections, it is hard to argue that HPTA shutdown would depend on how the T was delivered.
Without AI, some can be very miserable as they get a wild libido then that fades and they suffer from estrogen poisoning, mood problems etc. If more or less AI is needed, that will come out in the wash with lab work and dose adjustments that should be basic routine. Estrogen hell can be prevented.
It is very rare that TRT does not shut down LH, Brick seems to be the only one that I am aware of. You have the option of watching your testes shrink, pull up and perhaps ache 24x7, then introducing hCG if that happens. So you have that option. Better to have a script in hand if you need it or a doc that will phone in a script when you report problems.
I have a few patients that when test levels get normalized e2 drops.
Adex may not be needed if you get lifestyle, nutrition, and other factors in check.
I normally give guys 6 -8 weeks with natural recommendations to see if e2 comes down then move then on to adex if needed.
One just needs to find what works for them. i prefer less drugs less variables to deal with . Just lowering body fat and balancing liver pathways seems to work the most efficient.
I like to look at potential pathology of the issue rather then to look at just symptoms.
i love it how dr's treat one thing and person feels normal then when something else goes out they stick them on antidepressants. Problem with medicine today there are too many bandaids.
If you seek to get near serum E2=22pg/ml as a target, I expect that your passive success levels drop very low.
In many cases, you need to lower E2 to lower body fat as E2 can block fat loss, even with good T levels.
The lesson is "a few patients", and E2 drops to what?
Some may be on other non-avoidable meds that will never allow E2 to drop because of contention for liver enzyme pathway capacity.
Again, if E2 levels are below target, anastrozole dose can be reduced, and that routine process can lead to a dose of zero if need be. That is a much better outcome than a doc that does not test for E2 and/or refuses to use anastrozole under any circumstances.
I dont think its as simple as "estrogen makes guys fat"....
"Contrarian Endocrinology Revisited: Estrogen for Men?"
Estrogen has been reported to confer a number of health benefits in both males and females, such as the well described effects of increasing bone mass density. Here I want to examine some aspects of estrogen that may be of more immediate interest to bodybuilders and athletes. These include the lipolytic (fat mobilizing) and fat oxidizing properties of estrogen, as well as its anorectic (appetite suppressing) effect. Finally we will look at an emerging area of research: the relative contributions of the various metabolites of estrogen to the overall effects of the parent steroid.
Estrogen as a Lipolytic Hormone
Are male (and many female) bodybuilders misguided in their attempts to limit their exposure to estrogen? After all, it makes a person fat doesnâ??t it? And cause gynecomastia? Well, certainly for men using anabolic steroids that aromatize, too much estrogen can lead to gynecomastia in susceptible individuals. But what about those of us not using steroids? Should we treat estrogen as our fat producing enemy and even go so far as to attempt to prevent its production by using aromatase inhibitors? Or block its action at the estrogen receptor with agents like tamoxifen?
In fact, there are a wealth of data that implicate estrogen as both an anorectic and antiadipogenic hormone. It is much more likely that progesterone is the culprit in supporting higher levels of gluteofemoral fat that is prominent in women (men tend to store more fat in the abdominal area) (1). The model described in (1) has progesterone as the lipogenic hormone. Before menopause, both estrodiol and progesterone are secreted by the ovaries. After menopause, estrone becomes the primary circulating estrogen produced from aromatization of adrenal androgens (primarily the aromatization of androstenedione to estrone by adipose tissue), while progesterone levels drop dramatically since adrenal production of progesterone is minimal.
In premenopausal women progesterone increases lipoprotein lipase activity, which is greater in the gluteofemoral region, while estrogen suppresses it. Lipoprotein lipase is the bodyâ??s primary fat storage enzyme; it is responsible for allowing fats to leave the circulation and enter adipocytes. The progesterone wins out though and before menopause, women tend to have more gluteofemoral fat and less abdominal fat.
From an adaptational viewpoint, it has been argued that women's fat is designed to be stored until needed for lactation and child rearing. Men's is designed to be readily mobilized for fight or flight situations during defense and hunting. This theory may be a bit simplistic as well as sexist; but it does make sense to some degree.
Most likely the notion of estrogenic fat originated from the belief that estrogen upregulates alpha 2 receptors in fat cells, retarding lipolysis. This may be just one facet of estrogenâ??s actions. If one looks at the net result of estrogenâ??s effects, to quote a leading expert in the field â??Testosterone and GH inhibit LPL and stimulate lipolysis markedly. Oestrogens seem to exert net effects similar to those of testosterone.â?? (2)
For example, animal studies have shown that testosterone and the nonaromatizing DHT promote alpha 2 adrenoreceptor mediated antilipolytic activity, just as they promote beta adrenoreceptor mediated lipolysis (25).
Interestingly, recent research has even attributed at least part of testosterone's fat burning properties to its local aromatization to estradiol (3). For example when testosterone is administered along with an aromatase inhibitor, LPL activity has been shown to increase (4). This suggests that the aromatization of testosterone to estradiol is responsible for the noted ability of testosterone to inhibit LPL.
There are a number of animal studies where estradiol administration led to significant weight and fat loss. Citing just one, for example
The administration of 17 beta-estradiol (500 micrograms/kg, 2 or 4 weeks) to male rats significantly reduced the body weight...Basal lipolysis and adrenaline-induced lipolysis [due to increase in HSL action] were also significantly enhanced in the epididymal adipose tissue from the male rat treated either with 7 mg/kg estradiol 12 h ahead or with 500 micrograms/kg estradiol for 2 weeks. These results indicate that estradiol exerts strong effects on metabolism of the adipose and these effects seems to be mediated through cyclic-AMP. (5)
This research indicates that in addition to the abovementioned inhibition of LPL, estrogen also stimulates the lipolytic enzyme hormone sensitive lipase.
Some of the most compelling evidence for the antiadipogenic effect of estrogen in both males and females comes from studies of estrogen receptor knockout mice and humans with aromatase deficiency. Both the afflicted humans and the knockout mice exhibit obesity. A detailed look at this topic can be found in a study of estrogen receptor knockout mice (6) Quoting from that study,
The one known human male lacking ER had a body weight approximately 2 SD greater than normal. However, this individual also had increased height because of a lack of epiphysial plate fusion. Thus, continued growth may mitigate potential increases in WAT that might normally occur because of a lack of ER. However, men and women lacking aromatase manifest truncal obesity. This and the insulin resistance and impaired glucose tolerance observed in both humans lacking ER or aromatase and their murine counterparts emphasize that similar effects accompany loss of ER in both species and strongly suggest ER may regulate adipose tissue in men.
Estrogen as an Anorectic Hormone
I also mentioned that estrogen is a potent anorectic, hunger-suppressing hormone. This effect is thought to be due to an estrogen-induced inhibition in melanin-concentrating hormone (MCH) signaling (7). MCH is a neuropeptide found in the hypothalamus that is also thought to be involved in leptinâ??s regulation of appetite. Leptin, an anorectic hormone secreted from adipose tissue, acts on the specific receptor present on its target neurons in the brain, and suppresses the expression of both MCH and its receptor. So we see that the actions of both estrogen and leptin are at least partly mediated through interactions with MCH. In rats and mice, intracerebroventricular administration of MCH induces hyperphagia, whereas MCH deficiency induced by targeted gene deletion leads to a hypophagia syndrome and loss of body fat.
Under normal conditions, restricted food availability leads to a drop in leptin. Falling leptin levels in turn elevate Neuropeptide Y (NPY), a hunger inducing peptide, and decrease expression of pro-opiomelanocortin (POMC), the precursor of the anorexic melanocortin -MSH, a hunger suppressing hormone. Both these changes result in elevated MHC, and food seeking behavior is initiated. When high levels of estrogen are present, the normal food seeking brought on by the changes in NPY, POMC, and MHC described above is blocked, as depicted in the diagram below, adapted from (7)
Figure 1. Proposed model of the effects of estrogen on hypothalamic neuronal pathways involved in the regulation of energy balance. A, In response to energy restriction, circulating leptin and insulin levels decrease, resulting in increased gene expression of orexigenic peptides (e.g., NPY) and decreased gene expression of anorexic peptides (e.g., POMC) in neurons of the ARC. These neuronal responses are proposed to increase expression of the orexigenic neuropeptide MCH in neurons of the LHA, which in turn promote increased food intake. B, Estrogen-mediated weight loss and anorexia also lower plasma leptin and insulin, but the expected activation of MCH neurons fails to occur in the presence of estrogen, despite the preservation of "upstream" ARC NPY and POMC neuronal responses to reduced adiposity signaling. This inhibition of MCH neurons by estrogen is hypothesized to contribute to the sustained anorexia observed with chronic estrogen exposure in male rodents. Adapted from Mystkowski et.al. J Neurosci. 2000 Nov 15;20(22):8637-42.
Estrogen Promotes Fat Burning During Exercise
For ethical reasons, the bulk of the research described was carried out in females and male animals. However, one recent study looked at the effects of estrogen administration on energy expenditure in exercising men (8). In this study male subjects cycled for 90 min at an intensity of 65% VO2max following eight days of either estrogen supplementation (2 mg 17beta-estradiol/day) or placebo. Estrogen supplementation significantly decreased carbohydrate oxidation by 5-16% and leucine oxidation by 16% (indicating a sparing effect on glycogen and muscle) whereas it significantly increased lipid oxidation by 22-44% at rest and during exercise. The authors concluded that estrogen influences fuel source selection at rest and during endurance exercise in men characterized by a reduced dependence on amino acids and carbohydrate and an increased reliance on lipids as a fuel source.
The administered dose of estrogen in (8) resulted in an increase in plasma estradiol from a baseline of 125 pM/L to 876 pM/L.
The authors suggest that the change in substrate use during exercise caused by estrogen may result for estrogen related stimulation of beta and possibly alpha adrenergic receptors. I see a problem with this hypothesis, however, since research has shown that beta receptor stimulation during exercise actually has the opposite effect, sparing fat at the expense of glycogen oxidation (9). Whatever the underlying mechanism is, estrogen clearly promotes fat burning in men.
Studies Involving Male to Female Transsexuals
Studies where hormonal treatment was administered to male to female transsexuals are often cited as evidence that estrogen administration to men leads to accumulation of subcutaneous fat.
These studies are typically confounded by the co-administration of progestational antiandrogens along with estradiol (24). The observed increase in subcutaneous fat in these subjects could very well be due to the progestational antiandrogens and the resulting drop in testosterone, which itself is a lipolytic hormone in subcutaneous adipose tissue.
All Estrogens are Not Created Equal
So far we have dwelt on the effects of estrogen itself. However, considerable work has shown that the major metabolites of estradiol and estrone are those hydroxylated (possess an OH group) at either the C-2 or the C-16alpha positions, although forms hydroxylated at the C-4 and C-15alpha are present, but in relatively lesser amounts. There exists a complete divergence in the biological properties of the 2- and 16alpha-hydroxylated metabolites of estradiol. 2-hydroxyestrone (2-OHE1) has been found to exert a modest anti-estrogenic effect in some tissues (10) and is popularly called the â??good estrogenâ??. Studies on its ability to alter Lutienizing Hormone (LH) have yielded variable results, with some studies showing it increases LH production while others report either no change or a slight drop in LH with large doses of 2-OHE1.16alpha-hydroxyestrone on the other is a potent estrogen (11). In addition, it is associated with various cancers and has been shown to be a mutagen (cancer promoting agent).
Figure 2. Pathways of Estradiol metabolism, showing the so-called â??goodâ?? metabolite 2-hydroxyestrone and the â??badâ?? metabolite 16alpha-hydroxyestrone.
Figure 3. Schematic illustration of the metabolic pathway depicted in figure 2 showing additional estrogenic metabolites affected by DIM.
Phytochemicals such as indole-3-carbinol (I3C) are components of cruciferous vegetables, which exhibit antitumor activity associated with altered carcinogen metabolism and detoxification. The compound 3,3'-diindolylmethane, (DIM), is a major metabolite of I3C now available in supplement form. DIM directs estrogen metabolism away from â??badâ?? estrogen to the good 2-hydroxyestrone/estradiol metabolites. Moreover, DIM itself exhibits antiestrogenic properties according to some researchers, and estrogenic activity according to others, much as if it were a SERM (12, 24). Among the hypothesized mechanisms of chemoprevention by I3C and DIM is their ability to induce a number of phase I enzymes in liver and colon, including cytochrome P450 (CYP) 1A1, CYP1A2, and CYP 3A. Increased activity of phase I drug-metabolizing enzymes can protect against some carcinogens by increasing their rate of oxidative metabolism to less toxic metabolites.
So by taking supplements containing 3,3'-diindolylmethane we can possibly lessen the likelihood of developing prostate and possibly other cancers, since research has shown that 3,3'-diindolylmethane has direct anticancer effects on the prostate independent of its ability to suppress â??badâ?? estrogen (13). However, at least part of the ability of DIM to help prevent prostate cancer may lie is its antiandrogenic as well as antiestrogenic properties. Studies using prostate cancer (LNCaP) cells show that at physiologically obtainable levels DIM acts as a pure androgen antagonist that blocks expression of androgen-responsive genes and inhibits AR nuclear translocation (14).
One theory is that DIM appears to exert its antiestrogenic/antiandrogenic properties by acting as a weak agonist at the so-called aryl hydrocarbon receptor (AhR) (15). The AhR has been extensively studied due to the fact that a number of environmental toxins such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exert their effects by acting as strong agonists of the AhR. Dioxins are well known to disrupt reproductive activity in animals by deranging gonadal, pituitary, and CNS function. TCDD, like DIM acts as an antiestrogen in numerous tissues. At least part of TCDDâ??s antiestrogenic activity results from activation of proteosomes that degrade the estrogen receptor (16).
Itâ??s intriguing to speculate whether DIM might also be capable of ER degradation in the pituitary, which we noted possesses AhR receptors and is sensitive to TCDD. If so, DIM might block estrogen related negative feedback on the HPTA. Yet another theory on DIM action proposes that in some tissues it activates the estrogen receptor independently of the presence of estrogen by activating the so-called PKA- and MAPK signaling systems (22).
As noted above, some studies show 2-hydroxyestrone has no suppressive effect on the HPTA while other research shows either suppression or enhancement. Another metabolite of estradiol, depicted in figure 3, is 2-hydroxyestradiol. Animal experiments have shown that administration of 2-hydroxyestradiol can override the suppressive effect of estradiol on pituitary LH secretion in males (17). The same study showed that the bad estrogen 4-hyroxyestradiol was able to suppress LH production
As can be seen in figures 3 and 4, both 2-hydroxyestradiol and 2-hydroxyestrone are methylated during their metabolism by the body. Interestingly, 2-methoxyestradiol (2-MeOE2) has a significantly higher affinity for Sex Hormone Binding Globulin than do estradiol and even testosterone (18). This is significant in that 2-MeOE2, by virtue of its higher affinity for SHBG than testosterone, can displace testosterone from SHBG, possibly enlarging the fraction of free, or bioactive testosterone.
16alpha-hydroxyestrone may play a role in a number of diseases other than cancers. For example, the estrogen found in the synovial fluid of rheumatoid arthritis patients is primarily the proinflammatory 16alpha-hydroxyestrone and may be responsible for the inflammation associated with that disease (19, 20). DIM may prove useful in treating or ameliorating the symptoms of rheumatoid arthritis and other estrogen related autoimmune diseases that primarily affect women. Also of interest is the observation that while estradiol has well-known neuroprotective actions, 2-hydroxy-estradiol appears to be significantly more neuroprotective than its parent, estradiol (21). Of course, standard medical protocols should be followed and a physicianâ??s advice obtained, before self-medicating with DIM to treat any disease.
Since some evidence suggests DIM might generate estrogen metabolites that suppress LH production, it might not be advisable to use DIM as the sole agent during Post Cycle Therapy. When used post cycle with a SERM such as Clomid that stimulates the HPTA, DIM could offer a number of potential health advantages by shunting estrogen metabolites towards the more healthful 2-OH series while at the same time elevating free testosterone levels. Similarly, during a cycle of aromatizable steroids, when estrogen is high and the HPTA is suppressed, DIM use may offer a number of health benefits due to its actions described above.
For a person not using anabolics and unconcerned about the complexities of Post Cycle Therapy, DIM use may confer enough health benefits, such as possible cancer prevention, to warrant its use as a supplement. And, as mentioned above, we may get a boost in free testosterone as well. Long term safety studies in animals have failed to detect any toxicity due to DIM (23).
In summary, while certainly not advocating estrogen supplementation for men, I also believe it is not the evil hormone it is often made out to be. We should accept it for what it is, a naturally occurring part of or normal hormonal milieu, that can be manipulated in form and quantity to better suit the needs of male athletes and bodybuilders by focusing on altering the byproducts of estrogen metabolism.
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17) Franks S, MacLusky NJ, Naish SJ, Naftolin F. Actions of catechol oestrogens on concentrations of serum luteinizing hormone in the adult castrated rat: various effects of 4-hydroxyoestradiol and 2-hydroxyoestradiol. J Endocrinol. 1981 May;89(2):289-95.
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blah blah blah, when men get fat, T-->E2 increases and T levels drop. That promotes more fat and is a trap. Yes we need estrogen. No we do not want to take E2 to single digits as is often the case with extreme body building. But you are better off seeking optimal level.
With T+hCG I lost a lot of fat and gained muscle with no weight change [155 pounds]. But some fat lingered at my belt line and umbilicus [E2=3pg/ml]. When anastrozole was added to get to E2=22pg/ml, those areas and torso became lean - no weight change. No other changes to diet or activities... except for more libido driven pursuits.
With the lower E2 level, energy and mood improved. With E2=37 and high FT and TT numbers, I was irritable, lower E2 fix that. Good TRT TT and FT results are good, but E2 is a critical success factor.
Do docs understand these issues? Rarely!
"Looking at most guys post, it seems like docs start you out on testosterone with or without hcg, then add in arimidex based on follow up labs. IS it not smart to use something like an E blocker right from the get go??"
Most docs seem/claim to know little about anything other than T replacement - and even that, many are not successful in their protocols. Most docs have a narrow view on male hormonal treatment, and the one's that do inherently are apparently called "andrologists", which I had never heard of until visiting this site. Googling this term renders NO results w/docs w/this credential in my area.
Ultimately, you have to realize your body is a system that works together and in many cases, abnormalities in the system can be extremely complicated. I've learned you are the best proponent to finding out what's going on w/you, getting as many different viewpoints as possible and applying them to yourself.
If insurance is involved, docs are conditioned to not prescribe anastrozole before there are elevated lab numbers and symptoms. A few docs are proactive and will prescribe T+AI+hCG from the get-go, but that is very rare. A few have taken what they have learned here and had their docs like the approach and get it. Most often docs are dismissive about the concept that you might understand anything.
If a guy has obvious effects of estrogen dominance pre-TRT, it makes sense to add the AI immediately.
Docs do not understand anastrozole over-responder issues and whenever anastrozole is prescribed. Docs really need to be counseling about this; unless one has learned this from this site already.
I am one to look at the pathology of the person rather then just jump to TRT. It really is case specific and biggest factor is age. I have rebalanced alot of young 20 year olds through properly lifestyle, looking at their nutrition, and what supplements they are taking as well as n numberous other factors over looked by traditional medicine. Now genetic are playing a huge part if our ability to manage estrogens and I have fallen victim to this. Once this was finally identified I no longer need armidex and never though I did. Been off adex for 3 months having the best sex I have ever had 2-3 times a day. I use proviron as an anti estrogen which is very mild but enough to do the job
When did proviron become a FDA approved drug in the USA?
You are not telling guys how to manage their estradiol levels.
To manage estrogen levels one needs to look at the pathology of the problem which can be a multitude of things. Once the underlying cause is determined then proper recommendations can be made
1. nutrition imbalance
2. exposure to heavy metals (mercury and cadnium) other enviromonmental factors
3. low cortisol levels
4. liver congestion - improper phase 1 and phase 2 imbalances, methylation, ect
5. Gut dybiosis
6. Poor Lifestyle
7. genetic mutations
8. improper TRT adminstration
9. thyroid disorder
Adex is too strong for me and caused my lipids to get all out of wack. Now I am perfectly stable. Proviron I use to offset high shbg from thyroid meds which I am seeing more and more in people on t-3 which I speculate this is the same pathway that detoxifies estrogens. So people that are getting high shbg from t-3 also have amazingly have the hardest time controling estrodial. I know of several that fall into this category and I am one of them.
Gut dybiosis: Adverse gut bacteria. These can recycle metabolized estrogens in the liver bile then they can be absorbed again. Probiotics can address that problem.
When did proviron become a FDA approved drug in the USA?
Has not been approved, but have internet will travel..
Gut dysbiosis is much more complicated then just taking probiotics. I have several cases that have I had to bang my head against the wall trying to figure them out, but eventually I did figure them out and they got resolution of symptoms. To resolve these gut issues things had to be done in several different sequence with combination of lifestyle, stress management, and also changing the way one thinks, and medical intervention.