Do you think estrogen levels and Body fat levels are corelated?

[bananas]

`Since a lot of the aromatase enzyme is present in adipose tissue, do you believe that it would make sense that a person with a higher body fat, lets say 15% wil have mroe estrogen than a person who is 7% bf.

If so can you also conclude that a person with higher bodyfat will have a harder PCT then a person with lower body fat due to decreased estrogen.??

 

[Sworder]

The adipose tissue which provides a protective layer for the organs does have a lot of Estrogen Receptors and so does the subcutaneous fat. It is worth noting that there are more estrogen receptors in the hips, chest and in the belly versus other areas. If you have high estrogen you will see an increase in body fat in these areas. Often the high number of Estrogen Receptors will cause a decrease in lipolysis. Contrary to what Androgens do.

A person that has 15% bodyfat will have higher estrogen levels than somebody who is at 7%, typically.

I have read quite a lot about this subject and everything is hard to try to puzzle together. You won't find many straight conclusions because there are so many variables. Example: In a study they can measure the estrogen of 100 guys with 15% BF and 100guys with 7%BF. The 100 guys with 15% BF all have higher estrogen, what does this mean? So if I lower my estrogen does that mean I will lose weight? Letro has become the newest fatburner! Just kidding, don't take letro to lose weight. Point being, too many variables to make simple conclusions.

 

[MR10X]

What i dont understand is when you loose weight so to speak the fat cells only shrink in size and not in number. So you still have the same amount of cells with the same amount of enzyme producing cells.

 

[bananas]

What i dont understand is when you loose weight so to speak the fat cells only shrink in size and not in number. So you still have the same amount of cells with the same amount of enzyme producing cells.

Yeh but a cell that is 10 microns in size is more robust and "Active" as opposed to a cell that has shrunk and is now 4 microns in size. After all the enzymes are found in either the cytoplasm or the nucleus so it would make sense that the size decrease correlates with the amount of enzyme in it as well.

 

[Sworder]

That doesn't matter much though if you are still talking enzyme/estrogen related. Three different lipolysis enzymes I know of are: ATGL, Hormone sensitive lipase(HSL), and MGL. The Hormone sensitive lipase enzyme would be of interest in this discussion but I am posting this to show that just because one enzyme is receiving influence doesn't mean you can count the other two enzymes out of the equation. These are just some enzymes, there are many factors to include when talking about fat loss.

 

[BBC3]

There is no question that estrogen relates to body fat. The old schoolers used to simply state, that is you are over 12-15% body fat (depending on you), "steroids would not work". I suspect they were mostly referring to testosterone as that was the subject matter of my inquiry.

The mod is correct in that the fat cells do not go away or change in count, it is only their activity levels that changes. BUT THIS IS THE POINT.

Lately I have been pondering that hormones are not dependent upon SHBG (protein), but it is the other way around. And that the protien is dependent upon the HORMONE to deliver it. to the intended target. Thus the SHBG protein would be the key to unlocking or enabling cellular ACTIVITY. So if there is any thing to this, then you could consider that estrogens will be highly active if fats cells are currently in storage and expansion, and adrogens for muscle type tissue, both for bone (or really all to certain degees), etc. But you get it.

So then with that concept premised. A fat person may not necessarily be a estrogenic as the next fat guy. Meaning, if you took a really fat guy, and worked the shit out of him, thus turning off all fat storage signalling, then perhap his BF may only be as strong an estrogenic factor as the skinny guy, thus all fat related activity being more strickly based on FAT ACTVITY, and not so much FAT CONTENT. The propensity to store fat is both learned and genetic. Thus it may take a while to evoke this change depending on currnet lifestyle and the time spent as the behavior persisted. Its a thought for dinner. But you have to also further consider androgen factors like muscle which are heavily andrgoen specific, and what hormones they are encouraging./producing to get the overall activity formula.

But as far as testosterone goes, there is not doubt if you are fat - not only will it not work, but you may be harming yourself more via excess estrogen production.

 

[Sworder]

Also with this topic leaves you with "the chicken or the egg" question. Did the elevated estrogen make you fat or did the fat make your estrogen levels rise?

 

[macdaddy69]

So how do we slow estrogen production while on and off. Adex stops my libido. Im not fat but tend to hold fat on my hips.bloodwork while off is high normal estradial

 

[Bill Roberts]

Arimidex stops your libido only from using too much.

 

[BBC3]

I am starting to believe there is no chicken egg to it. I am of the current though that estrogen is designed to deliver fuel to supply fat tissue, along with others in both male and females, and that the corrolation is with ACTIVITY and not CONTENT. Thats just IMO.

Still it will remain somewhat mooted in not provable as SERUM COUNTS can only measure changes in status quo, and are geneticall present in component presence as a BLOOD BUFFER level to activity. There is simply no way to measure hormone metabolism rates on a serum count. This is a snapshot of one moment. I do suspect serum counts "refine and hone" with experience and always in the direction of ZERO, or death. And the longer we retain a given physical condition, the more accustomed the body becomes to handling a said amount of hormones.

Blood composition of hormones and with regard to SHBG MUST be defined by physical tissue properties given. More muscle (or fat) should equal more blood, thus equalling more space to carry hormones, protiens, fats, etc.. The RATE at which they are transacted (created, used, and eliminated) has to change with changes in tissue composition.

However consider:
(1) Total blood VOLUME may vary with individuals as we do not all "hold 4 quarts" etc..
(2) New tissue GROWTH will NOT equal the same about of new blood volume.
(3) New tissue ACTIVITY should increase hormone transfer rates equalling in muscle presence, POUND FOR POUND, given a set activity rate.
(4) Thus you have a 1:1 ration in muscle CONTENT vs. a non-linear blood volume as it relates.
(5) Homone metalbolism furrther varies with USAGE, CELL DENSITY, ETC...
(6) Therefore a 100 percent increase in muscle volume, if given fully active, will increase RECEPTORS 100 percent.
(7) Usage and Genetic Requirements (receptor appetite) will still vary, but should probably increase the VOLUME of hormones required for activity more than 1:1, if not exponentially.
(8) While Serum Counts do not depict this TO ANY PLAUSIBLE RELATION.
(9) It would seem that we should be able to discern a CURVE of INCREASING ACTIVITY as TT SERUM COUNTS increase, Estrogen OR androgen related and considered as a whole.
(10) We still do not know the "Hangtime" or duration or hormones at the point of cellular receptor involvement - if estrogens vary from androgens, or all different tissues specifically.
(11) So the long and short is that I would propose that if one had a serum count of 250, they might metabolize 3 mgs TT per day, 500ng/dl could equal 4mgs day, 750ng/dl than 8mgs/day, and so on.. So the higher the serum TT - the MORE TT we are metabolizing. But far greater than a one for one ratio. As logic would stand to reason that we would need more in available BLOOD SURPLUS if the rates were MORE DYNAMIC OR HIGHER - and the AS TWO ENTIRELY DIFFERENT PRICIPLE CONCEPTS...

If you consider a notion I have lately that hormones are merely fuel delivery "tags" or "keys" to distribution. Then this could also explain possible variation in hormone metabolism activity durations (how long it take a repector to spend an involved hormone)... I am suspecting that estrogens have a longer presence in the body to effectively do their job, and as a result there of. If you consider that perhaps estrogens are the principle delivery key for fat cellular activity, then this one would vary based on whether or not fat cells are currently being actively built or stored, and lower when they are not. Most of us carry a pretty much static level of fat, but it is also the one that continues to proliferation as MOST PEOPLE Age. But consider when one reaches a point of fat saturation where nothing is going into storage (what all want to achieve) then how much would estrogen activity decline if estrogens are indeed required to deliver the fuel to the fat cells? Obviously all fat related estrogen completely CEASES. Whereas we are always using muscle to walk talk and breath. It is given that estrogen is involved in these processes too.

But the key should still lie in the actual COUNT of cells. How many fat cells does a person have. How dense is their muscle tissue? THIS should vary greatly beween SOME individiuals. But not only the COUNT, but the current ACTIVITY LEVEL. So consider a person with a shitpile of fat cells, or the potential to be a bIG+EN. If they have activated and are currently storing in all available fat cells then what could the estrogen count being processes to deliver all this fuel be??!!?? A lot. Same for muscle. And surely there is a balance and perhaps even a notion of RECEPTOR COMPETITION is some tissue which can balance the end result of the concurrent effects as an overall. As far as argument as to the amount of cells that may "swing either way" or possibly be involved with both androgens and estrogens, and if competition exists, CONSIDER BOTH ESTROGEN AND ANDROGENS ARE REQUIRED FOR THE BUIDING ? FUELING OF BONE, MUSCLE, etc., I do wonder if androgens serve any pupose to fat at all. Perhaps they compete with the estrogen entry and fuleing of fat cells only??!!

Perhaps the term I am looking for is not competition, but interaction. Perhaps PROPORTIONS must be correct to encourage cetain tissue development, and thus too much of one in a cell that needs both, negates any effective action. But what is going on with all these hormones otherwise as they affect other tissues. Is there protection in proper proportion regardless of quantiites of hormones, or is exvess alway bad as collateral damage to a goal of muscle buidling? Do they negate or compliment in different proportions? Keep in mind the fuel in the blood which is being delivered is serving two purposes, depending on the tissue and time. It serves to provide for BOTH Fuel & Growth.

So the magic question I would have with regard to hormones and fuel delivery would be - would the human heart even function with no hormones if they are required to deliver fuel? Would it suffer. The question would be hard to answer considering there are other sources of androgens and estrogens in the body. And also the fact that these are only two in the complex symphony of life. Clearly though, they are critcal on a fundamental level thus demonstrated by their corrolation with both reproduction and survival as hormonal psychological preludes to states like aggression and lust.

So to Bill Roberts I would pose: Could tissue even grow at a developmental state without hormones such as TT? I am thinking not, and thus demonstrated by stunted growth of the hormonally deficient for reasons of illness or trauma.? So how critical are the TT related hormones to growth and development and fuel to function?? Further, I would pose: Are homones actively effective ON ANY LEVEL if not bound by SHBG? Like I proposed, if homones are indeed not bound and protected by SHBG, and in fact it is the protien that covets the hormone as a KEY to delivery for growth and activity, then are hormones that are unbound also serving purpose? HOW DO WE KNOW THAT IT TAKES A "FREE" TESTOSTERONE TO GROW A MUSCLE??!! Perhaps the testosterone only looks free at the point of cellular interation in that it has now done its job and delivered the payload. How closely amd true has this transactino actually been observed.

Perhaps the ONLY real function of Free Testosterone is to STIMULATE CNS. And hypothsizing that the common 2% of available Free testosterone is not a result of release for muscle activity, BUT WHAT IS LEFT OVER AFTER THE PROTIENS HAVE PICKED UP ALL THEY NEEDED. The excess left behind for another pupose potentially... After all, it makes no sense that it is that samll count in proportion. No sense. Protiens are not protecting it. they must be USING IT.

And not putting words in anyone's mouth as these are CLEARLY more ra,blings from the ADDLED MIND OF BBC..... LOL:drooling:

Anyone. Thoughts pleauuuzze...

Also with this topic leaves you with "the chicken or the egg" question. Did the elevated estrogen make you fat or did the fat make your estrogen levels rise?

 

[Michael Scally MD]

Take your pick!

Auyeung T-W, Lee JS, Kwok TC, et al. Testosterone but not estradiol level is positively related to muscle strength and physical performance independent of muscle mass - a cross-sectional study in 1489 older men. Eur J Endocrinol:EJE-10-0952. Testosterone but not estradiol level is positively related to muscle strength and physical performance independent of muscle mass: a cross-sectional study in 1489 older men

Objective: To examine the relationship among different measures of testosterone and estradiol, muscle mass, muscle strength and physical performance; and to test whether the association of sex hormone level with muscle strength and physical performance was independent of muscle mass.

Design and methods: A cross-sectional survey on 1489 community-dwelling men older than 64 years of age. Serum levels of testosterone and estradiol were measured by mass spectrometry and sex hormone binding globulin levels were measured by immunoradioassay. Muscle mass was examined by dual-energy X-ray absorptiometry and physical performance was assessed by hand-grip strength, gait speed, step length and chair-stand test.

Results: Appendicular skeletal mass (ASM) was positively associated with total testosterone (TT) (p<0.001), free testosterone (FT) (p<0.001), total estradiol (E2) (p<0.001) but not free E2 (p=0.102). After adjustment for age, SHBG and relative ASM, both TT and FT were significantly associated with grip strength, narrow-walk speed and the composite neuromuscular score. Higher total estradiol, but not free estradiol was associated with lower grip strength (p<0.05) after adjustment for age, FT, SHBG and relative ASM.

Conclusions: Testosterone level was related to both muscle mass, strength and physical performance. Total estradiol level, though related to muscle mass positively, affected muscle strength adversely in older men.


van den Beld AW, de Jong FH, Grobbee DE, Pols HA, Lamberts SW. Measures of bioavailable serum testosterone and estradiol and their relationships with muscle strength, bone density, and body composition in elderly men. J Clin Endocrinol Metab 2000;85(9):3276-82. Measures of Bioavailable Serum Testosterone and Estradiol and Their Relationships with Muscle Strength, Bone Density, and Body Composition in Elderly Men

In the present cross-sectional study of 403 independently living elderly men, we tested the hypothesis that the decreases in bone mass, body composition, and muscle strength with age are related to the fall in circulating endogenous testosterone (T) and estrogen concentrations. We compared various measures of the level of bioactive androgen and estrogen to which tissues are exposed.

After exclusion of subjects with severe mobility problems and signs of dementia, 403 healthy men (age, 73-94 yr) were randomly selected from a population-based sample. Total T (TT), free T (FT), estrone (E1), estradiol (E2), and sex hormone-binding globulin (SHBG) were determined by RIA. Levels of non-SHBG-bound T (non-SHBG-T), FT (calc-FT), the TT/SHBG ratio, non-SHBG-bound E2, and free E2 were calculated. Physical characteristics of aging included muscle strength measured using dynamometry, total body bone mineral density (BMD), hip BMD, and body composition, including lean mass and fat mass, measured by dual-energy x-ray absorptiometry.

In this population of healthy elderly men, calc-FT, non-SHBG-T, E1, and E2 (total, free, and non-SHBG bound) decreased significantly with age. T (total and non-SHBG-T) was positively related with muscle strength and total body BMD (for non-SHBG-T, respectively, beta = 1.93 +/- 0.52, P < 0.001 and beta = 0.011 +/- 0.002, P < 0.001). An inverse association existed between T and fat mass (beta = -0.53 +/- 0.15, P < 0.001). Non-SHBG-T and calc-FT were more strongly related to muscle strength, BMD, and fat mass than TT and were also significantly related to hip BMD.

E1 and E2 were both positively, independently associated with BMD (for E2, beta = 0.21 +/- 0.08, P < 0.01). Non-SHBG-bound E2 was slightly strongly related to BMD than total E2. The positive relation between T and BMD was independent of E2. E1 and E2 were not related with muscle strength or body composition.

In summary, bioavailable T, E1, total E2, and bioavailable E2 all decrease with age in healthy old men. In this cross-sectional study in healthy elderly men, non-SHBG-bound T seems to be the best parameter for serum levels of bioactive T, which seems to play a direct role in the various physiological changes that occur during aging. A positive relation with muscle strength and BMD and a negative relation with fat mass was found. In addition, both serum E1 and E2 seem to play a role in the age-related bone loss in elderly men, although the cross-sectional nature of the study precludes a definitive conclusion. Non-SHBG-bound E2 seems to be the best parameter of serum bioactive E2 in describing its positive relation with BMD.

 

[Sworder]

I am under the impression that high estrogen levels equate to higher body fat. This being that estrogen suppresses lipolysis while androgens promote lipolysis. Especially as individuals with high estrogen accumulate the body fat on areas of the body where the estrogen receptors are in the highest concentrations. Body fat increases in certain tissue is directly linked to high hormone levels. Also, androgens have been shown to increase lipolysis. But of course this is only talking about burning fat. I haven't read much upon the storage of fat in regards to androgens/estrogen only the burning portion. Logically, perhaps they don't have an effect on the storage of it. The decrease of burning will result in using other fuel and it may not be it is not getting stored more but it just isn't getting burned.

As we grow older our bodies slow down testosterone production because it is not needed. I do not think the body likes Testosterone.. If it NEEDS it it will be provided but I think the body would much rather be estrogenic. Over the past 100 years our testosterone levels have gone down by 25-50%(depending on the source). We do not like testosterone that is why it is going down. I think the explanation is biological and very simple. We do not need to be strong, we don't need to run fast, we do not need to lift more than 10 pounds to get through the day.... Why should our testosterone levels be high? I don't want to open a can of worms on this one but IQ and testosterone levels correlate with the reasoning, I don't need to be strong if I am smart.

That is why after a certain age the body notices. Ok, I am sitting down all day. Not moving too much. I am getting fed. I think that hunger signals are important to maintain high testosterone because these are the biological message of saying "get some food now". The body does everything for a reason and we just don't understand it or the pathway or preference. I definitely think that there is a natural way to combat low test/high estrogen. We just need to fool our body to think that we really really need test! All this talk about test when the subject is estrogen. But Test is the flip side of the coin and the one that the body doesn't like otherwise it wouldn't choose estrogen at the slightest whim of test not being needed. It makes a lot of sense too because why would the body want unnecessary muscle that is high maintenance.

I definitely think that within the next 100 years our testosterone will be even lower(estrogen higher).. The body wants to do bare minimum. Body fat is good and muscle is bad. That is what the body thinks and PREFERS otherwise it wouldn't be that way.

 

[Sworder]

Wanted to add to hunger signals increasing Testosterone production. Stress signals in an oxidative environment are seen as catabolic. This being obvious because we need more energy hence the stress, though stress signals must be anabolic in the long term.. What did the body learn from the stress signals and how does it collect it as a memory? The memory(biological clock if you will) is vital in keeping testosterone high and making the body think it needs to keep elevated T levels. Genes that are passed down the thing they are telling your child is how stressed you were, did you get to eat, and how can it prepare for a similar lifestyle. If we could emulate the right combination of stress signals/or the signals they trigger we shouldn't have a problem keeping testosterone levels high and estrogen low. This being done without gene modification(body-memory modification). When we are measuring blood serum levels we are only looking at the tip of the iceberg and even the what are they telling us about activity on a cellular level @ target areas.

My arguments being based solely on "logic" with the main argument, the body will do what it wants to do or it wouldn't do it