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New member
btw- interesting study.. will have to peruse more fully later..
drveejay11
New member
Counterstrike said:
Uhh......YES !!!!!!!!!!!!!!!!!!!!!!!
I don't think you can necessarily conclude that nolvadex will make you fat. The opposite is probably true. All I am saying is women seem to have a higher LPL activity in the lower body, presumably due to estrogen (1). Tamoxifen decreases LPL activity and possibly allows this fat to move to the viscreal area and the organs. I say "presumably" and "possibly" because there is not a ton of research to rely on. For instance, even though there is research showing that estrogen causes fat cells to make LPL(2), other research shows estrogen decreases the activity of that LPL (3). It's obviously complex and I'm no expert.
Whatever the role of estrogen, tamoxifen definitely seems to lower LPL activity, and since LPL is a major fat depositing enzyme, that is a good thing.
Macro's focus is on the alpha 2 adrenoreceptor control of fat. When that receptor is activated it puts the brakes on fat burning by blocking the action of lipolytic catecholamines (epinephrine, norepinephrine). Women have a higher concentration of these alpha 2 receptors in their lower body making it more difficult to lose fat there. They get a double whammy: high LPL and high alpha 2 receptor density. Women do have the advantage of having lower alpha 2 receptor density in their abdomens than men.
Yohimbine binds to this alpha 2 adrenoreceptor and blocks it so it can't put the brakes on fat burning. Estrogen DOES NOT bind this receptor, in spite of the claims of George Spellwin in his plug for yohimbine:
"HOW DOES YOHIMBINE WORK?
It binds to the A2 and blocks Norepinephrine (and other A2 agonist INCLUDING ESTROGEN) from binding to and agonizing it (which inhibits the release of fatty acids)- thus it allows for fatty acids to be "burned" and thus stubborn fat to be lost. "
http://www.elitefitness.com/articledata/efn/082001.html
This is flat out wrong. Estrogen does not bind to the alpha 2 adrenoreceptor and inhibit the release of fatty acids.
It is not known how exactly estrogen regulates the alpha 2 receptor density and activity. It does not bind to the receptor but may control where and how much of it there is in the body.
If estrogen does increase the number of these receptors then this would be another advantage of taking nolvadex.
(1) Med Hypotheses 2001 Aug;57(2):192-200
Modulation of adipocyte lipoprotein lipase expression as a strategy for preventing or treating visceral obesity.
McCarty MF.
(2) Przegl Lek 1998;55(5):266-70
[The role of estrogens in hormonal regulation of lipid metabolism in women]
Szafran H, Smielak-Korombel W.
(3) Am J Obstet Gynecol 1998 Jan;178(1 Pt 1):101-7
Estrogen regulation of adipose tissue lipoprotein lipase--possible mechanism of body fat distribution.
Price TM, O'Brien SN, Welter BH, George R, Anandjiwala J, Kilgore M.
Whatever the role of estrogen, tamoxifen definitely seems to lower LPL activity, and since LPL is a major fat depositing enzyme, that is a good thing.
Macro's focus is on the alpha 2 adrenoreceptor control of fat. When that receptor is activated it puts the brakes on fat burning by blocking the action of lipolytic catecholamines (epinephrine, norepinephrine). Women have a higher concentration of these alpha 2 receptors in their lower body making it more difficult to lose fat there. They get a double whammy: high LPL and high alpha 2 receptor density. Women do have the advantage of having lower alpha 2 receptor density in their abdomens than men.
Yohimbine binds to this alpha 2 adrenoreceptor and blocks it so it can't put the brakes on fat burning. Estrogen DOES NOT bind this receptor, in spite of the claims of George Spellwin in his plug for yohimbine:
"HOW DOES YOHIMBINE WORK?
It binds to the A2 and blocks Norepinephrine (and other A2 agonist INCLUDING ESTROGEN) from binding to and agonizing it (which inhibits the release of fatty acids)- thus it allows for fatty acids to be "burned" and thus stubborn fat to be lost. "
http://www.elitefitness.com/articledata/efn/082001.html
This is flat out wrong. Estrogen does not bind to the alpha 2 adrenoreceptor and inhibit the release of fatty acids.
It is not known how exactly estrogen regulates the alpha 2 receptor density and activity. It does not bind to the receptor but may control where and how much of it there is in the body.
If estrogen does increase the number of these receptors then this would be another advantage of taking nolvadex.
(1) Med Hypotheses 2001 Aug;57(2):192-200
Modulation of adipocyte lipoprotein lipase expression as a strategy for preventing or treating visceral obesity.
McCarty MF.
(2) Przegl Lek 1998;55(5):266-70
[The role of estrogens in hormonal regulation of lipid metabolism in women]
Szafran H, Smielak-Korombel W.
(3) Am J Obstet Gynecol 1998 Jan;178(1 Pt 1):101-7
Estrogen regulation of adipose tissue lipoprotein lipase--possible mechanism of body fat distribution.
Price TM, O'Brien SN, Welter BH, George R, Anandjiwala J, Kilgore M.
C
Counterstrike
Guest
So if i give a chick liquidex or nolvadex she will shed fat? age is 30. Will there be any sides for her age? how long should she take it for and which is better and safer nolva or liquidex? Also if she does los BF will she gain it again afte discontinuing nolva or L-dex?
Since I don't know of any double blind, placebo controlled trials of nolvadex for weight loss you would have to experiment, or ask one of the women over on their forum. It could work for the reasons I mentioned:
Nolva lowers LPL activity theoretically making it more difficult to hold and deposit fat. But as the study I cited showed, the women ended up with more visceral fat and serum triglycerides. This is not healthy.
Estrogen causes preadipocytes (immature fat cells) to proliferate. These grow into adult fat cells. This is another reason estrogen promotes fat deposition. Nolvadex or arimidex could block this.
As macro pointed out, there is a difference in the alpha 2 adrenoreceptor concentration in men and women, with higher alpha 2 levels in the thighs of women. These receptors bind catecholamines and blunt the fat burning the catecholamines would otherwise stimulate. If the distribution of these alpha receptors is regulated by estrogen, nolvadex might help fat burning by reducing their number.
There is another possibility that has been put forth by some researchers that estrogen actually lowers LPL activity and progesterone raises it. The progesterone wins out and women hold fat in their hips. This actually makes sense because after menopause progesterone disappears, but there is still some estrogen from the adrenal glands. Women tend to lose fat on their hips after menopause and develop more upper body fat.
This could happen if you blocked estrogen with nolvadex.
My wife gets good results with T3 and clen alternating with ECA and some AS thrown in to preserve muscle against T3 induced catabolism. This is what I would recommend if dieting and exercise have failed.
Nolva lowers LPL activity theoretically making it more difficult to hold and deposit fat. But as the study I cited showed, the women ended up with more visceral fat and serum triglycerides. This is not healthy.
Estrogen causes preadipocytes (immature fat cells) to proliferate. These grow into adult fat cells. This is another reason estrogen promotes fat deposition. Nolvadex or arimidex could block this.
As macro pointed out, there is a difference in the alpha 2 adrenoreceptor concentration in men and women, with higher alpha 2 levels in the thighs of women. These receptors bind catecholamines and blunt the fat burning the catecholamines would otherwise stimulate. If the distribution of these alpha receptors is regulated by estrogen, nolvadex might help fat burning by reducing their number.
There is another possibility that has been put forth by some researchers that estrogen actually lowers LPL activity and progesterone raises it. The progesterone wins out and women hold fat in their hips. This actually makes sense because after menopause progesterone disappears, but there is still some estrogen from the adrenal glands. Women tend to lose fat on their hips after menopause and develop more upper body fat.
This could happen if you blocked estrogen with nolvadex.
My wife gets good results with T3 and clen alternating with ECA and some AS thrown in to preserve muscle against T3 induced catabolism. This is what I would recommend if dieting and exercise have failed.
I'm not an MD but it is my understanding that fatty liver itself is actually a benign condition that is a symptom of some other problem. In this case it is presumably the hypertriglyceridemia (high triglyceride levels) that is causing fat to accumulate in the liver. Since the nolvadex is lowering LPL activity, less fat can get into adipocytes and more accumulates in the blood.
If a person really wanted to stay on nolvadex (or had to because of breast cancer) they might be able to lower triglycerides with a fibrate, a type of cholesterol lowering drug that also lowers triglycerides. The hypertriglyceridemia is what is potentially serious, not the fatty liver.
After doing a little more reading on this, it seems estrogen treatment also can cause hypertriglyceridemia. If estrogen lowers LPL activity in accord with the alternate theory I cited above:
"There is another possibility that has been put forth by some researchers that estrogen actually lowers LPL activity and progesterone raises it. The progesterone wins out and women hold fat in their hips. This actually makes sense because after menopause progesterone disappears, but there is still some estrogen from the adrenal glands. Women tend to lose fat on their hips after menopause and develop more upper body fat.
This could happen if you blocked estrogen with nolvadex"
then nolvadex is actually exerting an estrogenic rather than antiestrogenic effect on fat cells. This is certainly possible since as macro pointed out, nolvadex is a SERM, meaning it can exibit both estrogenic and antiestrogenic activity in different cells.
It might be wise to get blood lipids checked if one is planning on a long term course of nolvadex. I wonder if clomid can also cause hypertriglyceridemia, since it too is a SERM
If a person really wanted to stay on nolvadex (or had to because of breast cancer) they might be able to lower triglycerides with a fibrate, a type of cholesterol lowering drug that also lowers triglycerides. The hypertriglyceridemia is what is potentially serious, not the fatty liver.
After doing a little more reading on this, it seems estrogen treatment also can cause hypertriglyceridemia. If estrogen lowers LPL activity in accord with the alternate theory I cited above:
"There is another possibility that has been put forth by some researchers that estrogen actually lowers LPL activity and progesterone raises it. The progesterone wins out and women hold fat in their hips. This actually makes sense because after menopause progesterone disappears, but there is still some estrogen from the adrenal glands. Women tend to lose fat on their hips after menopause and develop more upper body fat.
This could happen if you blocked estrogen with nolvadex"
then nolvadex is actually exerting an estrogenic rather than antiestrogenic effect on fat cells. This is certainly possible since as macro pointed out, nolvadex is a SERM, meaning it can exibit both estrogenic and antiestrogenic activity in different cells.
It might be wise to get blood lipids checked if one is planning on a long term course of nolvadex. I wonder if clomid can also cause hypertriglyceridemia, since it too is a SERM
Quiet Storm
New member
this sucks ass
im on 25mg nolv ED and dieting right now, from what ive read i assume its not helping anything if not making it worse?
im on 25mg nolv ED and dieting right now, from what ive read i assume its not helping anything if not making it worse?
