Originally Posted by hackskii

You are talking visceral fat (intra-abdominal) right?
I have heard DHT drugs increase visceral fat.

Originally Posted by Greekgoddess

Lost it off my legs first, then a**e, face and neck, arms, stomach in that order.

Originally Posted by Macro

that is an androgenic fat pattern of fat loss. very uncommon for women (unless they have had hysterectomy or extreme PCOS).

you probably have signifcantly higher than average androgen to estrogen ratio

Originally Posted by Greekgoddess

On second thought- could it be something in the Lipo 6 I am taking that is having this effect????

My sex drive has been through the roof since I started taking it three months ago!

Originally Posted by hackskii

My GF is 52 and she is going through menopause and she has zero sex drive.

Originally Posted by maccer

haha Hacks isn't that a bit irrelevant?

I thought you were going to give an interesting answer about lipo 6 lol

Originally Posted by Macro

with respect to soft belly fat, yes. the intra-abdominal fat is due more to androgenic and insulin influence (gut and belly distention)

Originally Posted by Macro

you obviously dont understand this study or you would not have posted it. And certainly not highlighted that portion of the text. leptin insensitivity is linked to obesity, not low levels of leptin. Leptin levels in obese persons are actually generally very high. As are estrogen levels (due to aromatase). And to be clear there is a huge difference between hypoestrogenemic state (which is what that study refers to) and the hyperestrogenic being discussed in the article.

as to your criticism, the article does not say that estrogen is the cause of all adipose issues. What is says is that higher estrogen levels are linked to alpha2 proliferation (as well as female fat pattern and inhibition of lipolysis) and that aromatase increases due to fat gain increase levels of estrogen (primarily in men, but peripheral and local impacts of estrogen synthesis in women are also significant, highly linked to secondary conversion due to reduction of SHBG).

and because macro is nice and decidedly forgiving of your rudeness...

J Clin Endocrinol Metab. 2004 Apr;89(4):1869-78. Links

Estrogen controls lipolysis by up-regulating alpha2A-adrenergic receptors directly in human adipose tissue through the estrogen receptor alpha. Implications for the female fat distribution.

Pedersen SB, Kristensen K, Hermann PA, Katzenellenbogen JA, Richelsen B.
Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Aarhus University Hospital, Denmark. sbp@dadlnet.dk
Estrogen seems to promote and maintain the typical female type of fat distribution that is characterized by accumulation of adipose tissue, especially in the sc fat depot, with only modest accumulation of adipose tissue intraabdominally. However, it is completely unknown how estrogen controls the fat accumulation. We studied the effects of estradiol in vivo and in vitro on human adipose tissue metabolism and found that estradiol directly increases the number of antilipolytic alpha2A-adrenergic receptors in sc adipocytes. The increased number of alpha2A-adrenergic receptors caused an attenuated lipolytic response of epinephrine in sc adipocytes; in contrast, no effect of estrogen on alpha2A-adrenergic receptor mRNA expression was observed in adipocytes from the intraabdominal fat depot. These findings show that estrogen lowers the lipolytic response in sc fat depot by increasing the number of antilipolytic alpha2A-adrenergic receptors, whereas estrogen seems not to affect lipolysis in adipocytes from the intraabdominal fat depot. Using estrogen receptor subtype-specific ligands, we found that this effect of estrogen was caused through the estrogen receptor subtype alpha. These findings demonstrate that estrogen attenuates the lipolytic response through up-regulation of the number of antilipolytic alpha2A-adrenergic receptors only in sc and not in visceral fat depots. Thus, our findings offer an explanation how estrogen maintains the typical female sc fat distribution because estrogen seems to inhibit lipolysis only in sc depots and thereby shifts the assimilation of fat from intraabdominal depots to sc depots.

1: J Lipid Res. 1999 Sep;40(9):1559-71. Links

Regional and gender variations in adipose tissue lipolysis in response to weight loss.

Mauriège P, Imbeault P, Langin D, Lacaille M, Alméras N, Tremblay A, Després JP.
Lipid Research Center, Laval University, Ste-Foy, Québec, Canada G1K 7P4.
Catecholamine-induced lipolysis was investigated in 32 obese subjects (14 men and 18 premenopausal women), aged 36-50 years, whose body mass index ranged from 30 to 42 kg/m(2). Isolated subcutaneous (subc) abdominal and femoral adipocytes were studied before and after a 15-week weight reducing program, during which mean body weight loss averaged 9 vs. 10 kg in women and men, respectively (P < 0.0001). Participants were re-examined when they were weight-stable. Fat cell weight decreased by about 15;-20% in both depots (P values ranging from 0.01 to 0.05). Epinephrine (mixed alpha2-/beta-adrenoceptor (AR) agonist) induced antilipolysis at low concentrations and a net lipolytic response at higher doses, irrespective of subjects' fatness and anatomic location of fat. Basal lipolysis, maximal lipolytic responses to isoprenaline (beta-AR agonist), dobutamine and procaterol (beta1- and beta2-AR agonists, respectively) as well as maximal antilipolytic effects of epinephrine or UK-14304 (alpha2-AR agonist) were similar before and after weight reduction. However, both beta- and beta2-AR lipolytic sensitivities and the beta-AR density were increased in both genders after weight reduction, this effect being more marked in subc abdominal than in femoral adipocytes (P values ranging from 0.001 to 0.05). The alpha2-AR antilipolytic sensitivity was reduced in adipose cells from both regions in women, but only in subc abdominal adipocytes in men (P < 0.05), although the alpha2-AR density remained unchanged after weight reduction. In conclusion, a moderate weight loss leads to a higher adipose cell lipolytic efficiency which is associated with changes at receptor levels (mainly an increased beta2- and a decreased alpha2-AR sensitivities), in both genders.
1: Int J Obes Relat Metab Disord. 1997 Apr;21(4):314-20. Links

Lipolytic catecholamine resistance linked to alpha 2-adrenoceptor sensitivity--a metabolic predictor of weight loss in obese subjects.

Hellström L, Rössner S, Hagström-Toft E, Reynisdottir S.
Department of Medicine, Karolinska Institute, Huddinge University Hospital, Sweden.
OBJECTIVE: The weight loss achieved during treatment with very-low-calorie diets (VLCD) varies between individuals. The aim of this study was to investigate whether interindividual variations in catecholamine-induced lipolysis are of importance for the rate of weight loss during VLCD. DESIGN: Prospective study. SUBJECTS: Twenty-eight obese, but otherwise healthy and drug-free women aged 20-57 y with BMI 33.3-47.5 kg/m2 were investigated before entering a four week weight reduction program with a calorie-restricted diet. MEASUREMENTS: A subcutaneous adipose tissue biopsy was obtained from the abdominal area. Isolated fat cells were prepared and incubated in vitro with agents acting on lipolysis at defined steps in the lipolytic cascade. Glycerol release was measured and used as a lipolytic index. Following the biopsy, the subjects underwent a four week VLCD treatment. RESULTS: The decrease in body weight in the whole group ranged between 4.8 and 13.5 kg. Dietary compliance was ascertained by daily measurements of urine-ketones and regular interviews and was satisfactory in all subjects throughout the study. Based on percent body weight reduction, the material was divided into two equally sized groups, classified as rapid or slow weight losers. The rapid weight losers were 10-fold more sensitive to the lipolytic effect of noradrenaline (P = 0.04) and 10-fold less sensitive (P = 0.002) to the antilipolytic effect induced by the alpha 2-adrenoceptor agonist clonidine than the slow weight losers. In the whole material, weight loss was significantly correlated (adjusted r2 = 0.25) with alpha 2-adrenoceptor sensitivity. CONCLUSION: Rapid weight loss during VLCD is associated with increased adipocyte lipolytic sensitivity to catecholamines due to decreased alpha 2-adrenoceptor sensitivity, which in turn may promote lipid mobilization. It appears that variations in alpha 2-adrenoceptor sensitivity in adipocytes may be predictive of weight loss during VLCD.

1: Clin Endocrinol (Oxf). 2007 Mar;66(3):440-6. Links

Intra-adipose sex steroid metabolism and body fat distribution in idiopathic human obesity.

Wake DJ, Strand M, Rask E, Westerbacka J, Livingstone DE, Soderberg S, Andrew R, Yki-Jarvinen H, Olsson T, Walker BR.
Endocrinology Unit, Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Scotland, UK.
OBJECTIVE: Causes of visceral fat accumulation include glucocorticoid excess or decreased oestrogen/androgen ratio either in plasma or within adipose tissue. In obese subjects, the intra-adipose cortisol-generating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) is increased, but information on sex steroid signalling is sp****. We aimed to test associations between body fat or fat distribution and mRNA transcript levels for androgen and oestrogen receptors and for enzymes metabolizing sex steroids in adipose tissue. DESIGN: A cross-sectional study. PATIENTS: Forty-five healthy men and women with body mass index (BMI) 21-36 kg/m(2). MEASUREMENTS: In subcutaneous adipose biopsies we measured mRNAs for enzymes metabolizing local oestrogens (aromatase) and androgens [5alpha-reductase type 1; AKR1C2 (3alpha-HSD3); AKR1C3 (17beta-HSD5, 3alpha-HSD2)] and for sex steroid receptors [oestrogen receptor (ER)-alpha and androgen receptor (AR)]. We related these to body fat mass and distribution. RESULTS: Generalized obesity (BMI) was associated with increased aromatase mRNA (r = 0.35, P < 0.05). Central obesity (waist : hip ratio) was associated with mRNA for AKR1C2 (r = 0.28, P < 0.05) and AKR1C3 (r = 0.38, P < 0.01) but not aromatase (r = 0.06). 5alpha-Reductase type 1, ER and AR mRNA levels did not predict fat amount or its distribution. CONCLUSION: These data on transcript levels suggest that, in idiopathic obesity, increased intra-adipose oestrogen generation by aromatase predicts p