Let's Get a Simple Yes or No and Finally Resolve This: Do Steroids Burn Fat?

[MR. BMJ]

I agree with Juggy and TypeII. It's a benefit of most androgens, but has been noted with Anavar in relation to visceral fat. I am not sure if i did, but Big A had a thread up...oh, about 10 or so years ago (yea I know), and I think I may have posted a study or two in that thread. Not sure if that thread is even still accessible. This had been a topic over at CEM years back, and they posted some stuff on it...which I hope I put on that thread by Big A. I'm a loser though so i probably didn't lol.

I didn't use Anavar for so many years thinking it was just an expensive waste of money. When I started using it for the first time, it was one of the first things i noticed right away. Halo does the same...though i've not used that compound since the 90's, and that was Stenox from Mexico, lol.

 

[MR. BMJ]

This is the one that Juggy noted, I thjink it may have been posted already:

Oxandrolone DECREASES VAT
Nandrolone INCREASES VAT
TE INCREASED VAT (Note: this may be dose dependent from other studies on the matter. Simply too little and too much T can cause VAT).

In the full study, the authors point out that there were no differences between subQ fat loss between the different groups

Lovejoy JC, Bray GA, Greeson CS, Klemperer M, Morris J, Partington C, Tulley R. Oral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men. Int J Obes Relat Metab Disord. 1995;19(9):614-24.

ABSTRACT

OBJECTIVE: To compare the effects of testosterone enanthate (TE), anabolic steroid (AS) or placebo (PL) on regional fat distribution and health risk factors in obese middle-aged men undergoing weight loss by dietary means. DESIGN: Randomized, double-blind, placebo-controlled clinical trial, carried out for 9 months with primary assessments at 3 month intervals. Due to adverse blood lipid changes, the AS group was switched from oral oxandrolone (ASOX) to parenteral nandrolone decanoate (ASND) after the 3 month assessment point. SUBJECTS: Thirty healthy, obese men, aged 40-60 years, with serum testosterone (T) levels in the low-normal range (2-5 ng/mL). MAIN OUTCOME MEASURES: Abdominal fat distribution and thigh muscle volume by CT scan, body composition by dual energy X-ray absorptiometry (DEXA), insulin sensitivity by the Minimal Model method, blood lipids, blood chemistry, blood pressure, thyroid hormones and urological parameters. RESULTS: After 3 months, there was a significantly greater decrease in subcutaneous (SQ) abdominal fat in the ASOX group compared to the TE and PL groups although body weight changes did not differ by treatment group. There was also a tendency for the ASOX group to exhibit greater losses in visceral fat, and the absolute level of visceral fat in this group was significantly lower at 3 months than in the TE and PL groups. There were significant main effects of treatment at 3 months on serum T and free T (increased in the TE group and decreased in the ASOX group) and on thyroid hormone parameters (T4 and T3 resin uptake significantly decreased in the ASOX group compared with the other two groups). There was a significant decrease in HDL-C, and increase in LDL-C in the ASOX group, which led to their being switched to the parenteral nandrolone decanoate (ASND) after 3 months. ASND had opposite effects on visceral fat from ASOX, producing a significant increase from 3 to 9 months while continuing to decrease SQ abdominal fat. ASND treatment also decreased thigh muscle area, while ASOX treatment increased high muscle. ASND reversed the effects of ASOX on lipoproteins and thyroid hormones. The previously reported effect of T to decrease visceral fat was not observed, in fact, visceral fat in the TE group increased slightly from 3 to 9 months, although SQ fat continued to decrease. Neither TE nor AS treatment resulted in any change in urologic parameters. CONCLUSIONS: Oral oxandrolone decreased SQ abdominal fat more than TE or weight loss alone and also tended to produce favorable changes in visceral fat. TE and ASND injections given every 2 weeks had similar effects to weight loss alone on regional body fat. Most of the beneficial effects observed on metabolic and cardiovascular risk factors were due to weight loss per se. These results suggest that SQ and visceral abdominal fat can be independently modulated by androgens and that at least some anabolic steroids are capable of influencing abdominal fat.

 

[MR. BMJ]

Haloteston for it's effects on reducing/blocking 11beta-HSD1, and working as an anti-glucocorticoid, had been discussed at some length at CEM many years back. I have not looked over these in many years, it's a little out of my area. I found the Big A post from 2010, and was able to find these to add here for discussion.

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

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 signaling is sparse. 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 peripheral fat distribution, while androgen metabolism by AKR1C isoforms predicts central fat distribution, supporting the hypothesis that intra-adipose sex steroid metabolism is a determinant of gynoid vs. android patterns of body fat.


Obesity (Silver Spring). 2007 May;15(5):1155-63.

Omental 11beta-hydroxysteroid dehydrogenase 1 correlates with fat cell size independently of obesity.

Michailidou Z, Jensen MD, Dumesic DA, Chapman KE, Seckl JR, Walker BR, Morton NM.

Endocrinology Unit, Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.

OBJECTIVES: In ideopathic obesity, there is evidence that enhanced cortisol regeneration within abdominal subcutaneous adipose tissue may contribute to adiposity and metabolic disease. Whether the cortisol regenerating enzyme, 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1), or glucocorticoid receptor (GRalpha) levels are altered in other adipose depots remains uncertain. Our objective was to determine the association between 11betaHSD1 and GRalpha mRNA levels in four distinct adipose depots and measures of obesity and the metabolic syndrome. RESEARCH METHODS AND PROCEDURES: Adipose tissue biopsies were collected from subcutaneous (abdominal, thigh, gluteal) and intra-abdominal (omental) adipose depots from 21 women. 11betaHSD1 and GRalpha mRNA levels were measured by real-time polymerase chain reaction. Body composition, fat distribution, fat cell size, and blood lipid, glucose, and insulin levels were measured. RESULTS: 11betaHSD1 mRNA was highest in abdominal subcutaneous (p < 0.001) and omental (p < 0.001) depots and was positively correlated with BMI and visceral adiposity in all depots. Omental 11betaHSD1 correlated with percent body fat (R = 0.462, p < 0.05), fat cell size (R = 0.72, p < 0.001), and plasma triglycerides (R = 0.46, p < 0.05). Conversely, GRalpha mRNA was highest in omental fat (p < 0.001). GRalpha mRNA was negatively correlated with BMI in the abdominal subcutaneous (R = -0.589, p < 0.05) and omental depots (R = -0.627, p < 0.05). Omental GRalpha mRNA was inversely associated with visceral adiposity (R = -0.507, p < 0.05), fat cell size (R = -0.52, p < 0.01), and triglycerides (R = -0.50, p < 0.05). DISCUSSION: Obesity was associated with elevated 11betaHSD1 mRNA in all adipose compartments. GRalpha mRNA is reduced in the omental depot with obesity. The novel correlation of 11betaHSD1 with omental fat cell size, independent of obesity, suggests that intracellular cortisol regeneration is a strong predictor of hypertrophy in the omentum.


11beta-hydroxysteroid dehydrogenase type 1 mRNA is increased in both visceral and subcutaneous adipose tissue of obese patients.Desbriere R, Vuaroqueaux V, Achard V, Boullu-Ciocca S, Labuhn M, Dutour A, Grino M.
Service de Gynécologie/Obstétrique, CHU Nord, Marseille, France.

OBJECTIVE: Data from rodents provide evidence for a causal role of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) in the development of obesity and its complications. In humans, 11beta-HSD-1 is increased in subcutaneous adipose tissue (SAT) of obese patients, and higher adipose 11beta-HSD-1 was associated with features of the metabolic syndrome. To date, there is no evidence for an increased expression of 11beta-HSD-1 in human visceral adipose tissue (VAT), although VAT is the major predictor for insulin resistance and the metabolic syndrome. RESEARCH METHODS AND PROCEDURES: 11beta-HSD-1 and hexose-6-phosphate dehydrogenase (the enzyme responsible for the synthesis of nicotinamide adenine dinucleotide phosphate, the cofactor required for 11beta-HSD-1 oxoreductase activity) mRNA levels were measured using real-time quantitative reverse transcriptase-polymerase chain reaction in abdominal SAT and VAT biopsies obtained from 10 normal-weight and 12 obese women. Adiponectin mRNA was used as an internal control. RESULTS: 11beta-HSD-1 mRNA concentrations were significantly increased in both SAT and VAT of obese patients (720% and 450% of controls, respectively; p < 0.05) and correlated with hexose-6-phosphate dehydrogenase mRNA levels. The level of VAT 11beta-HSD-1 mRNA correlated with anthropometric parameters: BMI (r = 0.41, p = 0.05), waist circumference (r = 0.44, p = 0.04), abdominal sagittal diameter (r = 0.51, p = 0.02), and percentage fat (r = 0.51, p = 0.02). DISCUSSION: Our results demonstrate for the first time that 11beta-HSD-1 mRNA expression is increased in VAT from obese patients. They strengthen the importance of 11beta-HSD-1 in human obesity and its associated complications and suggest the need of clinical studies with specific 11beta-HSD-1 inhibitors

 

[Elvia1023]

YES

 

[NGL34]

Steroids promote higher rate of protein synthesis which ultimately manifests in more muscle tissue. More muscle tissue manifests in an increased rate of metabolism. Higher metabolism means higher rate of fat burning. Period. Dot.

This.

Tren and high dosed var are thes only steriods that I ever notice any real appreciable fat loss. I'm sure the high androgens in tren accelerated this effect. Var I have no clue why it worked for fat burning esp with it being such a mild steriod