Anavar only cycle experience (so far) (and some advice for the newbies :))

[Barch]

"I went from 94kg (204lbs) to 98kg (216lbs)"

Actually, 4 kilos is only a little over 8 pounds.


"The general consensus is that steroids will not burn fat. Not Var, not winny, not anything."

Isn't there a quite a bit of research that says that Var will help you lose fat? In particular from the trunk?

Anyway, good read, thanks Tor.

[PT]

"I went from 94kg (204lbs) to 98kg (216lbs)"

Actually, 4 kilos is only a little over 8 pounds.


"The general consensus is that steroids will not burn fat. Not Var, not winny, not anything."

Isn't there a quite a bit of research that says that Var will help you lose fat? In particular from the trunk?

Anyway, good read, thanks Tor.

thats completly false. there is not a single bit of evidance that states anavar will burn stomach fat. im well aware of the steroid profiles and thata why your saying what you are but i have seen this discussion many times and the evidance all points against var burning any noticable amount of fat

[NewMuscle83]

thats completly false. there is not a single bit of evidance that states anavar will burn stomach fat. im well aware of the steroid profiles and thata why your saying what you are but i have seen this discussion many times and the evidance all points agaings var burning fat

So, you're saying this is false? How about the study that was done in that article? http://forums.steroid.com/showthread.php?t=199816

"Now here’s some interesting stuff for anyone interested primarily in the fat burning properties of this stuff: Anavar may be what we’d call a “fat-burning steroid”. Abdominal and visceral fat were both reduced in one study when subjects in the low/normal natural testosterone range used anavar (4). In another study, appendicular, total, and trunk fat were all reduced with a relatively small dose of 20mgs/day (8), and no excercise. In addition, weight gained with ‘var may be nearly permanent too. It might not be much, but you’ll stand a good chance of keeping most of it. In one study, subjects maintained their weight (re)gains from anavar for at least 6 months after cessation (2)! Concomitantly, in another study, Twelve weeks after discontinuing oxandrolone, 83% of the reductions in total, trunk, and extremity fat were also sustained (8)! If you’re regaining weight, Anavar will give you nearly permanent gains, and if you are trying to lose fat (and you keep your diet in check), the fat lost with Anavar is basically looks to be nearly permanent."

Do you have a link to studies that say otherwise?

[Barch]

thats completly false. there is not a single bit of evidance that states anavar will burn stomach fat. im well aware of the steroid profiles and thata why your saying what you are but i have seen this discussion many times and the evidance all points agaings var burning fat

Here's one. There are a few others that I've seen, but I'll have to find them. I cut out a chunk of text in the middle, because it was over the maximum length for this board.


Treatment with oxandrolone and the durability of effects in older men
E. Todd Schroeder,1,4 Ling Zheng,2 Kevin E. Yarasheski,3 Dajun Qian,2 Yolanda Stewart,2 Carla Flores,2 Carmen Martinez,2 Michael Terk,4,5 and Fred R. Sattler1,2,4
1Division of Infectious Diseases, Department of Medicine, 2General Clinical Research Center, and 5Department of Radiology, Keck School of Medicine, and 4Department of Biokinesiology and Physical Therapy, University of Southern California, Los Angeles, California 90033; and 3Divisions of Metabolism, Endocrinology and Lipid Research and Cell Biology and Physiology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110

Submitted 31 July 2003 ; accepted in final form 17 October 2003



ABSTRACT
TOP
ABSTRACT
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGMENTS
REFERENCES


We investigated the effects of the anabolic androgen, oxandrolone, on lean body mass (LBM), muscle size, fat, and maximum voluntary muscle strength, and we determined the durability of effects after treatment was stopped. Thirty-two healthy 60- to 87-yr-old men were randomized to receive 20 mg oxandrolone/day (n = 20) or placebo (n = 12) for 12 wk. Body composition [dual-energy X-ray absorptiometry (DEXA), magnetic resonance imaging, and 2H2O dilution] and muscle strength [1 repetition maximum (1 RM)] were evaluated at baseline and after 12 wk of treatment; body composition (DEXA) and 1-RM strength were then assessed 12 wk after treatment was discontinued (week 24). At week 12, oxandrolone increased LBM by 3.0 ± 1.5 kg (P < 0.001), total body water by 2.9 ± 3.7 kg (P = 0.002), and proximal thigh muscle area by 12.4 ± 8.4 cm2 (P < 0.001); these increases were greater (P < 0.003) than in the placebo group. Oxandrolone increased 1-RM strength for leg press by 6.7 ± 6.4% (P < 0.001), leg flexion by 7.0 ± 7.8% (P < 0.001), chest press by 9.3 ± 6.7% (P < 0.001), and latissimus pull-down exercises by 5.1 ± 9.1% (P = 0.02); these increases were greater than placebo. Oxandrolone reduced total (-1.9 ± 1.0 kg) and trunk fat (-1.3 ± 0.6 kg; P < 0.001), and these decreases were greater (P < 0.001) than placebo. Twelve weeks after oxandrolone was discontinued (week 24), the increments in LBM and muscle strength were no longer different from baseline (P > 0.15). However, the decreases in total and trunk fat were sustained (-1.5 ± 1.8, P = 0.001 and -1.0 ± 1.1 kg, P < 0.001, respectively). Thus oxandrolone induced short-term improvements in LBM, muscle area, and strength, while reducing whole body and trunk adiposity. Anabolic improvements were lost 12 wk after discontinuing oxandrolone, whereas improvements in fat mass were largely sustained.




Safety Evaluation

One serious adverse event occurred during the study. A subject randomized to oxandrolone developed hypotension (systolic blood pressure <90 mmHg) when his primary doctor modified the patient's antihypertensive medications at the subject's request. His systolic blood pressure had been in the 140- to 155-mmHg range before, and during the study and he desired tighter control. Study therapy was suspended for 3 wk while his antihypertensive medications were adjusted; study therapy was then resumed without problem.

There were no new symptoms or physical findings that could be ascribed to oxandrolone. After 12 wk, there were only modest changes in blood chemistry (Table 3). In the oxandrolone group, serum albumin and alkaline phosphatase levels decreased more than with placebo. The decline in albumin could have reflected the new onset of subclinical inflammation, but there was no change in ultrasensitive CRP levels at week 12 (Table 3) or week 24. There were minimal increments in the liver transaminase levels that reached statistical significance, but ALT was only increased beyond the normal range in two subjects in whom it reached 71 and 99 U/l (1.5 times the upper limit of normal). Both subjects were asymptomatic without liver enlargement, and the ALT returned to normal in both at the week 24 evaluation. Finally, there was a small but significant decrease in PSA in the oxandrolone group.

As described in METHODS, we only measured serum testosterone levels at baseline and week 24. Oxandrolone and placebo groups had similar baseline (P = 0.28; Table 1) and week 24 testosterone levels (358 ± 119 ng/dl in the oxandrolone group and 421 ± 196 ng/dl; P = 0.26). There was a trend toward a greater decline in LH levels with oxandrolone, suggesting that oxandrolone treatment may have suppressed the hypothalamic-pituitary-gonadal axis.


DISCUSSION
TOP
ABSTRACT
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGMENTS
REFERENCES


These findings demonstrated that a relatively brief course of treatment with a potent anabolic androgen in men over 60 yr of age increased LBM as well as upper and lower body maximal voluntary strength more than placebo. The increase of 3.0 ± 1.5 kg in LBM in this study is approximately twofold greater than the increase in LBM reported by other investigators using testosterone supplementation in older men (6, 21, 46, 51). The only other study of androgen therapy to achieve comparable increases in LBM (4.2 ± 0.6 kg) used a dose of testosterone enanthate adjusted to produce nadir levels in the upper normal range, suggesting that dosing was "supraphysiological" because nadir levels were tested 2 wk after a prior intramuscular dose (11). Moreover, subjects were treated for 24 wk compared with 12 wk in our study. These observations suggest that the formulation and potency of the androgen, dose, and duration of therapy may affect the changes in lean tissue achieved, which is in keeping with a recent dose ranging study of testosterone in younger men (5).

The significant increases in both upper and lower body maximal voluntary strength in subjects receiving oxandrolone are noteworthy. In the few studies assessing the effects of androgen supplementation in older men, muscle strength was not tested (51) or was evaluated with either handgrip (31, 44) or isokinetic dynamometry (46, 52), which may measure different mechanistic aspects of strength [reviewed in Storer et al. (47)]. Therefore, these evaluations may not be representative of true changes in maximal strength for larger muscle groups important for optimal physical function in older persons. Moreover, only one study demonstrated substantial increases in 1-RM strength in both upper body and lower body muscle groups, although neuromuscular learning may have contributed to the gains in strength with testosterone because multiple baseline trials of maximal strength were not assessed (11). However, older adults typically produce their best performance (highest force production) on the second or third 1-RM trial (12, 40). Thus, studies to assess the affects of anabolic interventions on maximal voluntary strength should test strength on at least two separate occasions before study therapy is initiated.

The increases in muscle strength and CSA in the oxandrolone group suggest that a major portion of the anabolic androgen-induced increase in LBM was due to increases in muscle protein mass, because strength is closely related to muscle size (27). Oxandrolone and testosterone exert their actions by enhancing the rate of mixed muscle (11, 52) and myofibrillar protein synthesis (7), and by reducing the rate of muscle protein breakdown (43). However, our 2H2O dilution measurements indicated a disproportionate increase in TBW (2.9 kg) compared with the increase in DEXA-derived LBM (3 kg). If the entire increase in DEXA-derived LBM were protein, we would have anticipated only 2.3-kg increase in TBW. Also, the rapid loss of LBM (2.5 kg) after oxandrolone was discontinued suggests that tissue fluid was a component of the oxandrolone-induced increase in LBM. Future studies should measure muscle amino acid balance after androgen administration in elderly men at risk for physical frailty.

To our knowledge, this is the first study to determine the durability of the effects achieved with androgen therapy after the treatment was discontinued. We speculated that at least some portion of the gains in LBM and strength would be sustained 12 wk after treatment with oxandrolone. However, the fact that gains in both LBM and strength were largely lost within 12 wk after treatment was discontinued suggests that prolonged therapy with an anabolic androgen will be necessary to maintain and enhance increases in LBM and muscle strength. Other anabolic strategies with potentially better safety profiles such as resistance training, a potent stimulus for skeletal muscle protein synthesis in older persons (56), or specific androgen receptor modulators should be investigated for sustaining gains in muscle mass and strength during the aging process.

Another important and unique finding of this study was the oxandrolone-induced decrease in total and trunk fat that was largely sustained 12 wk after oxandrolone was stopped. In younger hypogonadal men, testosterone decreased total body and abdominal fat mass (4, 20, 54). However, it is not clear whether androgen therapy affects adipose tissue in eugonadal men. Bhasin et al. (4) reported no change in fat mass with replacement doses of 125 mg testosterone weekly over 4 mo in eugonadal, healthy men, although much higher supraphysiological doses reduced adipose tissue. Marin et al. (24) reported that low-dose androgen therapy reduced abdominal fat in middle-aged men with central obesity. However, the effects occurred primarily in subjects with low testosterone levels, which is consistent with observations that intra-abdominal fat is inversely correlated with free testosterone levels (42). Only five of our subjects had baseline total testosterone levels <270 ng/dl (lower limit of normal in our laboratory), but levels for the entire group were generally less than those of younger men. Whether the relative hypogonadism (compared with younger men) of our participants or the potency or structure of the synthetic androgen, oxandrolone, was primarily responsible for the reductions in whole body and trunk fat is uncertain.

These results do provide clarification as to whether metabolism of testosterone by aromatase to estradiol (40%) is largely responsible for changes in fat mass when men are treated with testosterone (18). The fact that adipocytes contain estradiol receptors and the observation that estrogen receptor knockout mice have increased adipose tissue have suggested that estrogen is important in downregulating fat mass (8). However, oxandrolone is not aromatized to estrogen, suggesting that the favorable declines in adipose tissue observed in the present study were due to direct and specific actions of oxandrolone.

The discordant effects of oxandrolone on lean tissue and fat mass 12 wk after study therapy was discontinued were puzzling. According to 3-day food diaries and self-report of exercise activity, subjects did not change their dietary or habitual activity during the study. Thus the durability of the effects of oxandrolone on adipose but not lean tissue likely reflect the biological differences in these tissues and/or the effects of other concurrent regulators of metabolism. In a population prone to obesity, it is remarkable that 80% of the reduction in total and central fat mass after a relatively short period of androgen therapy (12 wk) were sustained for at least 3 mo after treatment was discontinued. The reductions in fat mass observed in obese middle-aged men have been associated with decreases in visceral adipose tissue, improvements in insulin sensitivity, and declines in cholesterol, triglycerides, and diastolic blood pressure (24, 25). These effects are consistent with the known effects of androgens to decrease lipoprotein lipase and upregulate -adrenergic receptors on adipocytes, which would inhibit the accumulation of lipid and enhance the efflux of lipid from these cells in response to catecholamines (26, 38, 55). Further studies will be necessary to assess whether the reductions in fat mass observed in our older men would be associated with beneficial measures of metabolism and health in an aging population.

A limitation of this study is that we assessed a 17-methylated androgen and not generic testosterone. Thus we cannot extrapolate our findings to a dose of testosterone. Although we did not demonstrate short-term adverse clinical effects with oxandrolone, evaluation of anabolic androgens, including testosterone, as potential treatments for sarcopenia, must be investigated in sufficiently powered studies of long-term treatment to demonstrate their safety for prostate and cardiovascular health.

In conclusion, substantial gains in LBM and muscle size were achieved safely with a relatively short course of therapy with an anabolic androgen in 60- to 87-yr-old men. Moreover, these changes were associated with significant gains in maximal voluntary strength in the large upper and lower body muscle groups, which are important for normal physical function in older persons. However, the benefits were lost within 12 wk after oxandrolone was discontinued, suggesting that prolonged androgen treatment would be needed to maintain these anabolic benefits. Thus the long-term safety and efficacy of androgen therapy in older men need to be established. In addition, whole body and trunk fat mass decreased significantly during therapy, and the effects were largely sustained after treatment was discontinued. Whether the reduction in central adiposity with androgen therapy has tangible health benefits is uncertain. These observations, therefore, raise several important questions that must be addressed before androgen therapy is widely prescribed as long-term therapy for sarcopenia in older individuals.