Contest Gear choice for maintaining good lipid profile

Toxicwaste

New member
I have been working on controlling my lipid profile for the past year with mixed success using statins and now Zetia and diet changes. In the past when preparing for a show my cycles were dominated by 17AA gear in addition to Letrozole/Arimidex. The combination simply devestates my lipid panel. I have a show coming up and I do not want my lipids to return to the 400 level again (I am 33). Are there any gear suggestions that will not completely screw up my lipids? I am already aware of the damage 17AA can do.

Also, read a post that Aromasin can be taken as an anti-e without the damage to lipid profiles characteristic of letrozole/arimidex. Can anyone support or refute this claim?
 
Toxicwaste,
I share your concerns. At 33, i have also been researching the best lipid-friendly cycle. I came by a few articles claiming that Anavar did not significantly rasie overall lipid levels, however the HLD/LDL ratio was affected. I am looking into the use of Lipitor in conjunction with AAS, but Lipitor is not easy on the liver in the first place. I'll watch this post close and add whatever I find.
AngerOut
 
Lipid-profile

I've garnered from various information I've read that the esterfied AS tend to be less destructive to lipid panels then non-esterfied AS. Unfortunately, pre-contest, the non-esterfied 17AA gear is the typical choice. I'm thinking something such as test/eq would be the best but these are not great choices for precontest preparations. Especially the last 4 weeks.

Letro was very bad for my lipid counts. I've read Nolvadex is better but I am interested to hear whether anyone has an opinion or experience with Aromasin. As I said, there was a post indicating that Aromasin did not screw your lipid panel as Arimidex or Letro does.
 
You can't suppress estrogen without affecting plasma lipids... HDL usually goes down slightly (by about 10% or less)...
Some studies suggest that arimidex might be your best choice...



An overview of the pharmacology and pharmacokinetics of the newer generation aromatase inhibitors anastrozole, letrozole, and exemestane.

Buzdar AU, Robertson JF, Eiermann W, Nabholtz JM.

Department of Breast Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston 77030, USA. abuzdar@mdanderson.org

BACKGROUND: The newer generation, nonsteroidal aromatase inhibitors (AIs) anastrozole and letrozole have shown superior efficacy compared with tamoxifen as first-line treatments and compared with megestrol acetate as second-line therapy in postmenopausal women with advanced breast carcinoma. In an open-label, Phase II trial, it was reported that exemestane showed numerical superiority compared with tamoxifen for objective response and clinical benefit. Because these agents ultimately may be administered for periods of up to 5 years in the adjuvant setting, it is of increasing importance to assess their tolerability and pharmacologic profiles. METHODS: In the absence of data from direct clinical comparisons, the published literature was reviewed for the clinical pharmacology, pharmacokinetic characteristics, and selectivity profiles of anastrozole, letrozole, and exemestane. RESULTS: At clinically administered doses, the plasma half-lives of anastrozole (1 mg once daily), letrozole (2.5 mg once daily), and exemestane (25 mg once daily) were 41-48 hours, 2-4 days, and 27 hours, respectively. The time to steady-state plasma levels was 7 days for both anastrozole and exemestane and 60 days for letrozole. Androgenic side effects have been reported only with exemestane. Anastrozole treatment had no impact on plasma lipid levels, whereas both letrozole and exemestane had an unfavorable effect on plasma lipid levels. In indirect comparisons, anastrozole showed the highest degree of selectivity compared with letrozole and exemestane in terms of a lack of effect on adrenosteroidogenesis. CONCLUSIONS: All three AIs demonstrated clinical efficacy over preexisting treatments. However, there were differences in terms of pharmacokinetics and effects on lipid levels and adrenosteroidogenesis. The long-term clinical significance of these differences remains to be elucidated. Copyright 2002 American Cancer Society.
 
Back
Top