what 1 week of winstrol can do

MANWHORE getting shredded! Nice man. How long have you been cutting, and what're you running -- if anything?
 
That is interesting but an even more interesting experiment would have been what happens after 4 weeks of staying on and comparing the results, then possibly 6 weeks.

The body does tend to drive towards more homeostatic conditions, so it would be interesting to see how it continues to deal with the winny after more time.

Any volunteers?

Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis. Hugh McA. Taggarta, Deborah Applebaum-Bowdena, Steven Haffnera, G.Russell Warnicka, Marian C. Cheunga, John J. AlbersCorresponding author contact information, Charles H. Chestnut, William R. Hazzarda.

Abstract
The effects of stanozolol on lipoprotein levels were assessed in a short-term (6 wk) prospective study of 10 normolipidemic, postmenopausal, osteoporotic women. While total cholesterol and triglyceride levels remained constant, equal and offsetting responses were seen in low density lipoprotein (LDL) cholesterol (+30.9 ± 28.1 mg/dl [mean ± S.D.], p < 0.01, a 21% increase) and high density lipoprotein (HDL) cholesterol (?32.5 ± 11.9 mg/dl [mean ± S.D.], p < 0.001, a 53% decline). Hence the LDL/HDL ratio increased dramatically, from 2.5 ± 0.7 to 6.8 ± 2.5. Within HDL, stanozolol was associated with a greater decline in HDL2 (from 26.0 ± 7.4 mg/dl to 3.8 ± 1.9 mg/dl, p < 0.001, an 85% decrease) than HDL2 (which diminished from 35.7 ± 3.2 to 24.1 ± 5.8 mg/dl, p < 0.001, a 35% decrease). The major HDL apolipoproteins also declined (A-I by a mean of 41% and A-II by 24%, both p < 0.001). Postheparin hepatic triglyceride lipase increased (off treatment 74 ± 42 nmole free fatty acid min?1 mole?1, on treatment 242 ± 110, n = 6, p = 0.06). All changes were reversed by 5 wk following termination of the drug. These lipoprotein changes suggest caution in the long term prescription of stanozolol, particularly in those without overriding clinical indications for its use.
 
Awesome post Dutch really because it highlights some of the problems encountered with oral AAS.

But really SO WHAT !!! Goodness why all this alarmism? What you think happens when you eat steak and eggs for breakfast?

Remember this is spot test (which should be collected in the AM after an "overnight fast") and the the results don't mean squat (except Oral AAS adversely effect lipids and as DOC mentioned that's not new) in determining what influence an oral anabolic will have on the relative risk of developing ASCVD over a particular period of time.

The contrast (a spot test vs a few weeks of AAS) is particularly important because the Hepatic and lipid aberrations are brief lasting no more than 4-6 weeks. (I hope).
It's also known the development of ASCVD takes YEARS of chronic exposure to known risk factors. (I know there are RARE exceptions such as the familial lipid abnormalities)

What is one to do? Limit oral cycles to no more than 4 weeks and KNOW your ASCVD risk BEFORE CYCLING an ORAL AGENT! If your considered "high risk" orals should be avoided, IMO

Regards

jim
 
Awesome post Dutch really because it highlights some of the problems encountered with oral AAS.

But really SO WHAT !!! Goodness why all this alarmism? What you think happens when you eat steak and eggs for breakfast?

Remember this is spot test (which should be collected in the AM after an "overnight fast") and the the results don't mean squat (except Oral AAS adversely effect lipids and as DOC mentioned that's not new) in determining what influence an oral anabolic will have on the relative risk of developing ASCVD over a particular period of time.

The contrast (a spot test vs a few weeks of AAS) is particularly important because the Hepatic and lipid aberrations are brief lasting no more than 4-6 weeks. (I hope).
It's also known the development of ASCVD takes YEARS of chronic exposure to known risk factors. (I know there are RARE exceptions such as the familial lipid abnormalities)

What is one to do? Limit oral cycles to no more than 4 weeks and KNOW your ASCVD risk BEFORE CYCLING an ORAL AGENT! If your considered "high risk" orals should be avoided, IMO

Regards

jim

Thanks for the additional information. There's no alarmism intended; I just want to share the rapid changes the low dose triggered in my particular case. Both tests were taken conform protocol btw.
If everyone would stick to the type of use you suggested, they would indeed limit their time at risk for the build-up of plaques. But I wonder if ‘the average user’ lives up to these recommendations. Unfortunately a bad cholesterol ratio is also associated with other health problems that may not need lengthy exposure, ie immunological responses and mood. Do you have any reference on that?
 
Any volunteers?

Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis. Hugh McA. Taggarta, Deborah Applebaum-Bowdena, Steven Haffnera, G.Russell Warnicka, Marian C. Cheunga, John J. AlbersCorresponding author contact information, Charles H. Chestnut, William R. Hazzarda.

Abstract
The effects of stanozolol on lipoprotein levels were assessed in a short-term (6 wk) prospective study of 10 normolipidemic, postmenopausal, osteoporotic women. While total cholesterol and triglyceride levels remained constant, equal and offsetting responses were seen in low density lipoprotein (LDL) cholesterol (+30.9 ± 28.1 mg/dl [mean ± S.D.], p < 0.01, a 21% increase) and high density lipoprotein (HDL) cholesterol (?32.5 ± 11.9 mg/dl [mean ± S.D.], p < 0.001, a 53% decline). Hence the LDL/HDL ratio increased dramatically, from 2.5 ± 0.7 to 6.8 ± 2.5. Within HDL, stanozolol was associated with a greater decline in HDL2 (from 26.0 ± 7.4 mg/dl to 3.8 ± 1.9 mg/dl, p < 0.001, an 85% decrease) than HDL2 (which diminished from 35.7 ± 3.2 to 24.1 ± 5.8 mg/dl, p < 0.001, a 35% decrease). The major HDL apolipoproteins also declined (A-I by a mean of 41% and A-II by 24%, both p < 0.001). Postheparin hepatic triglyceride lipase increased (off treatment 74 ± 42 nmole free fatty acid min?1 mole?1, on treatment 242 ± 110, n = 6, p = 0.06). All changes were reversed by 5 wk following termination of the drug. These lipoprotein changes suggest caution in the long term prescription of stanozolol, particularly in those without overriding clinical indications for its use.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1724824/pdf/v038p00253.pdf
 
That is a "lipid panel" should be collected in the AM after an "overnight fast".

Sidhu D, Naugler C. Fasting Time and Lipid Levels in a Community-Based Population: A Cross-sectional Study. Arch Intern Med. 2012;172(22):1707-1710. JAMA Network | JAMA Internal Medicine | Fasting Time and Lipid Levels in a Community-Based Population:

Background Although current guidelines recommend measuring lipid levels in a fasting state, recent studies suggest that nonfasting lipid profiles change minimally in response to food intake and may be superior to fasting levels in predicting adverse cardiovascular outcomes. The objective of this study was to investigate the association between fasting times and lipid levels.

Methods Cross-sectional examination of laboratory data, including fasting duration (in hours) and lipid results, was performed over a 6-month period in 2011 in a large community-based cohort. Data were obtained from Calgary Laboratory Services, Calgary, Alberta, Canada, the sole supplier of laboratory services for Calgary and surrounding areas (source population, 1.4 million persons). The main outcome measures were mean levels of high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol, and triglycerides for fasting intervals from 1 hour to more than 16 hours. After differences in individual ages were controlled for, linear regression models were used to estimate the mean levels of cholesterol subclasses at different fasting times.

Results A total of 209 180 individuals (111 048 females and 98 132 males) were included in the study. The mean levels of total cholesterol and high-density lipoprotein cholesterol differed little among individuals with various fasting times. The mean calculated low-density lipoprotein cholesterol levels showed slightly greater variations of up to 10% among groups of patients with different fasting intervals, and the mean triglyceride levels showed variations of up to 20%.

Conclusion Fasting times showed little association with lipid subclass levels in a community-based population, which suggests that fasting for routine lipid levels is largely unnecessary.
 
Gaziano J. Should We Fast Before We Measure Our Lipids?. Arch Intern Med. 2012;172(22):1705-1706. JAMA Network | JAMA Internal Medicine | Should We Fast Before We Measure Our Lipids?

In summary, most of the reasons that we measure a lipid profile depend on total and HDL cholesterol levels for most of our decision making. The incremental gain in information of a fasting profile is exceedingly small for total and HDL cholesterol values and likely does not offset the logistic impositions placed on our patients, the laboratories, and our ability to provide timely counseling to our patients. This, in my opinion, tips the balance toward relying on nonfasting lipid profiles as the preferred practice.

Therefore, in practice, you can begin with a nonfasting lipid profile, and it is possible to use nonfasting levels for risk assessment, decisions about initiating treatment, and monitoring the effects of treatment. If you want to monitor triglyceride levels, then doing some sample fasting may useful. With this approach, most of our lipid profiles can be obtained in the nonfasting state, increasing convenience for our patients and ourselves and decreasing the burden on the laboratory, with no real adverse effect on clinical decision making.
 
Aldasouqi SA, Grunberger G. Is It Time to Eliminate the Need for Overnight Fasting for Lipid Tests in Patients With Diabetes?. JAMA Intern Med. 2013;173(10):936-937. JAMA Network | JAMA Internal Medicine | Is It Time to Eliminate the Need for Overnight Fasting for Lipid Tests in Patients With Diabetes?

We read with interest the recent study by Sidhu and Naugler. Corroborating the findings of several recent studies, this large cross-sectional study showed little association between fasting times and lipid subclass levels. The authors suggested that fasting for routine lipid levels is largely unnecessary. While this study underscores the futility and inconvenience of the “traditional requirement” for fasting for the purpose of lipid testing, we would like to take this opportunity to draw the attention of the medical community to a related safety issue within a vulnerable sector of the population, people with diabetes.

Therefore, we call on clinicians to refrain from routinely asking patients with diabetes to fast for lipid testing and limit fasting to the few patients whose clinical needs indeed require overnight fast.
 
Thx DOC! I'm reporting what many labs request, obviously they are wrong as was my suggestion :)
 
Hey Dutch my comments were not directed at you the MESSENGER but to some of the posts generated thereafter.
 
Let's assume you run (or want to run) a cycle containing orals such as winny or var. Let's say you're concerned about the adverse effects on your lipids.

You can't use a statin drug because you need a script. Why not experiment with natural alternatives that will lower LDL and TC?

For example
Cholesterol Control: Bergamot, Berberine, and Amla May Help | Nutritional Outlook

http://blog.case.edu/yxr10/2005/1/19/nm1135.pdf
Effects of a nutraceutical combina... [Nutr Metab Cardiovasc Dis. 2010] - PubMed - NCBI

To raise HDL you might consider Slo-Niacin
The SLIM Study: Slo-Niacin® and Atorvastatin Treatment of Lipoproteins and Inflammatory Markers in Combined Hyperlipidemia

Your thoughts
 
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You've got to be joking! If someone can acquire a scheduled III substance on the web with limited difficulty Iv'e absolutely no reason to believe obtaining a non-scheduled "Statin drug" would pose ANY difficulty.

This is particularly true regarding this class of medications (statins) since excluding relatively rare side effects these drugs have passed the test of time and as a consequence some Pharm companies have pushed HARD for OTC FDA approval!

JIM
 
Let's assume you run (or want to run) a cycle containing orals such as winny or var. Let's say you're concerned about the adverse effects on your lipids.

You can't use a statin drug because you need a script. Why not experiment with natural alternatives that will lower LDL and TC?

For example
Cholesterol Control: Bergamot, Berberine, and Amla May Help | Nutritional Outlook

http://blog.case.edu/yxr10/2005/1/19/nm1135.pdf
Effects of a nutraceutical combina... [Nutr Metab Cardiovasc Dis. 2010] - PubMed - NCBI

To raise HDL you might consider Slo-Niacin
The SLIM Study: Slo-Niacin® and Atorvastatin Treatment of Lipoproteins and Inflammatory Markers in Combined Hyperlipidemia

Your thoughts



My feeling on this echos that of Dr Jim. The increased risk of CVD from high LDL/low HDL cholesterol is a long term risk since CVD takes many years to develop, often decades. The lipid alterations from the use of oral AAS are temporary, and usually normalize within a few weeks post cycle. Therefore, so long as one keeps oral cycles short (4-6 weeks) and infrequent, the lipid alterations are not worth worrying about, let alone trying to mitigate by using even more drugs. As Doc mentioned, the real risk is the LFT's.

Regards
CBS
 
Let's assume you run (or want to run) a cycle containing orals such as winny or var. Let's say you're concerned about the adverse effects on your lipids.

You can't use a statin drug because you need a script. Why not experiment with natural alternatives that will lower LDL and TC?

For example
Cholesterol Control: Bergamot, Berberine, and Amla May Help | Nutritional Outlook

http://blog.case.edu/yxr10/2005/1/19/nm1135.pdf
Effects of a nutraceutical combina... [Nutr Metab Cardiovasc Dis. 2010] - PubMed - NCBI

To raise HDL you might consider Slo-Niacin
The SLIM Study: Slo-Niacin® and Atorvastatin Treatment of Lipoproteins and Inflammatory Markers in Combined Hyperlipidemia

Your thoughts

That would certainly be interesting. Personally I'm done with oral kick starts. I'm perfectly fine waiting a bit longer for visible results (probably age related LOL) and if I persue fast responses, I choose the esthers accordingly.
 
follow-up:

HDL 47 (35-54)
LDL 142 (80-150)

HDL up again, LDL still not down, but probably Christmas has something to do with these numbers too LOL.
 

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