noah_k
New Member
MANWHORE getting shredded! Nice man. How long have you been cutting, and what're you running -- if anything?
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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.
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
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.
That is a "lipid panel" should be collected in the AM after an "overnight fast".
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.
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.
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?
I will not touch it.
Nevermind me saying that. I would touch it...
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
The HDL decrease seen with AAS is resistant to niacin. http://thinksteroids.com/forum/steroid-forum/blood-tests-3-problems-134346471.html#post931196"]
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
