what 1 week of winstrol can do

[This came up in a recent message so I thought this would help clarify some of the reasoning for fasting.]

Historically, triglycerides have been measured in the fasting state for 2 reasons.

First, because of the marked increase in triglycerides after fat ingestion, the variability in triglyceride measurements is much smaller in the fasting state.

Second, before the availability of direct assays for LDL cholesterol (LDL-C),1 estimation of LDL-C was performed in clinical practice almost exclusively by use of the Friedewald equation, which requires that both the HDL-C concentration and the fasting triglyceride concentration divided by 5 be subtracted from the total cholesterol concentration.

The recommendations to measure triglycerides in the fasting state did not, however, derive from a consistent set of prospective cohort studies showing that fasting concentrations were superior to nonfasting concentrations for the detection of cardiovascular risk. Instead, following screening



Is it possible, then, that recommendations to measure triglycerides in the fasting state have systematically underestimated the impact of hypertriglyceridemia in clinical practice?



The inclusion criteria for all of these trials targeting triglycerides relied on fasting concentrations; however, if concentrations measured in the fasting state are not the best indicator of atherogenicity associated with hypertriglyceridemia, then it is possible that these trials may not have defined the best possible population for study.

Although the correlation between fasting and nonfasting triglyceride concentrations is high, the fact that postprandial triglycerides may be a more potent predictor of risk suggests that the concordance for individuals is only modest and that the variability in postprandial concentrations captures relevant information about an individual’s metabolism.

Ridker PM. Fasting versus Nonfasting Triglycerides and the Prediction of Cardiovascular Risk: Do We Need to Revisit the Oral Triglyceride Tolerance Test? Clinical Chemistry. 2008;54(1):11-3. http://www.clinchem.org/content/54/1/11.full
 
[This came up in a recent message so I thought this would help clarify some of the reasoning for fasting.]

Historically, triglycerides have been measured in the fasting state for 2 reasons.

First, because of the marked increase in triglycerides after fat ingestion, the variability in triglyceride measurements is much smaller in the fasting state.

Second, before the availability of direct assays for LDL cholesterol (LDL-C),1 estimation of LDL-C was performed in clinical practice almost exclusively by use of the Friedewald equation, which requires that both the HDL-C concentration and the fasting triglyceride concentration divided by 5 be subtracted from the total cholesterol concentration.

The recommendations to measure triglycerides in the fasting state did not, however, derive from a consistent set of prospective cohort studies showing that fasting concentrations were superior to nonfasting concentrations for the detection of cardiovascular risk. Instead, following screening



Is it possible, then, that recommendations to measure triglycerides in the fasting state have systematically underestimated the impact of hypertriglyceridemia in clinical practice?



The inclusion criteria for all of these trials targeting triglycerides relied on fasting concentrations; however, if concentrations measured in the fasting state are not the best indicator of atherogenicity associated with hypertriglyceridemia, then it is possible that these trials may not have defined the best possible population for study.

Although the correlation between fasting and nonfasting triglyceride concentrations is high, the fact that postprandial triglycerides may be a more potent predictor of risk suggests that the concordance for individuals is only modest and that the variability in postprandial concentrations captures relevant information about an individual’s metabolism.

Ridker PM. Fasting versus Nonfasting Triglycerides and the Prediction of Cardiovascular Risk: Do We Need to Revisit the Oral Triglyceride Tolerance Test? Clinical Chemistry. 2008;54(1):11-3. http://www.clinchem.org/content/54/1/11.full

No doubt triglyceride levels play a MUCH greater role in the genesis of ASCVD than was once believed.

So much so that not long ago TTL were discounted by many as being an irrelevant "risk factor" for ASCVD with the result being

That's not to suggest total or fractionated cholesterol quantification is no longer germane but to acknowledge the greatest risk occurs in patients with combined elevations of both of these lipids.
 
I posed pic of my abs on MeetMe and got
6 messages
2 profile views
1 friend request
and a date to this girls house tonight...

My aunt better get home fast,
cause I am still horny as fuck :drooling:
Are you from Tennessee also?
..cuz I think that thing with your aunt is illegal in the other 49 states....jus sayin :rolleyes:
 

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