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LDL and Response to Resistance Training: Is high LDL really that bad?
by Physics_phitness
So for those of us who are AAS users, one of the big things we look at when we get bloodwork done is lipids. HDL is generally crashed and LDL is way above normal range. Low HDL bounces back pretty quickly, and we don't seem to concern ourselves too much with that. However, LDL is a completely different story. Low Density Lipoprotein is the so called "bad" cholesteral, which is known for building up in arteries and cause atherosclerosis. For this reason, many people tend to shy away from fatty foods for fear of increasing cholesterol levels. What people do not appear to know about is the important role that LDL plays in the body in terms of protein synthesis. A study done with the Mycoplasma capricolum bacterium found a correlation between cholesterol levels and protein synthesis. “The regulatory role of cholesterol on phospholipid, RNA and protein synthesis was investigated in Mycoplasma capricolum. The addition of 2 micrograms/ml of cholesterol to cells growing slowly on lanosterol (compound from which steroids are derived) (10 micrograms/ml) caused an early stimulation of unsaturated phospholipid synthesis followed by a later stimulation of RNA and protein synthesis.
Epicoprostanol, a cholesterol antagonist, sequentially inhibited these three processes. Phospholipid served as the acyl donor for the acylation of membrane proteins. Membrane-bound cholesterol correlated with a decrease in the amount of [3H]amino acids and an increase in the amount of [3H]oleate found in two membrane proteins (MW 78 kDa and 26 kDa). Taken together, the results suggest that a small amount of membrane-associated cholesterol serves as a signal for membrane biogenesis and, in turn, macromolecular synthesis and cell growth.” (https://www.ncbi.nlm.nih.gov/pubmed/6210267)
While this is correlational and not necessarily causational, it does seem to appear that higher LDL levels will aid in muscle gain. But this was done on bacteria. What about humans? In 2011 Texas A&M University conducted a study that found that subjects who gained the most muscle mass also had the highest LDL levels.(http://www.futurity.org/ldl-doesn%E2%80%99t-deserve-black-hat-moniker/)
The study is linked below and is a very long read with a lot of numbers.
http://biomedgerontology.oxfordjournals.org/content/62/10/1164.abstract?sid=30e75210-518f-4eac-af26-3bdab424b797)(
To sum it up, here is an excerpt from the study:
”Total cholesterol and triglyceride levels did not change by study week 12 in either group. However, at study week 6, low-density lipoprotein (LDL) cholesterol increased (31 ± 41 mg/dL; p =.02) and by study week 12 was 23 ± 37 mg/dL greater (p =.06) than were baseline values in the oxandrolone group but returned to baseline values 12 weeks after study therapy was discontinued. For high-density lipoprotein (HDL) cholesterol, levels decreased (20 ± 7 mg/dL; p <.001) at study week 6 and by study week 12, remained decreased (19 ± 8 mg/dL, p <.001) in the oxandrolone group. The effects of oxandrolone on HDL cholesterol were not sustained, and 3 months following treatment there was a rebound to levels greater than baseline.”
So what does this all mean? Based on what I have read and studied over the last couple months, here is my hypothesis: High LDL from AAS use is not a bad side effect of the hormones. It is a logical and necessary reaction to the introduction of supraphysiological doses of androgens. There exists a correlation between LDL and protein synthesis, and I believe it is a two way street in regard to LDL levels and protein synthesis. Elevated LDL levels allow more protein synthesis to occur, and an increased necessity for protein synthesis will elevate LDL levels to help facilitate this process. It is my belief that the latter is what we see occurring in AAS users.
AAS allow for rapid muscle growth and recovery. Since we are forcing our bodies to synthesize protein at a much accelerated rate, our bodies respond by increasing LDL levels to fulfill this requirement (This would also explain why stronger androgens like Tren affect lipids more). Does this mean we should dismiss high LDL levels when we get bloodwork done? No, I do not think this is wise. The body craves homeostasis, and low HDL and high LDL is not typical homeostasis. But perhaps it can become a new homeostasis for the body; something that the body can grow accustomed to without causing long term health issues. This is something that would need to be studied further, and at the current time there just is not enough research to make even an educated guess.
There is also the little caveat about LDL dangers being more related to diet and genetics (which would mean elevated LDL levels pose little threat if one has a good, healthy diet and decent genetics), but that can wait for a different post. But overall my conclusion is that elevated LDL levels are a normal and necessary response to our increased capacity to pack on muscle, and are less of a health concern than previously thought.
by Physics_phitness
So for those of us who are AAS users, one of the big things we look at when we get bloodwork done is lipids. HDL is generally crashed and LDL is way above normal range. Low HDL bounces back pretty quickly, and we don't seem to concern ourselves too much with that. However, LDL is a completely different story. Low Density Lipoprotein is the so called "bad" cholesteral, which is known for building up in arteries and cause atherosclerosis. For this reason, many people tend to shy away from fatty foods for fear of increasing cholesterol levels. What people do not appear to know about is the important role that LDL plays in the body in terms of protein synthesis. A study done with the Mycoplasma capricolum bacterium found a correlation between cholesterol levels and protein synthesis. “The regulatory role of cholesterol on phospholipid, RNA and protein synthesis was investigated in Mycoplasma capricolum. The addition of 2 micrograms/ml of cholesterol to cells growing slowly on lanosterol (compound from which steroids are derived) (10 micrograms/ml) caused an early stimulation of unsaturated phospholipid synthesis followed by a later stimulation of RNA and protein synthesis.
Epicoprostanol, a cholesterol antagonist, sequentially inhibited these three processes. Phospholipid served as the acyl donor for the acylation of membrane proteins. Membrane-bound cholesterol correlated with a decrease in the amount of [3H]amino acids and an increase in the amount of [3H]oleate found in two membrane proteins (MW 78 kDa and 26 kDa). Taken together, the results suggest that a small amount of membrane-associated cholesterol serves as a signal for membrane biogenesis and, in turn, macromolecular synthesis and cell growth.” (https://www.ncbi.nlm.nih.gov/pubmed/6210267)
While this is correlational and not necessarily causational, it does seem to appear that higher LDL levels will aid in muscle gain. But this was done on bacteria. What about humans? In 2011 Texas A&M University conducted a study that found that subjects who gained the most muscle mass also had the highest LDL levels.(http://www.futurity.org/ldl-doesn%E2%80%99t-deserve-black-hat-moniker/)
The study is linked below and is a very long read with a lot of numbers.
http://biomedgerontology.oxfordjournals.org/content/62/10/1164.abstract?sid=30e75210-518f-4eac-af26-3bdab424b797)(
To sum it up, here is an excerpt from the study:
”Total cholesterol and triglyceride levels did not change by study week 12 in either group. However, at study week 6, low-density lipoprotein (LDL) cholesterol increased (31 ± 41 mg/dL; p =.02) and by study week 12 was 23 ± 37 mg/dL greater (p =.06) than were baseline values in the oxandrolone group but returned to baseline values 12 weeks after study therapy was discontinued. For high-density lipoprotein (HDL) cholesterol, levels decreased (20 ± 7 mg/dL; p <.001) at study week 6 and by study week 12, remained decreased (19 ± 8 mg/dL, p <.001) in the oxandrolone group. The effects of oxandrolone on HDL cholesterol were not sustained, and 3 months following treatment there was a rebound to levels greater than baseline.”
So what does this all mean? Based on what I have read and studied over the last couple months, here is my hypothesis: High LDL from AAS use is not a bad side effect of the hormones. It is a logical and necessary reaction to the introduction of supraphysiological doses of androgens. There exists a correlation between LDL and protein synthesis, and I believe it is a two way street in regard to LDL levels and protein synthesis. Elevated LDL levels allow more protein synthesis to occur, and an increased necessity for protein synthesis will elevate LDL levels to help facilitate this process. It is my belief that the latter is what we see occurring in AAS users.
AAS allow for rapid muscle growth and recovery. Since we are forcing our bodies to synthesize protein at a much accelerated rate, our bodies respond by increasing LDL levels to fulfill this requirement (This would also explain why stronger androgens like Tren affect lipids more). Does this mean we should dismiss high LDL levels when we get bloodwork done? No, I do not think this is wise. The body craves homeostasis, and low HDL and high LDL is not typical homeostasis. But perhaps it can become a new homeostasis for the body; something that the body can grow accustomed to without causing long term health issues. This is something that would need to be studied further, and at the current time there just is not enough research to make even an educated guess.
There is also the little caveat about LDL dangers being more related to diet and genetics (which would mean elevated LDL levels pose little threat if one has a good, healthy diet and decent genetics), but that can wait for a different post. But overall my conclusion is that elevated LDL levels are a normal and necessary response to our increased capacity to pack on muscle, and are less of a health concern than previously thought.
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