So after starting this thread I continued reading into the so called evils of cholesterol, and how resistance trainers might have different cholesterol levels compared to the revered 'safe' margins set by government regulatory bodies.
I already know liver values are affected by weightlifting (notably AST/ALT and Bilirubin - all three are markers of cell damage not necessarily liver cells.) Cholesterol is in fact manufactured by the liver too. It is transported around the body in your blood and performs a myriad of important functions, including a being a building block in the manufacture of testosterone.
In fact, every single cell in your body contains cholesterol and it's essential to maintain cell structure! It makes sense to me then, if we are in the business of breaking down and rebuilding cells through resistance training, that lifters would benefit from higher cholesterol.
Your body produces the majority of the cholesterol in your body, possibly higher than 80%. Wouldn't it make sense then, if there is a higher demand for cholesterol, that your body would produce more? It regulates all the other hormones and chemicals in your body so why would cholesterol be any different?
Below is an interesting article, one part mentions a study which suggests...
... that the restricting of cholesterol - while in the process of exercising - appears to affect building muscle mass in a negative manner. If it's true, as our findings suggest, that cholesterol may play a key role in muscle repair, we need to know exactly how that happens."
There are in fact no conclusive studies that can effectively link “high” cholesterol with heart disease. Much of this misinformation comes from flawed studies dating back to mid last century. Furthermore:
Nutritional guidelines used for diet and cholesterol are based on the dis-proved notion that cholesterol (solely) comes from fat...
I would encourage you to research the current cholesterol guidelines, how they were set, and by whom. The guidelines were based upon 5 studies, all of which were drug company sponsored. Then a panel of 9 physicians made their recommendations based upon those studies.
The National Institutes of Health publishes a financial disclosure revealing the reported conflicts of interest of those physicians. This is published on the net so each individual can make up their own mind if the data is acceptable in the presence of the financial relationships between those physicians and the drug companies.
It has been disproven that consumed cholesterol (eg. eggs) increases your cholesterol. As said, most of it is produced in your liver. Of the cholesterol in the blood, between 60 and 80 per cent is transported by LDL and is called ”bad” cholesterol. Only 15-20 percent is transported by HDL and is called ”good” cholesterol. A small part of the circulating cholesterol is transported by other lipoproteins.
Consuming saturated fat will
increase cholesterol but it increases both LDL and HDL, so the supposed 'approved ratio' remains the same. Again we are talking a small increase here compared with the cholesterol your body naturally produces.
During my reading I saw a lot of posts made by fit healthy athletic people with great diets, even vegetarians, that returned high levels of cholesterol. One interesting thing of note was all these athletes also had high levels of HDL cholesterol. This was supported in one of the studies I read:
Like total cholesterol, the impact of habitual aerobic exercise on LDL-C appears to be quite variable. However, the majority of studies comparing endurance athletes to sedentary controls or the general population reported that athletes have lower LDL-C levels, with leaner athletes frequently having the lowest values. Although it is not yet definitive, moderate and high intensity aerobic exercise training appears to be associated with elevated HDL-C values.
More info on athletes experiencing higher HDL: http://circ.ahajournals.o...naha/84/1/140.full.pdf
My HDL is quite low and I’m wondering if it is because I do virtually no cardiovascular excersie. Lifting may not be sufficient to raise HDL in the same manner. Inversely my LDL is higher than normal, and I'm wondering if this is because of the weight training and subsequent cell repair (SARM use aside- I returned high level prior to use.) Triglycerides are generally lower in trained individuals too, mine being very low. This is the chemical form of the fat that exists in your body. Triglycerides in our blood come from the fat present in our food, or are made in the body from other energy sources, like carbs.
As I posted above there is a school of thought that suggests a better indicator of cardiovascular health is the comparison rate between HDL and triglycerides. There is a growing theory too that cardiovascular disease is caused by inflammation of arteries rather than plaque buildup. Primary cause of this inflammation is suspected to be processed foods and diets rich in carbs.
In summary there is not enough research into cholesterol and how it effects the body. Much of it seems to be conjecture or just the same misinformation regurgitated over and over again, perpetrating the myth that cholesterol is an enemy of your body and it should be reduced to avoid having heart disease.
I suspect there is a lot more to the picture, especially where muscle building is concerned. Cholesterol could be a warning sign that something is wrong if it gets too high but if its just outside the 'normal' ranges I wouldn't be concerned. In fact, I am starting to suspect it is necessary for muscle building, and would be reflected in the changes in cholesterol when using muscle building compounds like SARMs or steroids.
Hope this helps someone looking into the same topic, although it is mostly for my own reference down the track lol.
Possibly one of the most well written and eye-opening arguments against cholesterol margins here: http://www.ravnskov.nu/2015/12/27/myth-1/
Some more interesting info: http://blog.paleohacks.co...te-guide-cholesterol/#
In the interest of full disclosure here is my most recent cholesterol levels converted to mg/dL: