The newest drug to address all your problems…fuckitol.
Thanks MODOK and that is a great new drug. We do have them for everything
Modok is absolutely right about cholesterols function and regulation, but I would like to expand on the pathophysiology of atherosclerosis.
The reason cholesterol and LDL was thought to be a major cause of atherosclerosis makes sense if you understand what the scientists found. Essentially, they collected plaques at various stages of progression and analysed them. What they found was macrophages had infiltrated the arterial wall and ‘set up camp’. These guys were in a pro-inflammatory state and actually began to necrose in serious cases. Naturally, they wanted to find out why these macrophages done this.
What they found was that these macrophages and the associated fatty streaks had extremely high levels of cholesterol. So they decided to find out where it came from. This proved more challenging, but they managed to see apoB lipoproteins ‘stuck’ in the arterial wall. Through many complex experiments, they determined that apoB lipoproteins became stuck in the arterial wall and the macrophages came to clean up the mess - by eating the lipoproteins.
Normally this happens all the time without issue. However, if the associated macrophage is in an activated state (new science) or there is lots of cholesterol to be eaten (found at the time), then the macrophages would not re-enter the circulation for extended periods of time. There is a limit to the amount a macrophage can eat before it forms a foam cell and it pretty much there for good. This IS the beginning of atherosclerosis.
Later, a lot of epidemiological studies came out and poor or no correlations were shown to LDL cholesterol. The size principal was used to explain this. Small dense LDL was able to penetrate the arterial wall much easier, thus increasing the flux of cholesterol through the wall and increasing the possibility of LDL getting stuck. Sounds good in theory and there is some in vitro (cell or model work) evidence to suggest this. There is one thing that was ignored because of this principal and that is chylomicron cholesterol. After a fast most of the cholesterol in the blood is found in LDL and HDL lipoproteins. Chylomicrons are released from the intestines after meals and carry the dietary fats around the circulation. These particles are much larger than LDL, HDL and VLDL (precursor to LDL) and thought to not penetrate the arterial wall. These particles are also apoB lipoproteins, just a different variant. It turns out that most of the ‘stuck’ lipoproteins were chylomicrons and not LDL.
So you can see why the confusion occured and why fasting measurements of cholesterol would not correlate with atherosclerosis. Nonetheless, cholesterol can be a major factor in atherosclerosis, but is not necessarily required or the only factor.
[quote]OzyNut wrote:
Modok is absolutely right about cholesterols function and regulation, but I would like to expand on the pathophysiology of atherosclerosis.
The reason cholesterol and LDL was thought to be a major cause of atherosclerosis makes sense if you understand what the scientists found. Essentially, they collected plaques at various stages of progression and analysed them. What they found was macrophages had infiltrated the arterial wall and ‘set up camp’. These guys were in a pro-inflammatory state and actually began to necrose in serious cases. Naturally, they wanted to find out why these macrophages done this.
What they found was that these macrophages and the associated fatty streaks had extremely high levels of cholesterol. So they decided to find out where it came from. This proved more challenging, but they managed to see apoB lipoproteins ‘stuck’ in the arterial wall. Through many complex experiments, they determined that apoB lipoproteins became stuck in the arterial wall and the macrophages came to clean up the mess - by eating the lipoproteins.
Normally this happens all the time without issue. However, if the associated macrophage is in an activated state (new science) or there is lots of cholesterol to be eaten (found at the time), then the macrophages would not re-enter the circulation for extended periods of time. There is a limit to the amount a macrophage can eat before it forms a foam cell and it pretty much there for good. This IS the beginning of atherosclerosis.
Later, a lot of epidemiological studies came out and poor or no correlations were shown to LDL cholesterol. The size principal was used to explain this. Small dense LDL was able to penetrate the arterial wall much easier, thus increasing the flux of cholesterol through the wall and increasing the possibility of LDL getting stuck. Sounds good in theory and there is some in vitro (cell or model work) evidence to suggest this. There is one thing that was ignored because of this principal and that is chylomicron cholesterol. After a fast most of the cholesterol in the blood is found in LDL and HDL lipoproteins. Chylomicrons are released from the intestines after meals and carry the dietary fats around the circulation. These particles are much larger than LDL, HDL and VLDL (precursor to LDL) and thought to not penetrate the arterial wall. These particles are also apoB lipoproteins, just a different variant. It turns out that most of the ‘stuck’ lipoproteins were chylomicrons and not LDL.
So you can see why the confusion occured and why fasting measurements of cholesterol would not correlate with atherosclerosis. Nonetheless, cholesterol can be a major factor in atherosclerosis, but is not necessarily required or the only factor.[/quote]
Thank you for that (I don’t have the medical background to argue either way).
So in conclusion, how do YOU play it safe?
I get regular blood tests because I donate blood for research purposes. I have never really had any significant changes in values for any markers, which in some cases is more important than the marker itself. Our research institute also does lots of post-prandial (after eating) work, so I also get time course measurements done for blood glucose and various lipids. These are usually much more sensitive to disturbances than fasting blood tests.
My resulting lifestyle is probably shared with many people here, possibly with a few exceptions. I lift weights, enjoy regular cardio and compete in a sport I love. That more than enough covers my physical activity requirements. My with nutrition, I have developed a style which limits saturated fats and cholesterol. I have a moderate intake of fat overall. Most of my calories come from carbohydrates, with the percentage increasing during bulking phases. I regularly take fish oil, whey protein and green tea (thanks to my Japanese better half).
I don’t think there are any surprises or secrets there. I have my interpretation of nutrition literature, which seems to differ somewhat to Modok (the pharmacy god). But I completely understand his point of view, I have just ranked things differently.