Interesting conversation guys and a good read. I think the process can be more easily summarised if we consider inflammation and damage as the triggers for atherosclerotic events, while cholesterol is an opportunistic infiltrator of arteries.
I'm not aware of any research that treats lipids or cholesterol as molecules that are actively 'recruited' in an attempt to repair endovascular damage. I believe the working hypothesis more sees cholesterol as an infiltrate, which is consumed by local macrophages in an attempt to 'clean' the site. Obviously, these macrophages cannot deal with such large levels of cholesterol and become foam cells which form the basis of vascular thickening.
Higher levels of cholesterol simply means a larger amount of cholesterol for the macrophages to consume.
It's well understood that inflammatory states are big risk factors for atherosclerotic and cardiovascular disease, which is why rheumatoid arthritis leads to heart and lung disease for example. But I don't think cholesterol can be ruled out so easily. Medical consensus doesn't ever come off the back of one study, or one person's work, it doesn't even stem from what is or isn't FDA approved seeing as medical consensus is global.
While our understanding of fat and cholesterol is still evolving, we do know that high blood cholesterol especially if associated with a low HDL is a strong risk factor for atherosclerotic-related diseases. It's more complex than more = worse, but in a broad sense, it does equal less = safer. The discord here is that the body can regulate its blood cholesterol, so high fat or cholesterol diets DO NOT have a relationship with high blood cholesterol, i quote "dietary cholesterol has a small effect on the plasma cholesterol levels with an increase in the cholesterol content of the LDL particle and an increase in HDL cholesterol, with little effect on the LDL:HDL ratio, a significant indicator of heart disease risk". Also, remember (western) high-fat diets don't only lead to hypercholesterinaemia but also obesity and other gastrointestinal conditions like reflux and biliary cholic etc.
With regards to the video you shared... well it falls into all of the pseudoscience pitfalls... ie. 1. "it's called a hypothesis because it's never been proven"; 2. using cute but physiologically irrelevant metaphors to try and explain-away the risks of fat consumption; 3. drawing loops through a graph that has a clear trend. So I'm not giving it too much credibility. I'd also like to say that this wasn't the work of one man in the hand of pharma companies, it was a broader scientific consensus very consistent with the data we had at the time.
@tfcoates Great analysis ! You mentionned that we need first a damage in the arterial wall, it can be caused by a lot of conditions and risk factors, then comes cholesterol as an opportunistic infiltrator.Well that's my point but still can high cholesterol levels cause arterial damage in the first place ? I checked your profile (By the way it's a great one )and i can see that you are a med student, so have you ever heard about Familial hypercholesterolemia (FH) ? It's a condition marked by high LDL and choesterol levels from birth, generally these individuals die from heart attacks before the age of 20 ! And that's only one dyslipidemia, there are countless diseases out there
Hey, thanks for that! Yes I've heard of the condition, though I'll admit I've never seen it in practice! I didn't know there were other forms of dyslipidaemia, I tend to use the term interchangeably with hypercholesterinaemia... thanks for the info, always love to learn new things!
Thanks ! Nice chatting with you ^^
@fancybrothers
@chloroform
Interesting conversation guys and a good read. I think the process can be more easily summarised if we consider inflammation and damage as the triggers for atherosclerotic events, while cholesterol is an opportunistic infiltrator of arteries.
I'm not aware of any research that treats lipids or cholesterol as molecules that are actively 'recruited' in an attempt to repair endovascular damage. I believe the working hypothesis more sees cholesterol as an infiltrate, which is consumed by local macrophages in an attempt to 'clean' the site. Obviously, these macrophages cannot deal with such large levels of cholesterol and become foam cells which form the basis of vascular thickening.
Higher levels of cholesterol simply means a larger amount of cholesterol for the macrophages to consume.
It's well understood that inflammatory states are big risk factors for atherosclerotic and cardiovascular disease, which is why rheumatoid arthritis leads to heart and lung disease for example. But I don't think cholesterol can be ruled out so easily. Medical consensus doesn't ever come off the back of one study, or one person's work, it doesn't even stem from what is or isn't FDA approved seeing as medical consensus is global.
While our understanding of fat and cholesterol is still evolving, we do know that high blood cholesterol especially if associated with a low HDL is a strong risk factor for atherosclerotic-related diseases. It's more complex than more = worse, but in a broad sense, it does equal less = safer. The discord here is that the body can regulate its blood cholesterol, so high fat or cholesterol diets DO NOT have a relationship with high blood cholesterol, i quote "dietary cholesterol has a small effect on the plasma cholesterol levels with an increase in the cholesterol content of the LDL particle and an increase in HDL cholesterol, with little effect on the LDL:HDL ratio, a significant indicator of heart disease risk". Also, remember (western) high-fat diets don't only lead to hypercholesterinaemia but also obesity and other gastrointestinal conditions like reflux and biliary cholic etc.
With regards to the video you shared... well it falls into all of the pseudoscience pitfalls... ie. 1. "it's called a hypothesis because it's never been proven"; 2. using cute but physiologically irrelevant metaphors to try and explain-away the risks of fat consumption; 3. drawing loops through a graph that has a clear trend. So I'm not giving it too much credibility. I'd also like to say that this wasn't the work of one man in the hand of pharma companies, it was a broader scientific consensus very consistent with the data we had at the time.
@tfcoates Great analysis ! You mentionned that we need first a damage in the arterial wall, it can be caused by a lot of conditions and risk factors, then comes cholesterol as an opportunistic infiltrator.Well that's my point but still can high cholesterol levels cause arterial damage in the first place ? I checked your profile (By the way it's a great one )and i can see that you are a med student, so have you ever heard about Familial hypercholesterolemia (FH) ? It's a condition marked by high LDL and choesterol levels from birth, generally these individuals die from heart attacks before the age of 20 ! And that's only one dyslipidemia, there are countless diseases out there
Hey, thanks for that! Yes I've heard of the condition, though I'll admit I've never seen it in practice! I didn't know there were other forms of dyslipidaemia, I tend to use the term interchangeably with hypercholesterinaemia... thanks for the info, always love to learn new things!