CHOLESTEROL is HEALTHY - Here's Why (Sience Based) 

Thank you very much for your comment. I'm glad that i could show you a different view on cholesterol and I respect anyone that is able to change its mindset. I had similar problems in the beginning of my research, not knowing who i could trust and whom i couldn't. However, understanding the basics of nutrition and looking in the past - what our ancestors were eating (so our natural diet) have given me this whole picture with which i can understand some of these studies a lot better. My goal is always to have the best life experience as possible and health is something you can feel

@@Lancelot-Health Thanks. I totally agree. “Ancestor Nutrition” is a very complex issue in itself, being so dependent on geography / ancestral food availability & subsequent regional human genetic adaptation. This should surely be part of the bigger picture, similar to advocating consumption of traditional, regional “in-season” plant (& animal) produce.

Thank you for your comment and critics, I did in fact overlook that. Still, the basic mechanism of cholesterol being a vital part of every cell and thus for the whole body as well as its anti-inflammatory properties cannot be doubted and a guideline is generally not anything i care too much about, just found it interesting when i saw it. Good health and have a nice day.

@@Lancelot-Health while it is true that cholesterol is a vital part of every cell membranes - it doesn't follow from this that having elevated LDL-C or ApoB is going to be beneficial or healthy. Nor does it follow that dietary cholesterol is beneficial or even a requirement for a healthy diet (considering the fact that we produce cholesterol endogenously). The anti-inflammatory effect of cholesterol is primarily attributed to HDL (not LDL-C). And HDL-C is considered non-causal in the development of CVD. So to imply that elevated LDL-C is not a risk factor for CVD because 'cholesterol is anti-inflammatory' is flawed on this basis. HDL-C's anti-inflammatory effects should not be used to dismiss the well-established evidence linking elevated LDL-C levels to increased cardiovascular risk. I agree we shouldn’t rely on dietary guidlines alone to form our views on nutrition, but the evidence on ApoB and it’s relation to CVD risk is extremely clear and one of the most well understood relationships within nutrition science and lipidology.

@@ItsJordaninnit My dude, HDL and LDL are proteins that carry cholesterol, maybe you should rewatch the video. They do not have any properties at all, except for carrying cholesterol. I did also say that high LDL is due to inflammation in the cells, thus you should focus on the cells. Whenever LDL is high it should not be lowered by statin drugs, because that is going to make the inflammation worse. The cholesterol is there to fight off the inflammation. I did never say that high LDL is healthy, but there might be genetics involved and some people might have higher ldl and have no inflammation in the cells. Understanding basic mechanisms of nutrition and certain processes in the body is superior than relying on studies, because otherwise there is no way one can understand studies.

@@Lancelot-Health *HDL and LDL are proteins that carry cholesterol… They do not have any properties at all, except for carrying cholesterol* HDL/LDL are lipoproteins (not proteins). They are composed of proteins and lipids. And while their main function is transporting cholesterol, they also have other functions within the body. *high LDL is due to inflammation in the cells, thus you should focus on the cells… Whenever LDL is high it should not be lowered by statin drugs, because that is going to make the inflammation worse* So you believe elevations in LDL particle count are a direct consequence of inflammation within the cells and therefore the best response to high LDL is to target cell inflammation, rather than LDL lowering? Okay - if this were true: 1. Why does LDL lowering reduce CVD events regardless of the pathway through which LDL is lowered? 2. Why does the reduction in CVD events track proportionally with the degree to which LDL is lowered? (Again - regardless of the mechanism of lowering) I should also point out that Statins themselves have an anti-inflammatory effect which contributes to the reduction in CVD risk (in addition to LDLc lowering). So it’s odd that you’d be ‘anti-statin’ - given your proposed hypothesis. *The cholesterol is there to fight off the inflammation* If this were true then those with genetically elevated cholesterol should be at a lower risk of CVD because they’re more equipped to fight off inflammation… right? Yet mendelion randomisation studies show the opposite. Those with genetically elevated cholesterol are at an increased risk of CVD and those with genetically low levels are at a reduced risk. *I did never say that high LDL is healthy, but there might be genetics involved and some people might have higher ldl and have no inflammation in the cells* While I agree inflammation is certainly a factor in the development of ASCVD. We have studies which control for inflammatory markers and ApoB/LDL-P/LDL-C/Non-HDL-C. And these studies find that total atherogenic particle count has an effect of CVD risk (independently of inflammation). *Understanding basic mechanisms of nutrition and certain processes in the body is superior than relying on studies, because otherwise there is no way one can understand studies* Mechanistic data is interesting, however it’s generally hypothesis generating in nature and shouldn’t be relied upon to form causal inferences - especially if the results run contrary to the human health outcome data and the preponderance of findings from RCTs on the subject. Basically - there’s a reason why mechanistic data resides at the bottom of the hierarchy of scientific evidence.

@@ItsJordaninnit 1. Why does LDL lowering reduce CVD events regardless of the pathway through which LDL is lowered? Because LDL can oxidize, especially with high omega 6 fat intake. - not mentioned in the vid. 2. Why does the reduction in CVD events track proportionally with the degree to which LDL is lowered? (Again - regardless of the mechanism of lowering) Again same answer as above. I am anti-statin, because I am against something that is unnatural, thus has side effects. Statins inhibit Acytyl-CoA, therefore inhibit it being converted to Coenzyme Q10 and Cholesterol. 2 one of the most important things in our body. Cholesterol is for example important for bile production, which is needed to absorb all fat-soluble vitamins and minerals. Another Example: The Masaai were known to have a diet (like all indigenous groups) high in animal products, therefore also cholesterol. Still, they have low ldl, so high ldl is not something that has to do with high cholesterol intake. LDL is only raised in the blood, if the intake is high and there is inflammation in the cells. This whole genetic thing is questionable anyways. I have just read things about it, but i am not sure whether it is actually true, again the focus should be to lower inflammation and cell damage from free radicals/inflammation, so LDL decreases. So we can have the benefits of Cholesterol > just to name a few again: bile production, hormone production and absorption of fat soluble vitamins and minerals. A deficiency in just one of these things lowers the life quality and even expectancy of every person.