4, not 5: due to lame sense of humour and lack of references. Thankfully I have my own references from my own research so what he says make sense.
Just after I’ve finished reading all of the trials on statins, PCSK9 inhibitors, their criticisms, their (pharma funded) praises, Lp(a) research, and over a thousand pubmed articles on cholesterol and heart disease, I have now realised that I know very little about heart disease. And if I know nothing about cholesterol and heart disease after reading this much, cardiologists don’t even know what cholesterol is. (they probably actually have no clue!)
But Kendrick? He’s one smart cookie, and although his sense of humour is questionable and a little lame, the man really knows how to read scientific research. He has the most thorough research and explaination of heart disease I have ever read. I mean, the man is talking about Lp(a) back in 2008 when cardiologists probably didn’t have a clue!
Now they do, and we have Big Pharma to the rescue, with Lp(a) destroying gene silencing drugs coming our way. I am very excited and waiting for Merck to publish their initial trials, with a side of pop corn, a drink and my thousand research papers and articles at the side. That is, IF they allow independent researchers such as myself to actually get hold of the data. They’re not very good with transparency. I’m still waiting for the CTT research team from Oxford to release their research on statins. They refuse to release their data for independent analysis. Why, oh why? Hmmm.
Some interesting facts I have learnt from my research:
- every cell in the body is made of cholesterol and phospholipids that are in turn made of a mix of saturated and unsaturated fatty acids.
- LDL HDL VLDL etc are not cholesterols they are proteins that carry cholesterol in the form of esters
- it is impossible for cholesterol esters from LDL to turn into cholesterol crystals in the plaque because there will have to be an enzymatic process to allow this de-esterification to occur. Therefore THE LDL-C HYPOTHESIS IS BIOLOGICALLY IMPLAUSIBLE.
- it is also biologically impossible for LDL particles to “slip underneath” the endothelial cell lining. The endothelial cells are not that leaky, even when dysfunctional. If so, you’d be leaking and bleeding to death (like in dengue or Ebola - haemorrhagic fevers where this does happen)
- eating carbohydrates makes your liver produce saturated fatty acids, turns them into triglycerides and then puts them out as VLDL, which then turns into LDL. The triglycerides then exchange with HDL, thereby causing “Dyslipidaemia” or low HDL-c.
- eating carbohydrates stimulates liver cholesterol production because it stimulates the growth hormone insulin, (which means more cell growth, and what do cells need? Cholesterol)which uptakes more cholesterol from LDL, therefore reducing LDL-C.
- fasting, or eating a low carbohydrate diet suppresses cell growth and reduces liver cholesterol production, therefore liver will pick up less cholesterol from LDL, increasing LDL-C. If you are a lean person with good muscle mass, or you have an apoE4 gene, you are likely to be excellent at using fat as energy, so your LDL-c will be high. ANY TIME THAT YOU GO FROM SUGAR BURNING TO FAT BURNING MODE, LDL-C goes up. And there is a diabetic drug (SGLT2i) which is the best drug studied so far, which reduces plaque size in the heart, heart attacks, dementia, etc which INCREASES your LDL-c.
- eating saturated animal fats suppresses liver fat production & insulin production, thereby reducing risk of metabolic disease; it also reduces Lp(a).
- eating cholesterol from egg yolk and animal fat means that our liver REDUCES cholesterol production in the liver because it needs to produce less cholesterol. Your cardiologist probably has no clue.
- the reason vegetable oils reduce LDL-C is by damaging normal cholesterol esters into cholesterol oxides. This isn’t tested on a blood test. Also, phytosterols are plant sterols that confuses our liver. Our body excretes these sterols because (well, we are not plants therefore our cells are made of CHOLE not PHYTO sterol). When we eat too much of this, our liver thinks it’s not getting enough cholesterol from the diet therefore absorbs more cholesterol from LDL.
- when we inhibit cholesterol production in the liver cells with a statin, our body desperately cries in the need of cholesterol, therefore absorbs more cholesterol from LDL. This reduces LDL-C. The benefit of statins lies in their anti-clotting and anti-inflammatory properties. Both of which are conferred by Aspirin - in my opinion a much safer drug without side effects of diabetes, dementia, cancer and heart failure (yes these are actual side effects of statins - especially lipophilic)
- LDL, a protein supplies cholesterol to a cell when its membrane is damaged, and is rich in antioxidants such as vitamin E, carotenoids and coq10. There is evidence that it localizes to damaged cell membranes. But if there is too much inflammation, LDL can get oxidized turning into oxLDL, which is picked up by a macrophages and turns into a “foam” cell that can form plaques. Those with high LDL-C live longer, are smarter, and have much lower risk of dying from cancer and infection. And there is no correlation between high LDL-C levels and heart attacks except in men under age of 50. Everything else is a so-called cholesterol “paradox”
- Paradoxes of note: French paradox (high saturated fat, low CVD), Israeli Paradox (high PUFA, high CVD), Sri Lankan Paradox(low fat consumption, low cholesterol, high CVD), European paradox (41 countries - inverse relationship between saturated fat and cardiovascular deaths), paradox in South Asians (low cholesterol, low BMI, mostly vegetarian diets, really high rates of CVD), Paradox in ALL Women (high cholesterol, low CVD), cholesterol paradox in heart failure and MI (those with higher cholesterol die less), stroke paradox(low cholesterol = higher risk of bleeding), paradox in centenarians (high cholesterol = live longer), paradox that cholesterol is much lower now than before but CVD is rising (DuBroff has a few papers on this)
🫠 there’s so many paradoxes I have found that I’ve abandoned the hypothesis itself🫠🫠🫠
- Lp(a) is a protein that helps stabilize blood clots, and neutralize oxidized LDL. The reason it’s increased in those with heart disease is because those with cardiovascular disease have high levels of inflammation and oxidative stress.