#22 - Tom Dayspring Part III of V: reverse cholesterol transport, CETP inhibitors, & apolipoproteins

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Peter Attia MD

Peter Attia MD

Күн бұрын

Пікірлер: 7
@umeshchhikara
@umeshchhikara 4 жыл бұрын
Great podcast Peter....thank you. Its highly informative. Although I don't intend to treat any patients being a sports scientist; it is still very helpful. Thank you. Wow....30 to 60% cholesterol in LDL comes from HDL. This changes my perception of looking at lipid panel 360 degrees. It has only started to get exciting for me after listening to this talk. So this is not where I finish my study but instead I am beginning :) Here is how I have understood so far: a) Excess cholesterol serves no purpose in the body. Excess cholesterol could turn out to be bad cholesterol (may be in sometime if not immediately) whether it is in TAG or LDL's or total, regardless of the diet you are eating. This is because our cells make 80% of the cholesterol needed by our body and rest is made in the liver. Liver then uses cholesterol for bile salts etc. which gets reabsorbed again to the tune of 90%. Fantastic. What do we need extra cholesterol for? b) The cholesterol level in our body should not rise in our body beyond a certain level as it solves no purpose. However, it is expected to rise (a bit more than normal levels) if we are on high fat diet because we are literally chewing more cholesterol. But it can't go beyond a point even then because if we are metabolising fat, then our body should be equally capable of excreting excess cholesterol. It's the function of the same machinery. Only when we can manage certain levels of cholesterol in our body can we claim to have a good fat metabolism? c) Beside liver & intestines, cholesterol can be transported out of cells by ABC transporters, Albumin, red blood cells or HDL particles. This proves that our body has several mechanisms to handle excess cholesterol and hence it leaves no explanation to carry excess cholesterol in plasma. And here is my hypothesis which may differ a bit from yours after looking at 10 reports across different age groups: a) TAG numbers are surely no indicators for anything unless the numbers come high consistently in multiple reports done over a period of time. In case of one of my clients, TAG's have come down to 120 from 340 mg/Dl. Whereas, in my case it raised to 140 from 90 and then came back to 70 mg/Dl staying on same diet. So there could be multiple factors driving the TAG numbers. b) You guys have completely rejected the lipid panel which is not fair to the industry per se. A lipid panel giving - total Cholesterol, TAG, HDL C, LDL C, VLDL etc. may not be sufficient to make an accurate assessment for a patient but they are pretty good indicators for general population. For example: if somebody is showing a continuous decline in TAG numbers, increase in HDL numbers and decrease in VLDL numbers; why would he need any other numbers to declare themselves fit in a healthy person? From my small study, it seems Dave Felman's triad works perfectly for a healthy body provided it is based on a few reports done over a period and not just one as he insists. But I agree with you that we need more information like Apo B and LDL particle count if the numbers are not consistent but still it doesn't reject Dave's hypothesis. c) KETO: it seems pretty clear that the ratio's - TAG to HDL or TAG to HDL or VLDL to LDL have no meaning especially where total cholesterol gives you a good ballpark figure on cholesterol carried in each particle. To what level ones TAG's and VLDL's come down, HDL C and LDL C goes up is highly individualistic and we can not set any marker for these numbers except for baseline. All these numbers are genetically influenced for sure as it came out in my studies where the average HDL (after improvement) hovers around 45 mg/Dl in a healthy body in my part of the world as compare to around 80 mg/Dl in LCHF community. Most of my clients have a total cholesterol around 220 mg/Dl. All this begs one big question: why keto for someone if it increases their cholesterol phenomenally? How about the right mix where you can keep our metabolism flexible keeping the numbers healthy? Cholesterol plays no role in energy. We do not have any mechanism or machinery as you stated. I ask again....what do we do with high cholesterol? Answer if you like people to understand this better..... thanks & regards, Umesh
@marcjacobson757
@marcjacobson757 Жыл бұрын
Tom Dayspring is always great. This was a real eye-opener, especially the complexity of HDL and the misunderstood roles of the different lipoproteins. This also sheds a lot of light on how severely the carnivore community misunderstands LDL and HDL. I still see doctors posting videos claiming it's only HDL and trigs that matter, when the reality is so much more complex than a simple number.
@8CIC8
@8CIC8 20 күн бұрын
Thanks
@SwoleTown
@SwoleTown Жыл бұрын
How are there only 3 comments and 5k views on this? Man, this is amazing info. People rather watch cat videos lol
@imtryinghere1
@imtryinghere1 Жыл бұрын
Do not disrespect Milo
@greendeane1
@greendeane1 3 жыл бұрын
My APO B is 140 but my LP(a) is is 03 nmol/L or 1.34 mg/dl, LDL-p 1097.
@robertusga
@robertusga 2 жыл бұрын
5mg Rosuvastatin + 10mg Ezetimibe here we come!
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