What are your thoughts on berberine and/or citrus bergamot supplementation to help lower LDL? Also, what would be the equivalent benchmark of 100mg/dl of LDL-C, in ApoB g/L?
Total cholesterol and all-cause mortality by sex and age: a prospective cohort study among 12.8 million adults Korea. Cholesterol levels 200 to 250 offer the most protection from all cause mortality.
Correct. Unfortunately, for those with a genetic mutation (FH) or diabetes it's not good. Also there is too high and too low in the health parameters of blood lipids.
I started WFPB vegan diet as prescribed by Dr. Caldwell Esselstein's research reversing heart disease. I was on this diet six weeks. I didn't do it perfectly. Cholesterol went down from 380 to 193 LDL - C from 280 to 125. No medication. I am diagnosed with familial hypercholesterolemia.
FHC is caused by only two nucleotide changes at position 21006289 on the ApoB gene in chromossome 2. It replaces the two typical guanine bases present there for two adenines. These changes causes the coded protein to be dramatically overexpressed raising total and LDL cholesterol to stratospheric degrees. Left untreated, it leads to death in the teen years to twenties from massive myocardial infarctions and strokes. Fortunately for people that have it, loweing APOB is relatively simple: statins and multi-gram niacin combined with a low-fat diet. It is much, much, much harder to deal with a dysfunctional ApoE than with ApoB. In fact, there is nothing that seems to counter the inceased risk of Alzheimer's and high LDL-c that comes from the terrible ApoE4 allele. This is why geneticists are working so hard to develop gene therapy to eliminate the E4 allele version of the gene or to overexpress ApoE2 through viral vectors in the brains of ApoE4 people, because having this allele is so catastrophic for health, especially for brain health.
Appreciate your comment. With specific regard to ApoE epsilon 4, my impression from reading so far that this is far from an environment-independent, directly causative factor in chronic disease process - in fact figured out to have been the original ApoE in human evolution. Risk amplifier - agreed. 'Terrible allele' sounds rather emotionally laden ... is this merited by an association? Gene therapy to eliminate genes without complete insight seems to me rather misguided of a proposition. Cautiously examining evolutionary history and function, and environment / epigenetics that render this gene a point of reduced or increased concern, is warranted in my opinion - a higher priority. I do think it is a very interesting discussion worth having, especially with how it allows for comparisons to be made between relatively slowly emerging processes of injury and acute injury - the latter showing remarkable similarities in certain regards to the former, described sometimes as appearing in most regards like acutely sped up aging. Rhonda Patrick comes to mind in this regard, as one of the people drawing attention to this. Great thing to keep the discussion open here on this topic, and again, appreciate the thoughts shared in your comment here.
@@yl1487 It's not predicative like the presinilin mutation is predicative of Alzheimer's or the werner helicase mutation is predicative of Werner's Syndrome, but it's still pretty damn bad. Having just one APOE4 allele raises your risk of dementia by your sixties by around 5 X, and having two copies raises your risk somewhere between 12 to 30 X. In fact, having two copies means a 75% to 90% chance of Alzheimer's before age 70. That is pretty damn bad. If you have two copies of APOE4, odds are that you are demented at 60 and dead at 70. There are some things that can mitigate that, like the KL-VS Klotho mutation or the rare SIRT1 rs3758391 T/T genotype almost completely neutralize the risk. But since than 10% of people have these rare beneficial SNPs, it's pointless. I don't think that there is anything that an APOE4 carrier can do that is proven to mitigate risk. There is some evidence that eating a Mediterranean diet and that supplementing with omega-3 might decrease the odds. There is also some evidence that metformin might improve the cognitive functioning of people with APOE4. But it's all a wash. Some studies show it has some effect, while others show that these things are nothing more than placebo. What makes APOE4 such a tragedy is that it increases the risk of Alzheimer's significantly *and* it is relatively common with 22% of all people having at least one allele. The presinilin mutations are much worse and cause severe Alzheimer's at a young age. But these mutations are very, very rare.
@@petercoderch589 perhaps there are inputs which I have been considering which you might like to consider, in order to alter your perception of there being little to be done. Light environment is hard to overestimate: recalling superior visual field ipRGCs relaying their EM wave input to SCN which in turn controls the pineal for melatonin synthesis, this being key mitochondrial antioxidant: just as a start. The landscape is complex, all the same, Pareto calls for getting our priorities sorted out.
@@yl1487 Melatonin has no effects whatsoever on decreasing the risk of Alzheimer's in APOE4 carriers. Also, you can just take melatonin. "Light therapy" is pseudoscience. Healthy diet and exercise might decrease risk, but most of the 70+ year olds with APOE4 that do not have Alzheimer's have other beneficial mutations that protect them from risk, like having an APOE2 allele(in the case of heterozygotes), or Klotho KL-VS, or the T/T genotype of rs3758391 on the SIRT1 gene, etc.
@peter coderch I don’t know how to send a message through RU-vid. Mr Coderch, if possible could you message me. I’d like to ask some questions- that you may have at least a recommendation. Thx.
Hello very thankful for this kind of videos ☺️. I am 42 with hefh (tc 340) and no medicine till this day. In general I feel very fit and healthy for my age . I think insulin sensitivity is the key to health but I want to share this: I am not functioning without dietary cholesterol and especially red meat. I know this since childhood. No sport and no mental health for me without meat. So , could it be that people with FH don't absorb cholesterol good enough and that's why they are hyper producers and not necessary hyper absorbers or bad cleaners ?
I appreciate your experience shared here and your thinking. As a matter of interest - may be a slight excursion away from your question, I recall recently exploring cholesterol synthesis, requiring about thirty (yes 30, three-zero) distinct steps, your question prompts me to take another look at it ... how do you manage with things like egg yolks by the way? Since becoming more familiar with phosvitin I've been getting particularly interested to hear from others how they cope with it ... on account of phosvitin as well as other substances too, actually, such as choline ...take care. Peace acetyl-CoA --> HMG CoA --> mevalonic acid 5P --> mevalonic acid 5PP --> isopntenyl PP --> dimethylallyl PP --> geranyl PP --> famesyl PP --> squalene --> epoxysequalene --> lanosterol ... [another 19 steps or so ... via lathosterol & friends ... ] --> 7-dehydrosterol --> cholesterol (!)
My question is does having FH and the excessive amount of LDL particles necessarily mean placquing (sp?)? If one has FH and no arterial inflammation is it still imperative that one reduces their intake of saturated fat and cholesterol? What’s the difference between lean mass hyper responders and those with FH that are lean healthy? It can’t be that FH people just have fewer LDL receptors or their livers are having trouble removing them because the end result is the same, a lot of LDL particles. Is it the quality of the particles? Low dense ones compared to big fluffy ones? And if that’s the case then wouldn’t it be more imperative to reduce insulin levels by reducing carbs and sugar? I’m asking because I recently had a heart attack and I thought I was more of a lean mass hyper responder since my triglycerides are always in the 50’s and my HDL was in the high 60’s and A1c is 5.5. My cardiologist has me on the maximum dose of Lipitor and a few other drugs and I feel like crap from the side effects.
Im not a docter, but I have FH. In my own research I found that particle number is important. Test for Apo B. Cholesterol can be transported in large and small lipoproteins. Metabolic issues like diabetes can cause very elevated particle numbers (Apo B). It is possible a lot of cholesterol is loaded on very large lipoproteins and the particle number is lower than expected.
@@cintiaspataro3205 Hi Cintia I have LDL 10.5mmol/L without medicin. I take statins every day 40mg rosuvastatin and 10mg ezetimib. It is a high dosage because I take birth control pills. The hormones accelerate the metabolism of the medicin and therefore the dosage must be increased. My grandmother died when I was 13 years old. It was her 3th blood clot, first one in the age of 42, second one age 58 and the last age 63. The good news is that my mother who has the FH gene is now 67 years old and she has never had any blood clots, she is even diabetic and obese. It is the statins that make it happening. She have had checked her heart and aortha. It looks good. I think it is very important to take statins. Do not be affraid of statins. Some statins can have side effects, but then you can try another type. I do not have any problems with rosuvastatin. My own daughter has FH. She is 15 years old. She will start statins when she is 16. I have taken statins from the age of 18. I had 3 years pause during pregnancy and breastfeeding. I have made a lot of research on FH. I would take statins for my self and my daughter. FH is not the same as elevated cholesterol due to obesity. It's different. I have experimented with my self. If I live extreemly healthy and follow all guide lines, perfect weight, exercise and all that... my LDL is only decreased by 1mmol/L. It is nothing. It will not matter. I hope you will take the statins ❤️ Live a long life and do not fear statins. Kind regards Serina
@@cintiaspataro3205 good luck on your journey. I’m looking for recipes and medical maintenance that has been effective for my 21 year old daughter. Best to you
Just thinking outloud. If she developes diabetes on top of that, in which rare cases does happen. Could there be a genetic cause of increased LDL caused by poor glucose partioning to beging with which statin increases a small liklyhood of, tipping them over when already vurneable that could explain their high LDL ? One has to ask what is the cause of the increased LDL cholesterol. And even in midst of having hypercholesteroolemia due to defect to the LDL receptor, if that had already led up to bad metabolic health and the statin just tipped them over. To manage in such a scenario as to know more, I would be very curious as to see if incrased lipolysis could actually lower their LDL as a piece of a puzzle to what is going on. If she already had weight and was metabolicly unhealthy, I would see if weight management would lower need for insulin and settle where cholesterol was its lowest without comrpomissing their metabolic health by forcing the body to depend on other energy substrates than triglycerides. But with leaner fit and a very high carb diet low fat diet if person responds well with faster clearence of insulin and increased insulin sensitivy, would be than ideal to lower cholesterol.
@@MrPerfume1979 I endeavoured to follow your comment, you have a lot of details packed in there. Please excuse me for addressing it less than comprehensively, at least for now (hoping to get back later if I get the chance). The discussion between Cyris + Robbie with Paul (Saladino) comes to mind: Cyris in particular, in relation to your closing sentence (his intake being particularly VHC-VLF. In that case though there was a confluence of AI conditions including T-1 diabetes. Very interesting.
Is there any good herbs to lower insulin besides berberine? Berberine gives me low grade stomach pain.. And what else can raise my SHBG? Thyroid is fine.
The cholesterol debate is often manipulated by those who (as we all can) become fearful without comprehension of functionality. Cholesterol is vital for optimal health as such to say high levels are detrimental then its disingenuous as if a car has half a tank of gas is it problematic to the car or if the tank is full is it also problematic? yet less gas in the tank has more probability to having problems . This simplistic example is by no means literal however common sense isn't as common in many. Unlike Chris masterjohn who has abundance sense.
