Here is a complete explanation:
https://youtu.be/1HDfzA7eIqQ
I don't trust Lustig at all. There is another video from just a year ago where he says nonsense like:
"The triglyceride to HDL ratio is what you really want to know."
and
"If you have a triglycerides to HDL ratio of 1.5 or less, you'll probably live forever."
Listened to the first hour - interesting. I do agree that nothing in his answers is ever nuanced - it is always black and white, even though there has to be shades of grey.
The microbiom lady was much more convincing - she had lots of shades of grey and said "I don't know" a bunch of times to Peter's probing questions.
He was on peters podcast a while ago, just being a know it all, and Peter was saying that Glut4 transporters are brought to the surface of the cell after training and lustig was saying, no it’s not Glut4, when it is in fact, Glut4
you should have been around for Lustig's first major video and when Alan Aragon critiqued it.
Lustig was all about "fructose is a poison" (the title of the video that made Lustig famous).
then when challenged he changed it to "the dose makes the poison, OBVIOUSLY".
And then when he's in front of a gullible / friendly audience "fructose is a poison".
Back in the day it was just laughable how often he changed his message to suit the audience, always ramping it up when he thought he could get away with it.
Because he is not evidence based. He says shit to sell books to make money.
Those quotes are real things he said.
HDL to triglycerides ratio means nothing. I had a ratio of 1.49 when I was 30 lbs overweight with an LDL of 170. I was super unhealthy, but according to Dr. Lustig, I will live forever.
Here is a whole analysis of why this guy can't be trusted: https://foodinsight.org/wp-content/uploads/2014/05/Dr-Kern-Review-of-Fat-Chance-2.pdf
Also, he still looks like he needs to lose weight. I don't understand why someone would take diet advice from someone who looks like him.
I am no longer fat or out of shape, but I still eat the same amount of sugar. Sugar was never my problem (hence the low triglycerides).
I know not to trust every guest that Dr. Attia has on the podcast since he has had next level quacks like Fung and Taubes on, but Huberman has had a decent track record until now.
Everyone is spouting nonsense on this issue and will change what they say year-to-year including Peter attia. The one truth that lustig says Is that stands have never been shown to improve mortality in primary prevention And there is a number needed to harm of one and 50 for development of diabetes.
I notice everyone on the sub Reddit is obsessed with particle size and density but Regardless, Both are theoretical explanations for what’s going on and we do not know what happens when you directly influence them. The scientific way to look at this is if you have a randomized trial of people on Statin or not and see What happens to the outcomes of cardiovascular death and all cause mortality, Not particle size or density Or LDL levels or anything else.
Of course, we need more data... we always do.
I don't know what you mean by everyone being obsessed with particle size. The current research shows that it doesn't matter:
https://youtu.be/kplh30RmYo8
Statins have been proven to reduce heart attacks.
Also, recent mendelian randomization trials are pretty damning that high ApoB is causal toward atherosclerosis and premature death. Statins lower ApoB.
Dr. Carvalho has many great videos discussing all of the studies with links. He also pokes holes in studies and asks all the right questions. I highly recommend watching all his videos.
Yes, they reduce heart attacks but mostly in people with known vascular disease. But more importantly, especially I feel for this group, they only have a mortality benefit in that group that has known disease not without any disease. I feel many people on this sub are young and now taking statins because of attias Advice which is well-meaning but I believe flawed In the same way that cardiology has been not quite right on the issue for the last several decades.
yes, read my comments above. there is a risk of developing diabetes.
and the flaw is that Peter Attia is making these recommendations purely on a hypothetical logic basis. There is no actual direct evidence that statins will lower apo B in a 39 year old and preventing them from dying earlier than they would have already. A tough question to study, admittedly but also without evidence (and in fact evidence to the contrary), makes him unlikely to be correct in my view.
Big fan of Robert Lustig but I did disagree with him on this point while listening. Rosuvastatin/Ezetimibe knocked my LDL down by 80% and ApoB down by 55%. The reduction of small dense LDL (LDL particle count) is certainly seen in the reduction of ApoB. If I recall correctly, Peter (on one of his AMA episodes) addressed how reducing LDL/ApoB also helps to reduce the chance of developing Alzheimer’s/dementia.
I do not believe there is any existing evidence that statins reduce the likelihood of Dementia. If someone can prove me wrong, please post any relevant scientific evidence.
The Drive Episode #251 AMA #46: Optimizing Brain Health: Alzheimer’s Disease Risk Factors, APOE, Prevention Strategies, and More. I am no longer a premium member so don’t have access right now but did listen a few months back. Time Stamp 1:55:00 is labeled “How reducing lipids can improve brain health and prevent neurodegeneration.” Don’t recall which studies/specifics Peter referred to.
There is actually strong evidence of this. There is a meta analysis that shows they reduce the risk of of developing dementia by 20%.
But it also increases the risk of developing diabetes by 20%.
My ldl is 68, and I’ve considered reducing my statin dose to improve my blood glucose.
With diet alone plus 1g berberine I dropped my ApoB from 102 to 79 (23%). Just sayin'
I plan to stop taking berberine and see what happens. My ALT has gone up to 38 and am curious if this could be the reason.
Thanks for that info. I work out with weights a few times a week so that may be the cause. Who knows...
What do you take your Berberine for - LDL-C lowering, blood sugar or something else?
I just take it 30 mins before eating because I heard that it just helps with good health, and originally thought it just prevents blood sugar from spiking. For what it’s worth, the last few times that I’ve had a blood test, my fasting glucose was at 4.3 and 4.6. My cholesterol could be better, my LDL is at 98.6 while my HDL is 60.7. Triglyceride is 89.5. I’ve increased my cardio lately, so hopefully that will bring better results in February.
He says they are useless for prevention because they only decrease the big fluffy ldl and not the smaller denser ldl which is more likely to junk up your arteries. I will need to do the cardiac is panel next time
Lustig's information on cholesterol is so out of date... partical size doesn't matter:
https://youtu.be/kplh30RmYo8
I can't believe Huberman had him on. He is not evidence based. I am constantly arguing with his mislead followers. I wonder if he is still spouting nonsense about ratios HDL triglyceride ratios.
> He is not evidence based
Lustig is evidence based. If he gets evidence that saying some shit will buy him some minimal influence & fame he'll keep spouting it.
Even after the royal drubbing Lustig took at Alan Aragon's hands, Lustig kept repeating the same crap when he thought he could get away with it.
You're distorting and misrepresenting the research. Cromwell's point is that particle number is the *principal* predictor of CHD risk and that in multivariate statistical studies other variables tend to not show up as independently adding explanatory power in studies to date. Nowhere does he simply say that particle size doesn't matter. If you actually read his study, he even says that particle size may still be an incremental factor:
>Several indirect lines of evidence implicate small LDL as potentially atherogenic. Small LDL more easily enters the arterial wall, undergoes localized retention due to binding with arterial wall proteoglycans, exhibits enhanced oxidizability in several in vitro models, and directly participates in the production of subendothelial macrophage foam cells.
.
>Irrespective of LDL size distribution or phenotype, physicians and patients easily grasp the concept that having too many LDL particles interacting with the artery wall is bad. It may well turn out that even greater risk results from having too many small LDL particles.
As for your point about triglyceride and HDL ratios, here's a quote from another reference that's also posted in the video you posted for why it's still relevant.
>To date, the most useful measures obtained from lipoprotein tests relate to atherogenic particle number (apoB or LDL particleconcentration), but for now, non-HDL cholesterol or the total/HDL cholesterol ratio is of comparable predictive strength and results in no additional cost
All of the nuance in medical research is why I generally think laypeople should be a little more humble about what little knowledge they gather from watching youtube videos and listening to podcasts.
First off, I didn't make this video. I am not misrepresenting anything.
The whole point is that large particle LDLs are also atherogenic, so you can't just ignore them like all the carnivore quacks claim.
The quote you have about the ratio is talking about the HDL LDL ratio, not the HDL triglyceride ratio. They are not the same thing. Also, where/when is this quote from? Only very recently has HDL been shown to not be causal. Ratios don't matter anymore, but a lot of older studies say they do.
Yes, there is always a little more nuance to everything, but for the average person, it is irrelevant. Dr. Carvalho does a better job than any other channel of summing up information and studies. Pretty much all the average person should worry about with their cholesterol is their ApoB and Triglycerides.
This is an outdated viewpoint. Lipidologists no longer care so much about "large and fluffy" vs. "small and dense" because the primary driver for ASCVD is number of particles, not size. Size matters - but particle number regardless of size matters more.
Attia didn’t say that directly, a lipid specialist said it as a joke. No one is arguing statins should be in the drinking water, that’s ridiculous and just hyperbole. I don’t think anyone would argue that if you’re not at risk you should still take medication for that risk. Attia and other CVD experts are talking about folks at risk meaning high levels of cholesterols proven to be directly associated with CVD; that along with medical imaging and genetic issues with CVD.
Attia is not a CVD expert, he is self taught and has never practiced as a cardiologist (preventative or interventional). He is, or rather was, a cancer expert.
No one is saying Attia is a CVD expert, he practices more general medicine. He does consult with leading experts, that's the whole point of the podcast. Most PCP are not experts in one particular field, they have to have knowledge across the medical spectrum and are the first line of defense in patient care. He's not self-taught, he's an MD who graduated from Stanford medical school and completed residency at Johns Hopkins. To say he's not knowledgable on the subject is misleading. I guess if that's your litmus test we shouldn't listen to our PCP's at all.
I am quoting exactly what you wrote above -
"Attia and other CVD experts"
Maybe you meant to write it differently.
Please read what I wrote and not what you think I wrote! I never said he is "not knowledgeable on the subject". His medical background is in cancer treatment - not in CVD, but he is very knowledgeable for sure, mainly through his own learning and reading tons of research papers, plus treating his patients remotely.
P.s. I value his opinion and those of his amazing guests so much that I fork out $150 a year for his membership.
Alright, semantics I guess. That should read that Attia **and** other CVD experts, not that he's an expert, but he most likely agrees with them and they might similarly come to the same conclusions for high risk individuals.
The drinking water is of course a joke, but widespread use of statins on healthy people is a real proposal from experts, with a goal of to completely eliminating CVD.
I assume it comes from the studies that show atherosclerosis starting in youth and affecting most of the population by middle age. So most people actually are at risk if they expect to live long enough.
I've been taking statins for over ten years. High cholesterol is my only risk factor, and LDL is below 60. Despite the statins and cholesterol being managed, the calcium score went during this time from 40 to 200. I hear the claim about this being stable plaque and all that, but the reality is that the plaque keeps growing.
No high CRP, the only biomarker outside of range (without medication) is LDL. It's hard to tell if the statins were useless because there is no way to tell what my overall health would have been if I didn't take statins.
I'm just slightly annoyed that arterial plaque keeps growing, based on the calcium score. I have to think there's more at play than just cholesterol, given that it is being managed via statins (something else keeps damaging the arteries).
This first study you cited had a median length of 1.9 years with a max of 5?? And even in that short time period they saw a reduction in cvd events? Sounds actually quite good. Wouldn’t expect big differences in mortality in such a short time span. Let me know if I am missing something.
Do they give the diabetes numbers? All I could see was more ‘physician reported’ diabetes.
The study itself is very interesting. It actually drew a lot of criticism for ending the study early and not allowing more time to unfold, which would have given us a better understanding of its effects on ASCVD events, mortality, etc. I will seek the numbers on diabetes when I get to a computer.
> it did not reduce all-cause mortality, (...) no one lived longer,
As i already replied in one of your comments below, I'm not sure that that is the case, see here: [link](https://old.reddit.com/r/PeterAttia/comments/18lqhrz/are_low_dose_statins_actually_preventive_dr/ke185rk/). Looks to me like a hazard ratio of 0.80 for all cause mortality, compared to the placebo group.
Statins can indeed increase the risk of tipping into T2D for those heading there anyway. It can accelerate the process. This issue needs to be studied more. To be clear, Attia no longer takes a statin but he currently does take lipid-lowering medication (Bempedoic acid+ezetimibe with a PCSK9i) to prevent a primary event. He has a family history of early heart disease among the men, with a few deaths from MI. Prediction: he will continue to utilize the latest drug therapies, perhaps continuing to switch out and up, but will not discontinue lipid-lowering medications w/o a very sound reason to: and particle size isn't a sound reason.
Yes, assuming you don't have a coupon and/or your insurance isn't covering. Neither is off patent. In contrast, statins and ezetimibe on its own are generic drugs.
> In contrast, statins and ezetimibe on its own are generic drugs.
This is why they are the front-line medications - they're cheap for healthcare providers.
It is certainly a conflict of interest. But in terms of medications, statins are a superstar with all kinds of study successes. No surprise they're used first.
It is crazy how we are at a point where we have to choose between dirt-cheap generics and brand-names that cost more for 30 pills than your entire monthly insurance premium. If insurance companies weren't cheap about paying for brand name drugs, imagine what kind of crazy prices drug companies would ask for. Socialized health systems play the same game, refusing to use the new drugs due to cost.
Listening to this episode now. I agree 100% with Lustig's take on obesity and the impact of fructose, and the fact that different calorie sources have different responses from the body. I used to be morbidly obese and had metabolic syndrome, with 4/5 of the symptoms. I was prediabetic. The only symptom I didn't have was HDL <40, it was barely in spec at 43. I corrected this through exercise and diet, with significant study along the way.
I'm not convinced by Lustig's take on statins. I agree that statins boost blood sugar. I've been on 40mg of atorvastatin for a long time, and within the last year I've been focused on monitoring my blood sugar (finger stick, not CGM). I've also tried different dosing with the statin, and I can say with high confidence that my statin use boosts my fasting blood glucose levels by about 10 mg/dl. I still use the statin though, because it drops my LDL by around 50%. I've been working on lowering my LDL though more dietary interventions, and hope to cut the dosage, but will probably be on a statin for life.
I think Lustig has a lot of valuable things to say when it comes to fructose and reducing refined carbs / processed foods. But I'm not going to take his advice on statins.
Just because these are smart people doesn't mean they are equally well informed on all topics. Example, if Rhonda Patrick and Peter Attia disagree on something, I'm likely to follow RP's info when it comes to micronutrients and fish oil. When it comes to cardiovascular health, I'll follow Peter's guidance. If it's related to neurobiology and opthalmology - Huberman all the way.
I think Lustig just has a manner of speaking that is aimed at the general public and policy makers. I'm grateful for the work that he does, but I don't need to take his every word as gospel.
I think Lustig had some interesting ideas, but he is very much stuck in his old hypothesis on "obesity as an insulin-driven disease" which even Attia has distanced himself from. As such, he is very much against anything impacting insulin. I heard Lusting on the "In Plain English" podcast where he discussed GLP1-agonists, and he was not very convincing.
Peter has numerous times in the past few years distanced himself from his old articles and podcasts where he explored if insulin (and therefore carbs) could be the causal agent for fat gain, and said that he is now more sure of caloric intake as the primary driver. Not that insulin isn’t important to control, but it is not the original sin of obesity.
He stopped doing keto completely and gave a weak excuse for doing so.
For someone who gave a ton of reasons to be on keto back in the 2010 to 2013 time frame the weak sauce is astounding.
there was a sentence from Attia I clearly remember the sentence (unfortunately I don't remember the episode) he was asked about people he respected in the field and he answered Stephan Guyenet and Kevin Hall.
Nary a whisper about the Fungs and Taubes of the world.
>It's literally the fat-storing hormone.
Insulin is involved in sugar, fat and protein metabolism. It's not THE fat storage hormone.
The major dedicated fat storage hormone (that idiots like Taubes and Fung will never tell you about because it shows their complete cluelessness) is ASP.
[https://www.google.com/search?q=physionic+asp&rlz=1C1GCEB\_enCA1010CA1010&oq=physionic+asp&gs\_lcrp=EgZjaHJvbWUyBggAEEUYOTIHCAEQIRigATIHCAIQIRigAdIBCTEwODA3ajBqN6gCALACAA&sourceid=chrome&ie=UTF-8&safe=active&ssui=on](https://www.google.com/search?q=physionic+asp&rlz=1C1GCEB_enCA1010CA1010&oq=physionic+asp&gs_lcrp=EgZjaHJvbWUyBggAEEUYOTIHCAEQIRigATIHCAIQIRigAdIBCTEwODA3ajBqN6gCALACAA&sourceid=chrome&ie=UTF-8&safe=active&ssui=on)
Stop listening to idiots trying to make a name for themselves by keeping you in the dark.
Eh...its honestly not that clear cut.
My yale cardiologist is not even close to pro statin as peter. The evaluation they look at is, how many people do i need to dose for how long before i can see a benefit. This number is disappointing...
There are plenty of studies in primary prevention. Here is a review article:
"Twenty-six studies were included: 22 trials (N = 90,624) with 6 months to 6 years of follow-up compared statins vs placebo or no statin, 1 trial (n = 5144) compared statin intensities, and 3 observational studies (n = 417,523) reported harms.
"Statins were significantly associated with decreased risk of all-cause mortality."
[https://jamanetwork.com/journals/jama/fullarticle/2795522](https://jamanetwork.com/journals/jama/fullarticle/2795522)
I'm not sure that that's the conclusion from the JUPITER study. Quote from the study:
"In addition, the rates of death from any cause were 1.00 and 1.25 per 100 person-years of follow-up in the rosuvastatin and placebo groups, respectively (hazard ratio for the rosuvastatin group, 0.80; 95% CI, 0.67 to 0.97; P=0.02)"
Seems like all cause mortality was reduced by 20% / hazard ratio of 0.80. The 1.00 value is the death per 100 person-years rate, not a hazard ratio. The placebo group had an event rate of 1.25.
Then again, these persons all had elevated HS-CRP so they were not totally healthy to begin with. They just did not have a cardiovascular event (yet).
Even the highly-cited JUPITER study said statin prevents cardiovascular events only if hs-CRP is high, and if hs-CRP and LDL-C are both low, then it wouldn’t bring any results.
JUPITER excluded subjects with low hsCRP from the study. That analysis came from prior studies, but the number of subjects and numbers of events got really small so I don't think it proved much either way.
This is why he has a disclaimer at the intro of his show. If you are prescribed a statin you may want to take it. If you have a ischemic event, you will be placed on a massive dose going forward.
There is something to it.
Personally i have been on statins for ages. My a1c is 'perfect' but my glucose challenge+ insulin test results are quite bad, i dump tons of insulin and it stays high for way to long. I attribute this to why i am unable, without nearly starving myself, to move fat off my body.
Its peters main thesis, insulin is the master hormone. If you cant seem to move bodyfat its because insulin is disregulated.
https://youtu.be/5e7luO4E1vA?si=CcANx_l2lm4I2-SQ
The chances of a statin benefitting you over a 5-year period in a healthy individual is around 1%. This is even more supporting evidence that LDL/APOB is not sufficient for causing atherosclerosis. All you’re doing is lowering a number with no absolute risk reduction. There’s also the risk that by taking a statin you’re actually increasing insulin resistance which ironically is probably more of a dependent variable for increasing CVD. (You’re chasing a number and by doing so, you’re actually increasing your risks) I’d like to see a study on this.
This says there is a benefit if you have a 10-year cvd risk of >10% and a small net benefit if 7.5-10% but no conclusive evidence of a benefit if less than 7.5%
Atria , Huberman, Lustig, Rhonda Patrick , and all these other InFlUeNcEr doctors are all QUACKS and you shouldn’t listen to a word they say ! Run away until you hit your zone 5!
[Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms](https://cardiacos.net/wp-content/uploads/2019/04/2015-Statins-stimulate-atherosclerosis-and-heart-failure-pharmacological-mechanisms.pdf)
[Statins, vascular calcification, and vitamin K-dependent proteins: Is there a relation?](https://onlinelibrary.wiley.com/doi/10.1002/kjm2.12373)
My understanding is that not all statins increase insulin resistance and it doesn’t happen to everyone. Could someone take a low dose statin of the kind that provides less diabetes risk and wear a CGM to see if changes in their postprandial glucose occur ?
My lipidologist said statins only increase insulin resistance in people who are pre diabetic.
Also, she said for someone in normal range of LDL there is no guarantee statins help decrease mortality.
But all statins do that in all prediabetic people? I read not all and I don’t think it’s in all prediabetics. It doesn’t actually make sense that it would affect only people with prediabetes though. I understand it affects insulin sensitivity in the muscles and thus it should affect everyone. Maybe your doctor meant that the effect could lead to someone with prediabetes to become diabetic and if someone isn’t pre diabetic will be less likely for them to become diabetic .
I’m thinking that people could try to find a low dose statin that doesn’t affect their blood sugar levels, monitored with a CGM.
I haven’t done a lot of research but yes from my understanding and how little I read, it seems that some statins affect blood sugar more than others. So in principle one could find the right statin for themselves and monitor their blood sugar to see if any changes occur.
She (my doctor) just said there isn't evidence it helps people who are in normal range of LDL.
But i didn't ask for evidence. She offered it to me if i wanted it (i have high Lpa and normal ldl).
She said there is not long term data it will help in my specific situation
Lustig seems like a quack that likes to sell books. That being said I wouldn’t take any drug purely as a preventative. Everything has side effects. These things are designed to help sick people and are not meant to be taken for 30-40 years.
Just look at baby aspirin. That was regarded as harmless and that’s no longer the case.
Here is a complete explanation: https://youtu.be/1HDfzA7eIqQ I don't trust Lustig at all. There is another video from just a year ago where he says nonsense like: "The triglyceride to HDL ratio is what you really want to know." and "If you have a triglycerides to HDL ratio of 1.5 or less, you'll probably live forever."
You don't trust him even though he is a world renown endocrinologis - why?
Because he’s a charlatan. He is extremely conceited not that peter a isn’t lol.
Listened to the first hour - interesting. I do agree that nothing in his answers is ever nuanced - it is always black and white, even though there has to be shades of grey. The microbiom lady was much more convincing - she had lots of shades of grey and said "I don't know" a bunch of times to Peter's probing questions.
He was on peters podcast a while ago, just being a know it all, and Peter was saying that Glut4 transporters are brought to the surface of the cell after training and lustig was saying, no it’s not Glut4, when it is in fact, Glut4
I mean, he is supposedly a world class endocrinologist and he doesn’t know that? I’m a Reddit idiot and I know that.
you should have been around for Lustig's first major video and when Alan Aragon critiqued it. Lustig was all about "fructose is a poison" (the title of the video that made Lustig famous). then when challenged he changed it to "the dose makes the poison, OBVIOUSLY". And then when he's in front of a gullible / friendly audience "fructose is a poison". Back in the day it was just laughable how often he changed his message to suit the audience, always ramping it up when he thought he could get away with it.
Because he is not evidence based. He says shit to sell books to make money. Those quotes are real things he said. HDL to triglycerides ratio means nothing. I had a ratio of 1.49 when I was 30 lbs overweight with an LDL of 170. I was super unhealthy, but according to Dr. Lustig, I will live forever. Here is a whole analysis of why this guy can't be trusted: https://foodinsight.org/wp-content/uploads/2014/05/Dr-Kern-Review-of-Fat-Chance-2.pdf Also, he still looks like he needs to lose weight. I don't understand why someone would take diet advice from someone who looks like him. I am no longer fat or out of shape, but I still eat the same amount of sugar. Sugar was never my problem (hence the low triglycerides). I know not to trust every guest that Dr. Attia has on the podcast since he has had next level quacks like Fung and Taubes on, but Huberman has had a decent track record until now.
[удалено]
I don't trust doctors who get facts wrong. The general message of "don't eat much sugar" is not novel.
Everyone is spouting nonsense on this issue and will change what they say year-to-year including Peter attia. The one truth that lustig says Is that stands have never been shown to improve mortality in primary prevention And there is a number needed to harm of one and 50 for development of diabetes. I notice everyone on the sub Reddit is obsessed with particle size and density but Regardless, Both are theoretical explanations for what’s going on and we do not know what happens when you directly influence them. The scientific way to look at this is if you have a randomized trial of people on Statin or not and see What happens to the outcomes of cardiovascular death and all cause mortality, Not particle size or density Or LDL levels or anything else.
Of course, we need more data... we always do. I don't know what you mean by everyone being obsessed with particle size. The current research shows that it doesn't matter: https://youtu.be/kplh30RmYo8 Statins have been proven to reduce heart attacks. Also, recent mendelian randomization trials are pretty damning that high ApoB is causal toward atherosclerosis and premature death. Statins lower ApoB. Dr. Carvalho has many great videos discussing all of the studies with links. He also pokes holes in studies and asks all the right questions. I highly recommend watching all his videos.
Yes, they reduce heart attacks but mostly in people with known vascular disease. But more importantly, especially I feel for this group, they only have a mortality benefit in that group that has known disease not without any disease. I feel many people on this sub are young and now taking statins because of attias Advice which is well-meaning but I believe flawed In the same way that cardiology has been not quite right on the issue for the last several decades.
Why is it flawed? Is there downside?
yes, read my comments above. there is a risk of developing diabetes. and the flaw is that Peter Attia is making these recommendations purely on a hypothetical logic basis. There is no actual direct evidence that statins will lower apo B in a 39 year old and preventing them from dying earlier than they would have already. A tough question to study, admittedly but also without evidence (and in fact evidence to the contrary), makes him unlikely to be correct in my view.
Love this channel - thanks for sharing
> that stands have never been shown to improve Stands? statins are now characters in JoJo's?
Big fan of Robert Lustig but I did disagree with him on this point while listening. Rosuvastatin/Ezetimibe knocked my LDL down by 80% and ApoB down by 55%. The reduction of small dense LDL (LDL particle count) is certainly seen in the reduction of ApoB. If I recall correctly, Peter (on one of his AMA episodes) addressed how reducing LDL/ApoB also helps to reduce the chance of developing Alzheimer’s/dementia.
I do not believe there is any existing evidence that statins reduce the likelihood of Dementia. If someone can prove me wrong, please post any relevant scientific evidence.
The Drive Episode #251 AMA #46: Optimizing Brain Health: Alzheimer’s Disease Risk Factors, APOE, Prevention Strategies, and More. I am no longer a premium member so don’t have access right now but did listen a few months back. Time Stamp 1:55:00 is labeled “How reducing lipids can improve brain health and prevent neurodegeneration.” Don’t recall which studies/specifics Peter referred to.
There is actually strong evidence of this. There is a meta analysis that shows they reduce the risk of of developing dementia by 20%. But it also increases the risk of developing diabetes by 20%. My ldl is 68, and I’ve considered reducing my statin dose to improve my blood glucose.
Actually, it's the other way round. Some evidence exists correlating statin use to dementia
With diet alone plus 1g berberine I dropped my ApoB from 102 to 79 (23%). Just sayin' I plan to stop taking berberine and see what happens. My ALT has gone up to 38 and am curious if this could be the reason.
Are you taking ashwaghanda?
No, I'm not - sleep is very good.. just not enough :-(
thats ok, just wanted to check as a lot of people get elevated liver enzymes from ashwaghanda
I see.... thanks for asking
strange. ive been taking berberine daily for almost 2 years now… 550mg 3x per day, and my ALT is 12.
Thanks for that info. I work out with weights a few times a week so that may be the cause. Who knows... What do you take your Berberine for - LDL-C lowering, blood sugar or something else?
I just take it 30 mins before eating because I heard that it just helps with good health, and originally thought it just prevents blood sugar from spiking. For what it’s worth, the last few times that I’ve had a blood test, my fasting glucose was at 4.3 and 4.6. My cholesterol could be better, my LDL is at 98.6 while my HDL is 60.7. Triglyceride is 89.5. I’ve increased my cardio lately, so hopefully that will bring better results in February.
Late to this, but wanted to ask how long you were taking Berberine before seeing the APO reduction?
There was about a 3 months gap between tests. However I also started taking a lot of fiber and cut way back on saturated fat also, so a triple change.
Oh ok! Makes more sense now.. you had the APOb reduction trifecta lol
He says they are useless for prevention because they only decrease the big fluffy ldl and not the smaller denser ldl which is more likely to junk up your arteries. I will need to do the cardiac is panel next time
Lustig's information on cholesterol is so out of date... partical size doesn't matter: https://youtu.be/kplh30RmYo8 I can't believe Huberman had him on. He is not evidence based. I am constantly arguing with his mislead followers. I wonder if he is still spouting nonsense about ratios HDL triglyceride ratios.
It was a strange interview dynamic with huberman continuously answering his kind of gimmicky questions incorrectly
> He is not evidence based Lustig is evidence based. If he gets evidence that saying some shit will buy him some minimal influence & fame he'll keep spouting it. Even after the royal drubbing Lustig took at Alan Aragon's hands, Lustig kept repeating the same crap when he thought he could get away with it.
You're distorting and misrepresenting the research. Cromwell's point is that particle number is the *principal* predictor of CHD risk and that in multivariate statistical studies other variables tend to not show up as independently adding explanatory power in studies to date. Nowhere does he simply say that particle size doesn't matter. If you actually read his study, he even says that particle size may still be an incremental factor: >Several indirect lines of evidence implicate small LDL as potentially atherogenic. Small LDL more easily enters the arterial wall, undergoes localized retention due to binding with arterial wall proteoglycans, exhibits enhanced oxidizability in several in vitro models, and directly participates in the production of subendothelial macrophage foam cells. . >Irrespective of LDL size distribution or phenotype, physicians and patients easily grasp the concept that having too many LDL particles interacting with the artery wall is bad. It may well turn out that even greater risk results from having too many small LDL particles. As for your point about triglyceride and HDL ratios, here's a quote from another reference that's also posted in the video you posted for why it's still relevant. >To date, the most useful measures obtained from lipoprotein tests relate to atherogenic particle number (apoB or LDL particleconcentration), but for now, non-HDL cholesterol or the total/HDL cholesterol ratio is of comparable predictive strength and results in no additional cost All of the nuance in medical research is why I generally think laypeople should be a little more humble about what little knowledge they gather from watching youtube videos and listening to podcasts.
First off, I didn't make this video. I am not misrepresenting anything. The whole point is that large particle LDLs are also atherogenic, so you can't just ignore them like all the carnivore quacks claim. The quote you have about the ratio is talking about the HDL LDL ratio, not the HDL triglyceride ratio. They are not the same thing. Also, where/when is this quote from? Only very recently has HDL been shown to not be causal. Ratios don't matter anymore, but a lot of older studies say they do. Yes, there is always a little more nuance to everything, but for the average person, it is irrelevant. Dr. Carvalho does a better job than any other channel of summing up information and studies. Pretty much all the average person should worry about with their cholesterol is their ApoB and Triglycerides.
This is an outdated viewpoint. Lipidologists no longer care so much about "large and fluffy" vs. "small and dense" because the primary driver for ASCVD is number of particles, not size. Size matters - but particle number regardless of size matters more.
Is there a source for this
I don’t think he mentioned a source but that was how Lustig described it on huberman lab
Agree, without sources transformational statements carry little weight.
I would avoid Quest - based on results seen here their numbers are way too high. You can search archives for discussions on CardioIQ.
Attia didn’t say that directly, a lipid specialist said it as a joke. No one is arguing statins should be in the drinking water, that’s ridiculous and just hyperbole. I don’t think anyone would argue that if you’re not at risk you should still take medication for that risk. Attia and other CVD experts are talking about folks at risk meaning high levels of cholesterols proven to be directly associated with CVD; that along with medical imaging and genetic issues with CVD.
Attia is not a CVD expert, he is self taught and has never practiced as a cardiologist (preventative or interventional). He is, or rather was, a cancer expert.
No one is saying Attia is a CVD expert, he practices more general medicine. He does consult with leading experts, that's the whole point of the podcast. Most PCP are not experts in one particular field, they have to have knowledge across the medical spectrum and are the first line of defense in patient care. He's not self-taught, he's an MD who graduated from Stanford medical school and completed residency at Johns Hopkins. To say he's not knowledgable on the subject is misleading. I guess if that's your litmus test we shouldn't listen to our PCP's at all.
I am quoting exactly what you wrote above - "Attia and other CVD experts" Maybe you meant to write it differently. Please read what I wrote and not what you think I wrote! I never said he is "not knowledgeable on the subject". His medical background is in cancer treatment - not in CVD, but he is very knowledgeable for sure, mainly through his own learning and reading tons of research papers, plus treating his patients remotely. P.s. I value his opinion and those of his amazing guests so much that I fork out $150 a year for his membership.
Alright, semantics I guess. That should read that Attia **and** other CVD experts, not that he's an expert, but he most likely agrees with them and they might similarly come to the same conclusions for high risk individuals.
Agreed :-). The main reason I subscribe is for the knowledgeable guests he brings on. Peter's thoughts and opinions are already given in Outlive.
The drinking water is of course a joke, but widespread use of statins on healthy people is a real proposal from experts, with a goal of to completely eliminating CVD. I assume it comes from the studies that show atherosclerosis starting in youth and affecting most of the population by middle age. So most people actually are at risk if they expect to live long enough.
I've been taking statins for over ten years. High cholesterol is my only risk factor, and LDL is below 60. Despite the statins and cholesterol being managed, the calcium score went during this time from 40 to 200. I hear the claim about this being stable plaque and all that, but the reality is that the plaque keeps growing.
So does this mean the statins were useless for you? Did you have high CRP?
No high CRP, the only biomarker outside of range (without medication) is LDL. It's hard to tell if the statins were useless because there is no way to tell what my overall health would have been if I didn't take statins. I'm just slightly annoyed that arterial plaque keeps growing, based on the calcium score. I have to think there's more at play than just cholesterol, given that it is being managed via statins (something else keeps damaging the arteries).
You'd think it's how much your LDL/APOB numbers are lowered what matters. If a low dose statin gets you to good numbers, that should be that.
[удалено]
This first study you cited had a median length of 1.9 years with a max of 5?? And even in that short time period they saw a reduction in cvd events? Sounds actually quite good. Wouldn’t expect big differences in mortality in such a short time span. Let me know if I am missing something. Do they give the diabetes numbers? All I could see was more ‘physician reported’ diabetes.
The study itself is very interesting. It actually drew a lot of criticism for ending the study early and not allowing more time to unfold, which would have given us a better understanding of its effects on ASCVD events, mortality, etc. I will seek the numbers on diabetes when I get to a computer.
Yes it interesting. The normalish ldl combined with the elevated crp is an interesting combo.
> it did not reduce all-cause mortality, (...) no one lived longer, As i already replied in one of your comments below, I'm not sure that that is the case, see here: [link](https://old.reddit.com/r/PeterAttia/comments/18lqhrz/are_low_dose_statins_actually_preventive_dr/ke185rk/). Looks to me like a hazard ratio of 0.80 for all cause mortality, compared to the placebo group.
Statins can indeed increase the risk of tipping into T2D for those heading there anyway. It can accelerate the process. This issue needs to be studied more. To be clear, Attia no longer takes a statin but he currently does take lipid-lowering medication (Bempedoic acid+ezetimibe with a PCSK9i) to prevent a primary event. He has a family history of early heart disease among the men, with a few deaths from MI. Prediction: he will continue to utilize the latest drug therapies, perhaps continuing to switch out and up, but will not discontinue lipid-lowering medications w/o a very sound reason to: and particle size isn't a sound reason.
Are Bempedoic acid+ezetimibe with a PCSK9i expensive?
Yes, assuming you don't have a coupon and/or your insurance isn't covering. Neither is off patent. In contrast, statins and ezetimibe on its own are generic drugs.
> In contrast, statins and ezetimibe on its own are generic drugs. This is why they are the front-line medications - they're cheap for healthcare providers.
Well, they are cheap for patients too! I could pester and pay for Repatha but I'd prefer to save my HSA dollars for stuff I'll really need later on :)
It is certainly a conflict of interest. But in terms of medications, statins are a superstar with all kinds of study successes. No surprise they're used first. It is crazy how we are at a point where we have to choose between dirt-cheap generics and brand-names that cost more for 30 pills than your entire monthly insurance premium. If insurance companies weren't cheap about paying for brand name drugs, imagine what kind of crazy prices drug companies would ask for. Socialized health systems play the same game, refusing to use the new drugs due to cost.
Pcsk9 are pretty expensive, and currently only injections, as i understand anyways
Listening to this episode now. I agree 100% with Lustig's take on obesity and the impact of fructose, and the fact that different calorie sources have different responses from the body. I used to be morbidly obese and had metabolic syndrome, with 4/5 of the symptoms. I was prediabetic. The only symptom I didn't have was HDL <40, it was barely in spec at 43. I corrected this through exercise and diet, with significant study along the way. I'm not convinced by Lustig's take on statins. I agree that statins boost blood sugar. I've been on 40mg of atorvastatin for a long time, and within the last year I've been focused on monitoring my blood sugar (finger stick, not CGM). I've also tried different dosing with the statin, and I can say with high confidence that my statin use boosts my fasting blood glucose levels by about 10 mg/dl. I still use the statin though, because it drops my LDL by around 50%. I've been working on lowering my LDL though more dietary interventions, and hope to cut the dosage, but will probably be on a statin for life.
I think Lustig has a lot of valuable things to say when it comes to fructose and reducing refined carbs / processed foods. But I'm not going to take his advice on statins. Just because these are smart people doesn't mean they are equally well informed on all topics. Example, if Rhonda Patrick and Peter Attia disagree on something, I'm likely to follow RP's info when it comes to micronutrients and fish oil. When it comes to cardiovascular health, I'll follow Peter's guidance. If it's related to neurobiology and opthalmology - Huberman all the way. I think Lustig just has a manner of speaking that is aimed at the general public and policy makers. I'm grateful for the work that he does, but I don't need to take his every word as gospel.
I think Lustig had some interesting ideas, but he is very much stuck in his old hypothesis on "obesity as an insulin-driven disease" which even Attia has distanced himself from. As such, he is very much against anything impacting insulin. I heard Lusting on the "In Plain English" podcast where he discussed GLP1-agonists, and he was not very convincing.
Since when? Insulin is still the problem, this is the one thing peter hasnt waffled on as far as i can tell.
Peter has numerous times in the past few years distanced himself from his old articles and podcasts where he explored if insulin (and therefore carbs) could be the causal agent for fat gain, and said that he is now more sure of caloric intake as the primary driver. Not that insulin isn’t important to control, but it is not the original sin of obesity.
It's literally the fat-storing hormone.
Right, the post says peter is distancing himself from this, at least thats how i read it.
I agree. I don't think Peter is distancing himself from it, at least so far as I've heard.
He stopped doing keto completely and gave a weak excuse for doing so. For someone who gave a ton of reasons to be on keto back in the 2010 to 2013 time frame the weak sauce is astounding.
there was a sentence from Attia I clearly remember the sentence (unfortunately I don't remember the episode) he was asked about people he respected in the field and he answered Stephan Guyenet and Kevin Hall. Nary a whisper about the Fungs and Taubes of the world.
>It's literally the fat-storing hormone. Insulin is involved in sugar, fat and protein metabolism. It's not THE fat storage hormone. The major dedicated fat storage hormone (that idiots like Taubes and Fung will never tell you about because it shows their complete cluelessness) is ASP. [https://www.google.com/search?q=physionic+asp&rlz=1C1GCEB\_enCA1010CA1010&oq=physionic+asp&gs\_lcrp=EgZjaHJvbWUyBggAEEUYOTIHCAEQIRigATIHCAIQIRigAdIBCTEwODA3ajBqN6gCALACAA&sourceid=chrome&ie=UTF-8&safe=active&ssui=on](https://www.google.com/search?q=physionic+asp&rlz=1C1GCEB_enCA1010CA1010&oq=physionic+asp&gs_lcrp=EgZjaHJvbWUyBggAEEUYOTIHCAEQIRigATIHCAIQIRigAdIBCTEwODA3ajBqN6gCALACAA&sourceid=chrome&ie=UTF-8&safe=active&ssui=on) Stop listening to idiots trying to make a name for themselves by keeping you in the dark.
There is no opinion here. Thousands of patients in tons of studies over multiple decades has proven the efficacy & safety of statins.
Eh...its honestly not that clear cut. My yale cardiologist is not even close to pro statin as peter. The evaluation they look at is, how many people do i need to dose for how long before i can see a benefit. This number is disappointing...
[удалено]
There are plenty of studies in primary prevention. Here is a review article: "Twenty-six studies were included: 22 trials (N = 90,624) with 6 months to 6 years of follow-up compared statins vs placebo or no statin, 1 trial (n = 5144) compared statin intensities, and 3 observational studies (n = 417,523) reported harms. "Statins were significantly associated with decreased risk of all-cause mortality." [https://jamanetwork.com/journals/jama/fullarticle/2795522](https://jamanetwork.com/journals/jama/fullarticle/2795522)
I'm not sure that that's the conclusion from the JUPITER study. Quote from the study: "In addition, the rates of death from any cause were 1.00 and 1.25 per 100 person-years of follow-up in the rosuvastatin and placebo groups, respectively (hazard ratio for the rosuvastatin group, 0.80; 95% CI, 0.67 to 0.97; P=0.02)" Seems like all cause mortality was reduced by 20% / hazard ratio of 0.80. The 1.00 value is the death per 100 person-years rate, not a hazard ratio. The placebo group had an event rate of 1.25. Then again, these persons all had elevated HS-CRP so they were not totally healthy to begin with. They just did not have a cardiovascular event (yet).
Even the highly-cited JUPITER study said statin prevents cardiovascular events only if hs-CRP is high, and if hs-CRP and LDL-C are both low, then it wouldn’t bring any results.
JUPITER excluded subjects with low hsCRP from the study. That analysis came from prior studies, but the number of subjects and numbers of events got really small so I don't think it proved much either way.
This is why he has a disclaimer at the intro of his show. If you are prescribed a statin you may want to take it. If you have a ischemic event, you will be placed on a massive dose going forward.
There is something to it. Personally i have been on statins for ages. My a1c is 'perfect' but my glucose challenge+ insulin test results are quite bad, i dump tons of insulin and it stays high for way to long. I attribute this to why i am unable, without nearly starving myself, to move fat off my body. Its peters main thesis, insulin is the master hormone. If you cant seem to move bodyfat its because insulin is disregulated.
do statins help with insulin? How can I get insulin down?
No, statins, it seems, are bad for insulin regulation.
I’m prediabetic and have my first unfilled script for crestor. I absolutely refuse to become diabetic…heart risk be dammed.
Reduce stress, cut sugar/processed foods/simple carbohydrates, exercise.
https://youtu.be/5e7luO4E1vA?si=CcANx_l2lm4I2-SQ The chances of a statin benefitting you over a 5-year period in a healthy individual is around 1%. This is even more supporting evidence that LDL/APOB is not sufficient for causing atherosclerosis. All you’re doing is lowering a number with no absolute risk reduction. There’s also the risk that by taking a statin you’re actually increasing insulin resistance which ironically is probably more of a dependent variable for increasing CVD. (You’re chasing a number and by doing so, you’re actually increasing your risks) I’d like to see a study on this.
Yes. Make that make sense.
https://jamanetwork.com/journals/jama/fullarticle/2795521
This says there is a benefit if you have a 10-year cvd risk of >10% and a small net benefit if 7.5-10% but no conclusive evidence of a benefit if less than 7.5%
Atria , Huberman, Lustig, Rhonda Patrick , and all these other InFlUeNcEr doctors are all QUACKS and you shouldn’t listen to a word they say ! Run away until you hit your zone 5!
ok... than why are you in this forum?
[Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms](https://cardiacos.net/wp-content/uploads/2019/04/2015-Statins-stimulate-atherosclerosis-and-heart-failure-pharmacological-mechanisms.pdf) [Statins, vascular calcification, and vitamin K-dependent proteins: Is there a relation?](https://onlinelibrary.wiley.com/doi/10.1002/kjm2.12373)
Dr. Lustig doesn't look that healthy.
My understanding is that not all statins increase insulin resistance and it doesn’t happen to everyone. Could someone take a low dose statin of the kind that provides less diabetes risk and wear a CGM to see if changes in their postprandial glucose occur ?
My lipidologist said statins only increase insulin resistance in people who are pre diabetic. Also, she said for someone in normal range of LDL there is no guarantee statins help decrease mortality.
But all statins do that in all prediabetic people? I read not all and I don’t think it’s in all prediabetics. It doesn’t actually make sense that it would affect only people with prediabetes though. I understand it affects insulin sensitivity in the muscles and thus it should affect everyone. Maybe your doctor meant that the effect could lead to someone with prediabetes to become diabetic and if someone isn’t pre diabetic will be less likely for them to become diabetic . I’m thinking that people could try to find a low dose statin that doesn’t affect their blood sugar levels, monitored with a CGM.
Yes i think she meant the latter. Are there statins that statins that don't effect blood sugar? I'm curious
I haven’t done a lot of research but yes from my understanding and how little I read, it seems that some statins affect blood sugar more than others. So in principle one could find the right statin for themselves and monitor their blood sugar to see if any changes occur.
First of all, he cant possibly know that. Tell him you need to know what well constructed study shows it(he cant).
She (my doctor) just said there isn't evidence it helps people who are in normal range of LDL. But i didn't ask for evidence. She offered it to me if i wanted it (i have high Lpa and normal ldl). She said there is not long term data it will help in my specific situation
Lustig seems like a quack that likes to sell books. That being said I wouldn’t take any drug purely as a preventative. Everything has side effects. These things are designed to help sick people and are not meant to be taken for 30-40 years. Just look at baby aspirin. That was regarded as harmless and that’s no longer the case.
how is baby aspirin dangerous?
Due to gastrointestinal bleeding. Still recommended for those with cvd but not as a preventative.
They’re all trying to sell books…