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58 minutes ago, Todd Allen said:

It's increasingly looking like most people could achieve cholesterol numbers similar to mine if they tried.  All that is needed is to get quite lean, be physically active and strictly limit dietary carbohydrates.  There isn't any data suggesting this is unhealthy.  

Hmmm... Is that true though?

https://www.tctmd.com/news/keto-diet-linked-hypercholesterolemia-higher-ascvd-risk

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4 hours ago, Dean Pomerleau said:

Where's the study?  I wouldn't bet my life on this without the details of the cohort, the methods, the data and analysis.

Here's a short video regarding preliminary results of a study of a cohort relevant to me and I am looking forward to it's completion.

Quote

Dave interviews Professor Matthew Budoff, Chair of Preventive Cardiology at Harbor-UCLA Medical Center and Principal Investigator of the Lean Mass Hyper-Responder (LMHR) Study. LMHR are individuals who exhibit extremely high LDL cholesterol (LDL-C) on a ketogenic diet, along with low triglycerides and high HDL-C, indications of good metabolic health. This prospective study aims to assess atherosclerotic plaque development in 100 LMHR using the most sensitive non-invasive imaging technology available, a coronary artery calcium scan with coronary CT angiography. In the interview, Dave discusses the findings from the baseline scans of the 64 LMHR recruited to date (August 2022). Highlights include that: Participant a mean age is 53 years; Have been on a ketogenic diet with extremely high LDL-C (mean of 233 mg/dl) for an average of 4 years; And, consistent with prior literature (below), LDL-C levels were normal (mean 135 md/dl) prior to their ketogenic diet, they were negative for monogenetic familial hypercholesterolemia, and were indeed leaner than the average American (mean BMI 22.6 kg/m2). Given the participants’ age and duration of time with LDL-C levels in the top 0.1% of the population, one might expect a substantial amount of plaque in their coronary arteries. However, about two-thirds of participants have 0 Total Plaque Score; and, across all 64 participants, the highest plaque score was 8, out of a 45 scale. Professor Budoff reports the plaque findings are “much lower than I anticipated” (4:45).

 

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1 hour ago, Todd Allen said:

LMHR are individuals who exhibit extremely high LDL cholesterol (LDL-C) on a ketogenic diet, along with low triglycerides and high HDL-C, indications of good metabolic health.

Don't let's forget that atherosclerosis is the result of the cumulative effect of the impacts of apolipoprotein particles on the arteries' walls. AFAIK, 4 years would perhaps enough just to see the inception of atherosclerosis and what we see in that study is 44% patients with the inception of calcific plaques accumulation, that is, the inception of atherosclerosis.

So, the study just confirms what Snidermann, Daysprings et al. affirm, that very high levels of LDL pose a risk of atherosclerosis on a temporal horizon whose length is 30 years. The study should go on 30 years, then we could draw the conclusions, with the percentages of hard plaques, soft plaques, eventual CV events (almost unavoidable in a large cohort, maybe avoidable in a small one).

Even then, we might expect some people who will not develop atherosclerosis, enjoying, in the words of Daysprings, some unknown protective mechanisms and maybe this phenotype of LMHRs does enjoy some protection with respect to non-LMHRs.

At the end, the cited study just confirms that a ketogenic diet in hyper responders, even if LMHR, is likely to cause the inception of an atherosclerotic process in about half the population after an average of 4 years, that is, a quick negative effect considering the very long time horizon this process takes to unfold.

Also, the data should be stratified and detail the population which exhibits plaques, they are may be the older ones in the cohort.

A criticism of the study, why they didn't measure directly ApoB, in this kind of detailed and specific models LDL-C may not be the best risk indicator although it may remain a good proxy.

At the end, the study is surely interesting but equally surely it would not encourage me to walk around with an LDL-C level at the 99.99th percentile, even if I had a lean mass.

Edited by mccoy
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There is a known multiplier coefficient - blood pressure. Those who have it higher will speed up the plaques formation (imho 1.5-3 times), especially at a few well-known places where the flow hits the walls the highest (dynamic pressure at these places will increase not the same 10% but much higher).

From this perspective, those with low blood pressure will have longer times to accumulate enough hits that result in plaques. Hard to say if LMHR studies are not heavily biased towards such groups, I never checked the publications personally.

And less known and hard to assess multiplier - "particles affinity" - how likely they will stick and aggregate. This is not yet ready to be assessed with confidence anyhow.

But as Mccoy pointed - 4 years is not enough time anyway to draw any conclusions, especially against really large amount of already accumulated mechanical evidence.

Br,

Igor

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1 hour ago, IgorF said:

But as Mccoy pointed - 4 years is not enough time anyway to draw any conclusions, especially against really large amount of already accumulated mechanical evidence.

the existing literature is a very strong point which reiterates the correlations between serum LDL and the atherosclerotic risk.

The article posted by Todd is a case of a very specific subgroup where plaques did show up after 4 years of LDL-repleted blood serum in a significant part of the population. Those are the plaques in coronary arteries, we know nothing about other arteries and we might expect more.

Anyway, the LMHR study in a way may be considered encouraging. In those extreme conditions, it takes time  to develop a serious condition of atherosclerosis. with the LDL levels of the majority of this forum members (and the lack of other risks like blood pressure, diabetes smoking and so on), we may be reasonably sure that our risk is very, very modest.

We may nonetheless desire perfection and wish to achieve zero risk. Zero risk is a more useful concept if contemplated in one's twenties. But even in one's sixties it has its benefits if we wish to live and be fit until 100. 

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11 hours ago, mccoy said:

AFAIK, 4 years would perhaps enough just to see the inception of atherosclerosis and what we see in that study is 44% patients with the inception of calcific plaques accumulation, that is, the inception of atherosclerosis.

Which is why I am looking forward to the completion of this study.  Everyone gets retested in a year and we will get to see who has progressed and by how much.  Conventional wisdom is that an LDL of 200 is far worse than twice as bad as 100.  The 233 LDL was the average over their time since going keto but most have been rising so there should be a fair number at 300 for the year tracked, some at 400, 500 even 600 and perhaps one or two as high as 800.  So despite the small cohort this should be a wonderful opportunity to see a dose response relationship.  The imaging is the best available which sees both hard and soft plaque with high resolution in great detail and 1 year of tracking using this imaging is common practice for drug studies.  Unlike the vast majority of studies this study was funded by donations of the members of this community who want answers and all data collected will be released.  I did not enroll in the study because I would never take a covid vaccine and during the recruitment period Chicago was increasingly enacting coercive restrictions on the unvaccinated preventing access to public places potentially interfering in my ability to travel to and from California for the testing.  But as I understand it the data collected goes far beyond the imaging and will have things like ApoB, Lp(a) and much more.

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Todd, I see it like this. The experiment is sure interesting, if the conclusions are exposed correctly, then it will be useful to illustrate the gambling risks of a high saturated fats ketogenic diet and everyone with a large risk appetite will be able to make an informed choice. 

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On 6/8/2023 at 1:44 PM, mccoy said:

I heard many experts in the field and they all agree that, as a rule, diet and lifestyle cannot solve serious cases of hypercholesterolemia. Also, as a rule, diet and lifestyle cannot bring cholesterol values down to neonatal values. That seems reasonable. Nobody said that diet and lifestyle have no use

Diet and lifestyle cannot solve serious genetic issues, but they may mitigate many of them, sometimes dramatically (like type 1 diabetes, which for some may be entirely controlled by low fat vegan diet). Todd obviously knows far more about hypercholesterolemia than I do, but my guess is that even there, a balanced whole-food plant-based diet that is very low fat should be expected to help a bit, and also keep other aspects of one's health in better shape. If I remember, Todd has tried that, although the devil may be in the details. Anyway, Todd seems to be an outlier and I am happy that his high-fat diet works for him, of course. But based on my knowledge, I would go low fat balanced HF vegan instead 🙂

I have certainly heard Attia repeatedly dismiss diet, other than his large protein recommendations. He used to do it more vehemently in the past, especially when he was essentially promoting keto, but still does it, particularly with regards to the issues with cholesterol and microbiota. Attia has personally had CV issues and may personally be justified in using pharmaceuticals, but I think he sprinkles some potentially damaging to some conclusions within his otherwise generally valuable videos.


mcccoy, thanks for posting The Proof interview in another thread here. Dayspring still uses his "eat 20 eggs a day" quip for those who are genetically lucky, which is clearly a fallacy, even based on his own statements elsewhere, such as the actual amounts of absorption and how they are influenced by diet. Interestingly, he may have retired, as in Part 3 of the interview he is far more open to diet influences than I've ever heard him to date.
 

Edited by Ron Put
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11 hours ago, mccoy said:

The experiment is sure interesting, if the conclusions are exposed correctly

It's not about drawing conclusions.  It is about producing data.  People have long been jumping to conclusions in what is an essentially data free domain.  My expectation which I admit is little better than a hunch is the data produced will not show much if any correlation at all between any lipid markers such as LDL-C, ApoB, Lp(a), HDL or triglycerides and plaque development among this cohort.  Among the general population there is a correlation between increasing adiposity and rising LDL but among this population that is strongly reversed.  Something is clearly different here.

 

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21 minutes ago, Ron Put said:

Anyway, Todd seems to be an outlier and I am happy that his high-fat diet works for him, of course. But based on my knowledge, I would go low fat balanced HF vegan instead 🙂

Normally I don't put much weight on mouse studies but this one so perfectly matched what I was already experiencing that I suspect it is relevant:

Glycolytic-to-oxidative fiber-type switch and mTOR signaling activation are early-onset features of SBMA muscle modified by high-fat diet

Quote

The performance of control mice fed the HFD was significantly decreased, as expected, whereas that of AR113Q mice was restored to normal. The HFD also increased the force of gastrocnemius (Supplementary Fig. 21f). Importantly, the HFD extended the median life span of AR113Q mice from 161 days to 322 days (χ2LR = 3.955, P = 0.047; Gehan–Breslow: P = 0.046) (Fig. 5g). These results show that the HFD attenuates disease manifestations in knock-in SBMA mice.

Note, the HFD (high fat diet) is a mix of highly refined crap such as soybean oil, sucrose and casein which produces or aggravates disease most everywhere it is tried.  I've come to see my disease as my superpower.  I've gone from feeling 90 years old when I was 50 to feeling like a teenager at 58.  I have next to zero concern about heart disease risk, as best I can tell I don't have any indications of CVD and I have yet to hear of anyone with my disease ever dying from a heart attack.  Even if the LMHR study were to show a massive CVD risk increase I'd probably gamble on being the one spared.  Even if wrong dying from a heart attack could be a pleasant surprise.  I nearly died of frailty and anything and everything which continues moving me further away from that is desirable.

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Hm,

Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5837225/

 

Quote

 

We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.

Conclusion

Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.

 

Quote

Considered together, the strong and consistent evidence from the genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized intervention trials discussed here, supported by mechanistic evidence to be presented in the second Consensus Statement on LDL causality, establishes that LDL is not merely a biomarker of increased risk but a causal factor in the pathophysiology of ASCVD.

Well, this is not an ordinary article, this is a kind of "pinnacle" text later being used by decision takers and so on.

They are using very strong wording as for scientific parlance, to state the things mentioned by other people whose opinions could be argued due to any reason. 

There exista definitely not attributable to LDL cases of ASCVD, no doubts on this topic exist but when I tried to search what share LDL has in total cases I failed to find some good assessment. Actually I decided to go with the reverse way - to try to understand what coefficient in weighting models being used is attributable to it and in two steps found the article above. Do we reallly, really have some argument being even 10% strong to beat what they conclude?

 

 

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Hm, I read it, it is a criticism targeted at every possible place where there could be some weak point or an "interpretation flip" could be made by data representation and so on.

But I was asking rather - do we have data, in the amount of 10% of pro-ldl but contra? Not the methodological criticism but data? And a better theory to support it? Usually such a thing is critical enough for the proponents to stop ignoring it like cited "but we received no answer" and to work on expansion of the mainstream to include it. And during this work sometimes happens that the mainstream understanding is changed drastically.

Right now, from 2023 it does not look even close to this, pro-ldl researchers are filling hte gaps on their side and what is the progress from critics? Do they have even raw contra-theory instead of hundreds of small statements that nobody have time to struggle against.

For my intuition, when I see this type of criticism I remember tobacco history with the same tactical approach - "we don't know what causes cancer but definitely not smoking."

So if not ldl - what is the killer sequence for HoFH in their childhood and HeFH in their midages? Is this already covered with a strong data and strong theory being developed with satisfiable mechanistic explanation? So this core topic will weight enough to move away from all the other built on it arguing?

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Hm, it seems there is a thing that makes it harder to focus on the substancial area of the question. Like a way to sell the idea with catchy motto "zero risk" that is being used by "pro-ldl-lowering party" (Mccoy just re-used the wording flying around) and that is itself controversial because in an enormously complex environment like a living animal there are no math/philosophical abstractions like "zero", there are probabilities in [0:1]. And there are other types of ignition mechanisms that can power the same mechanics apoB uses (the same way as to grow a crystal in the supersaturated solution of something it is not mandatory to use the same molecule type to initiate the process).

Also since we are here not to coin the bulletproff theory about how the things really works but rather to focus on personal life-related strategies it would be imho better to understand what weight to put on ldl topic. Todd in another topic raised a question - if a person is otherwise healthy (I understand it as - has no well-known risk factors) - will it be at substancially higher risk just from ldl elevation?

That is something deeply entwined within other data from 99% of available materials, those who pay money for research are focusing on large groups, mass effect and so on, that is expected because they are targeting their goals and areas of interest/responsibility.

But for personal answers we need to have some weight coefficients behind the risk factors, "purified" from other risks.

Studies done by volunteers on themselves maybe will be useful but they will never reach the coverage wide enough to draw well-grounded conclusions (there will never be 300000 volunteers to cut out all possible modifiers).

 

Here are some things from hypertension perspective:

 

Risk of Myocardial Infarction
Attributable to Elevated Levels of
Total Cholesterol Among Hypertensives
Nicole L. Glazer, Nicholas L. Smith, Susan R. Heckbert,
Carine J.M. Doggen, Rozenn N. Lemaitre, and Bruce M. Psaty

Quote

Background: Although cholesterol is an important risk
factor for coronary heart disease (CHD) among hyperten-
sives, the burden of CHD among hypertensives that may be
due to elevated cholesterol has not been well documented.
This study aimed to estimate the proportion of incident myo-
cardial infarction (MI) among hypertensives that may be
attributable to elevated total cholesterol, and to investigate
how well the National Cholesterol Education Program Adult
Treatment Panel III (ATP III) classification method repre-
sents risk of MI among hypertensives.
Methods: A population-based, case-control study of pa-
tients aged 30 to 79 years enrolled in a health maintenance
organization, treated pharmacologically for hypertension, and
who were not using lipid-lowering medication. Cases were
diagnosed with an incident fatal or nonfatal MI between 1986
and 2000 (n   1535). Controls were randomly sampled and
frequency-matched to cases by sex, 10-year age category,
and year of event (n   3743). Subjects’ most recent total
cholesterol values were categorized according to ATP III
guidelines.
Results: Overall, 31% (95% confidence interval: 23–
39) of incident MIs among hypertensives could be ex-
plained by total cholesterol level above the optimal level
of 200 mg/dL. Among participants in the highest ATP III
risk stratum, 41% (95% confidence interval: 9–62) of the
incident MIs were attributable to total cholesterol levels
 160 mg/dL, but total cholesterol  200 mg/dL accounted
for the majority of these excess events.
Conclusions: The ATP III risk stratification ap-
proach improves detection of the CHD burden due to
elevated total cholesterol among hypertensives at high-
est risk. A strategy to improve cholesterol control in
hypertensive patients might prevent a substantial part of
the burden of morbidity and mortality from MI.
Am J
Hypertens 2005;18:759–766 © 2005 American Journal
of Hypertension, Ltd.
Key Words: Cholesterol, myocardial infarction, li-
poproteins, hypertension, coronary disease.

doi:10.1016/j.amjhyper.2004.12.015

They did it with pre-2000 data and this is good because lowers probabilities of skewness due to efficient lipid lowering drugs agenda.

They attribute TC >160 with majority of cases of >200 as 30% additional factor when HT is present.

 

Here is a kind of modern approach

https://www.nhlbi.nih.gov/news/2022/calculating-risks-heart-disease

->

https://academic.oup.com/clinchem/article/68/10/1302/6651094

As I understand in their model TC accounts for approx 10% as an independent factor but they do have HDL thus it could act as a proxy for bad lipid profile - ok, TC up to 20% iin the overall model could be a max.

 

I don't remember but in some similar tool from the end of 90ies TC was also 2-4 points in total 7-9 total weight model, thus the figures are comparable.

 

In other words - since the most people under the overnutrition pressure that seems will not change to better in the coming decades will not cut out all the modifiable risks and age is a 40%+ factor on its own (yes, discussable) then the big players / decision takers are going to eliminate an important part of the mechanism in those at the higher risk.

Those who are not - are left at the same position - they can't yet just buy lipid lowering drugs and use on their own and they will definitely will be able to do it in the coming years outside of the government regulations. If they will ever want to do so.

Keeping in mind that when "pro-lowering party" is using catchy persuasion techniques (older one "statins in the tap water" the current one "zero risk") they are doing it for something (not only because of money, inertia of the whole mankind also needs some tool to be changed) but they should not convince us per se - they just have to sell the idea and that is the way it works.

If somebody has better data on TC risk of its own (not FH cases because for the personal purposes of risk assessment of non-FH people this can not be used, it is not about mechanism discovery in such cases) please share, we will all benefit from it.

 

Br,

Igor

 

 

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13 hours ago, IgorF said:

But I was asking rather - do we have data, in the amount of 10% of pro-ldl but contra?

Hibernating bears can have extremely high cholesterol.  But unfortunately they lack insurance or capacity to pay for treatment so this isn't treated as an emergency with a massive effort to find a pharmacological solution to "Save the Bears!"

Brown Bears (Ursus arctos) Seem Resistant to Atherosclerosis ­Despite Highly Elevated Plasma Lipids during Hibernation and Active State

Edited by Todd Allen
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17 hours ago, Todd Allen said:

A Critical Review of the Consensus Statement from the European Atherosclerosis Society Consensus Panel 2017

While data I've seen generally seems to indicate that statins are beneficial to the average Joe who can't accept the idea of a dinner without a steak, Todd's link helps explain why IMO, the reasoned answer to mccoy's original question about healthy people using statins to manipulate their lipids should probably be "No."

From Todd's link: "recent pharmacological/biochemical studies, as summarized in this review and elsewhere, have revealed that atherosclerosis is caused by statins taken to lower LDL-C, as well as by warfarin and some types of vegetable fats and oils, in the absence of significantly elevated LDL-C levels. Thus, the promotion of statin treatment by the Statement is rather risky and we do not feel that the conclusions are justified for the prevention of ASCVD." 

Again, Attia already has had CVD issues, as has Dayspring. So, in their case there may be some confirmation bias in their dismissal of diet and in arguing for pharmaceuticals for healthy people, in addition to other factors (at least some of which are commercial).

Also, I may have mentioned it before, but in the third part of The Proof interview mccoy posted, Dayspring appears to attribute more importance to diet than I've ever heard him do before. Nevertheless, in part two he still repeats the bombastic nonsense that if you are genetically lucky, you can eat 20 eggs a day without any absorption. 

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1 hour ago, Todd Allen said:

Hibernating bears can have extremely high cholesterol. 

Sorry, this is not applicable to humans. Chole levels IMHO are "semi-rigorously" bound (cancelling out dietary modifiers to simplify it now) to RBCs and RBCs are strictly regulated within species by the optimal oxygen delivery capabilities requirements which are very different in different species (Daniel E. L. Promislow had an interesting article on it - "The Evolution of Mammalian Blood Parameters: Patterns and Their Interpretation" before he started his more famous Dog Aging project). Even better-studied lab models are not comparable to humans from chole topics perspective, many researchers mentioned that they are doing it biochemically different.

 

Also, when I digged for a famous Inuits on the topic of their "protected" status this was interesting to be found:

Low incidence of cardiovascular disease among the Inuit*/what is the evidence?
Peter Bjerregaard a,*, T. Kue Young b, Robert A. Hegele c

https://www.researchgate.net/publication/10943329_Low_incidence_of_cardiovascular_disease_among_the_Inuit_-_What_is_the_evidence

I know people like autors of chole sceptics manifesto will argue against but they are not credible in the area of discussion and obviously we can't replay the 50-80 years old studies, so I am just taking it as it is, probably trustworthy.

Thus - some heavy evidence is needed, not by me personally but by those thousands and thousands of researchers who are adding and adding bricks into the building of ldl studies. So they will start questioning the things they are being researching for the whole their lives and will be convinced to either expand their theory or rethink it. The same way it happened many times in science when evidence was heavy enough.

Br,

Igor

 

 

Edited by IgorF
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1 hour ago, IgorF said:

Sorry, this is not applicable to humans.

So you fervently believe the cholesterol rise in humans when fasting has no physiological relationship to that of hibernating mammals?  That in humans fasting destroys cardiovascular health because cholesterol can rise in obese diabetic humans and there is a correlation among that population between rising cholesterol and CVD risk?  These two things must be exactly equivalent because LDL-C moves in the same direction despite very notable differences in the lipoproteins and their cargos between fasted healthy people and obese diabetics with chronic hyperinsulinemia?  Did you know that gluconeogenesis provides substrate for increased cholesterol synthesis seen in fasting while at the same time in the fasted state there is down regulation of LDL receptors so both synthesis is increased and clearance decreases?  It certainly is amazing that mammals survived this double mistake of evolution without clever drugs to save them.

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3 hours ago, Ron Put said:



From Todd's link: "recent pharmacological/biochemical studies, as summarized in this review and elsewhere, have revealed that atherosclerosis is caused by statins taken to lower LDL-C, as well as by warfarin and some types of vegetable fats and oils, in the absence of significantly elevated LDL-C levels. Thus, the promotion of statin treatment by the Statement is rather risky and we do not feel that the conclusions are justified for the prevention of ASCVD." 

 

 

I'm sorry - but did you, Ron and Todd, even read that article past the abstract? The article does not deliver what it claims in the abstract.

 

The only article cited that makes any statement to that claim is:

https://www.tandfonline.com/doi/abs/10.1586/17512433.2015.1011125?journalCode=ierj20

It's an article by THE SAME AUTHORS. It's not a trial. It's not an analysis of an RCT or association study. It's purely in-vitro science - mechanistic evidence.

Generally these authors love to cite themselves to "prove" their strongest claims. But none of their self-references contain an analysis of clinical trials - it's all mechanistic evidence.

Their claim that none of the statin trials after 2004 showed a benefit in outcomes or mortality is just plain wrong. JUPITER (2008) and HOPE-3 (2016) were 2 major statin trials for Rosuvastatin and showed that early and aggressive LDL-lowering has a propotional benefit in lowering all-cause mortality and events.

Their only trial data that they try to spin as evidence against statins is from cohort studies. But as there are a range of factors that influence LDL (diet; sickness; genetics; LDL-medication because of prior heart attacks etc.) that's just not good data to proof anything about LDL - e.g. these studies almost never correct for pre-existing conditions.

 

In summary: this article is highly misleading - the claim in the abstract is almost a lie; depending how generous you are with your goodwill.

Edited by Guest
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57 minutes ago, Guest said:

I'm sorry - but did you, Ron and Todd, even read that article past the abstract?

Guest, you are correct, I did not read beyond the abstract. But my point is not the safety of statins.

My point is that while people who have abnormal lipids may benefit, some perhaps greatly, healthy people should rely on diet and lifestyle to maintain or optimize their health, not get on statins as Attia suggests.

For healthy subjects, unneeded pharmaceutical lipid lowering interventions, including statins, may cause unintended deleterious consequences. At least based on what I know of the currently available options.

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12 hours ago, Todd Allen said:

So you fervently believe the cholesterol rise in humans when fasting has no physiological relationship to that of hibernating mammals? 

I don't want to believe in anything, I need a research published that describes the mechanics of what happens. With calculation of probabilities, with times, with description of binding sites, with description of similarities in proteoglycans in bears and humans and so on. Also atherosclerosis statistics on bears is needed.

I understand that details will never be satisfiable enough but I have to have at least some, to conclude that we really can derive from bears existance the idea that ldl is so insignificant that the whole lipidology as it is known today makes no sense.

Is there something worse to read on this topic?

 

EDITED TO ADD:

I was surprised to chase exactly what I wanted to see in bears case, and yes, as expected they are different enough comparing to humans in this topic:

Vasculoprotective properties of plasma lipoproteins from brown bears (Ursus arctos)
Matteo Pedrelli,1,2,∗ Paolo Parini,1,3,4 Jonas Kindberg,5,6 Jon M. Arnemo,6,7 Ingemar Bjorkhem,1 Ulrika Aasa,8 Maria Westerståhl,9 Anna Walentinsson,2 Chiara Pavanello,10 Marta Turri,10 Laura Calabresi,10 Katariina Öörni,11 Gérman Camejo,1 Ole Fröbert,6,12 and Eva Hurt-Camejo1,2,∗

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8131316/

 

Quote

 

LDL binding to human arterial PGs

The binding of isolated LDL to human arterial PGs was measured ex vivo. Although CE and UC content in bear LDL is higher in winter than in summer (Table 1), Fig. 4A shows that the winter LDL binds significantly less to human arterial PGs. These differences were observed even when adjusting the values of binding of LDL to PGs for the amount of LDL-TC added to the wells (Fig. 4B). Interestingly, both the winter and summer LDL from the bears bound 5 to 10 times less to the arterial PGs than the human LDL tested in the same analytical runs (Fig. 4).

 

(bold is mine, IF)

 

I also need to mention that the ldl researchers were already puzzled which model to choose for deeper experimenting and pigs are the preferred models for the areas most close to humans, mice are the second line due to significant differences in many areas related to the ldl biochemistry.

(I cross-checked if I am fresh with the topic via "Atherosclerosis Methods and Protocols" Humana Press 2022, section "In Vivo Model Systems for Atherosclerosis Research" https://link.springer.com/protocol/10.1007/978-1-0716-1924-7_24 written by https://metabolism.uchicago.edu/program/faculty/godfrey-s-getz whose credibility on the area of research raises no questions)

 

Br,

Igor

 

ps:

Perhaps bears as an offtopic could be closed here, the focus of this topic is different.

Edited by IgorF
added some related bear data
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  • 2 weeks later...
On 6/28/2023 at 1:02 PM, Mike Lustgarten said:

 

Thanks for making the video, Mike.Of course, the correlation may be (and it more likely is) due to other factors, such as various mostly terminal diseases that in advanced stages result in lower cholesterol.

Or, it may be that many of those on the lower end are on high statin regimens, and side effects like increased blood sugar disregulation and possibly onset of diabetes contribute to their demise (Attia's followers who disregard diet in favor of farmaceuticals to keep Apo B low should be a bit weary of stuff like this).

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