They Were Wrong About Cholesterol?
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- Опубликовано: 27 сен 2024
- Become a patient: prevmedhealth.com
There is a big problem when talking about cardiovascular prevention, trying to encapsulate prevention into LDL and Apo B, even though can save a lot of people, it can still overlook many people with other cardiovascular risk factors, we discuss with Dave Feldman and Nick Norwitz the nuance behind lipids and heart disease
Want to know more about how I reversed my plaque:
• How I Cleaned Out My A...
See our latest discussion on LDL and Apo B: www.youtube.co...
Check out Dave Feldman's channel: / @realdavefeldman
Check out Nick's Channel: / @nicknorwitzphd
@nick love your take on nuance. Reminds me of an Albert Maysles quote.. "tyranny is the deliberate removal of nuance."
I’m a mathematician. I have studied thousands of peer reviewed medical studies. It’s obvious to me that at least half of the studies. Totally misinterpret the statistical laws that they claim to invoke. Anyone who says “the science says” is full of it. The quality of so-called peer review health studies is abominable. You might be interested in reading the recent study, entitled “why are all scientific studies wrong?”
The only way real progress is made is when people like Dr Brewer and his educated patients use a combination of the best science, the best common sense, and the best clinical practice.
Bravo! Science demands the checking/leaving of egos at the door of the lab. Otherwise, you’re not practicing the scientific method…period!
Outstanding comment! 👍
You are so correct. In peer reviewed studies the actual data is never read by the reviewers as most of the time they simply review the initial report. We only seem to find out the data said something totally different when a graduate student reviews the study for a report.
Attia has a financial background and they're the worst offenders of misapplying statistical laws.
They need to stop calling epidemiological studies as science. They need to be reffered to what they are “a study of associations” and why they are used “to generate hypothesis” so that later you have something to do real science with.
“No statistical correlation between LDL and plaque”. THANK. Finally we have adults in the room.
I'm one of those people who have high HDL (105), low triglycerides (40), and high LDL (168). According to Precision Health Reports I have no markers for Metabolic disease, and I am very insulin sensitive. I'm lean (BMI 20.2), fit at 67 years old, and I believe my high LDL is protective against all-cause mortality. Why would I want to lower my LDL cholesterol? or APO B which is a protein attached to my LDL cholesterol? The Lipid Theory has so many holes in it, it's laughable...like 73% of first heart attacks occurred in people with "normal" cholesterol levels, OR most of the FH population live normal lives, even longer lives if they make it to 65 or older. How is that possible if the Lipid Theory is correct? My favorite is the Minnesota Heart Study, done in 1973, and published 40 years later because the results were "inconvenient." This study found for every 1% you lowered cholesterol; you increased your risk of death by 1%. Seriously, we need to stop beating around the bush and call out this FRAUD that has been perpetrated on the public for 60 years! Then we can start to turn our attention to the true causes of Heart Disease - damage to the endothelial lining of the blood vessels and any defect in the process that the body uses to repair the damage (spoiler alert- it involves a blood clot).
Thank you David Feldman on your work with lean mass hyperresponders.
Thank you very much. Yes. Our patients typically know more about this than their original doctors.
Thanks Dr Brewer!
I live in the UK and started Keto 2 years ago. My total cholesterol rose from "normal" to 12.2 mmol. My doctor swore at me and ordered me to start taking statins. I refused, and challenged this, did my own research and started to ask questions. I asked if the NHS could tell me the partial size of my LDL, they could not. I asked them if they had a view on my HDL/triglycerides ratio, which was 0.1, they did not have a view on this The whole ordeal was very stressful and I found myself under a lot of pressure to change my diet and start taking drugs. I feel soooo good on a low carb diet, but feel under peer pressure to change. I very much welcome this research, I hope it makes its way into the mainstream, especially the NHS. ❤
Thank you for sharing that.
Well done you. Visited a UK Cardiologist a few days ago, his tool kit consisted primarily of statins, said they were now aiming to keep patients at an LDL of 1.4mmols (
I am 66 yrs old and in the exact situation. I reluctantly stated statin a couple of weeks ago as recommended by a neurologist due my mild memory issues (though my brain MRI is normal).
@@ThanhNguyen-wn5czYou started statins to improve memory? I have seen studies that indicate lower cholesterol is correlated with worse memory. If I were you, I would stop statins and start CoQ10, which is exactly what I did and my memory has improved.
@@catchristo9406 thank you, I absolutely understand you reaction :-) I do take CQ10.
As my blood test result showed high LDL, the specialist recommended statin, her reason was to prevent clogging brain (causing dementia)!
I started statin coz I was so scared of developing dementia but I have stopped and I am now at peace with the decision thanks to the recent findings.
I reversed type 2 diabetes under a keto diet. I felt the best I’d felt in my life. Even anxiety and depression seemed to basically disappear after years of dealing with it.. and despite significant life issues continuing. All poor bloods turned good.. except my LDL rocketed. I was 56 years old. I felt amazing. Everyone told me to start carbs again. Except my wonderful young progressive informed doctor .. who told me to stay the course because ‘high LDL has never killed anyone’. This is a HUGE issue. These guys might just change the world. Thank you. BTW I have nil calcium too just for interest.
As a child in in America during the 1960's I listened to the argument of fat is bad and looked to my grandparents ( farmers) and knew that bad fat is a lie! At 67 years old I can out work people in their 20's 😇
My grandfather was able to do the same. Then he died suddenly of atherosclerosis at 84
Thanks to Dr. Brewer and Dr. Nick Norwitz and Dave Feldman.
I'm a 61 year old LMHR. I have been on keto/ketovore WOE for 2 years. Zero CAC score plus no more fibromyalgia, IBS, or depression. Grateful for Dave and Nick for doing this and I support the Citizen Science Foundation as much as I can afford to.
Thanks to them, my doctor seems comfortable that I am healthy even though I have high LDL and total cholesterol.
Thank you for sharing that.
Waiting for heart attack???
@@leelajapheth4051waiting without fibromyalgia, IBS & depression. Sounds like someone got their life back.
@leelajapheth4051, you really need to open your eyes and think with a brain.
@@beardumaw24 I did.
Now it's your turn.
when you need a software engineer to create a trial to shine the light of truth on a decades old core controversy in medicine, it begs several critical questions.. the answers that logically follow (occam's razor) regarding the intentions of the major players in the medical system are terrifying in their ramifications.. my eyes are wide open, naive assumptions on who is trustworthy are crumbling,.. institutions that were once revered are now looked at in an entirely new light (verging on fear).. be very cautious, and do the due diligence on your health.. the truth is out there, just not where you previously thought it resided..
Afraid? Fearful?
Conspiracy?
Evil philosophy or religion.
Yes.
The government socialists with their medical industry lie and manipulate. It is and was all a lie and manipulation.
Look at covid excess deaths for another current example. See Dr J Campbell
Look at the cancer standard of care failure for another current example. See Dr T Seyfried.
Why?
Because the evil philosophy of the archons fights against the philosophy of liberty and freedom. See Tucker Carlson, everyone seems to know this, yet will not talk about it.
What if we were actually free?
SPQR; The Empire Never Ended. VALIS, PKD; creating Christ, J Valiant; Caesars Messiah, J Atwill.
It’s tragic really.
in addition, never ignore the role that the various "guidelines" play in funneling patients into the cattle chutes (eat your 200 grams of carbs daily, along with a max dose of metformin.. ignore the effect on insulin, thank you very much, it just muddies the water and is not covered by the am diab assoc) .. many professionals in denial that they are wearing "blinders" not unlike those on the poor horses pulling buggies on the highway.. necessary, lest some pesky practitioners start to wander too far off script.. commerce and the cookie-cutter assembly line have their imperatives.. a nightmare, and we haven't even mentioned "insurance"..
“It is difficult to get a man to understand something when his salary depends on his not understanding it.” Upton Sinclair
Outsiders are always needed. They are also called inventors, innovators, entrepreneurs. The status quo never challenges itself.
I think this is going to end up being groundbreaking - this will redefine what constitutes healthy metabolism. Huge!
unfortunately not, the establishment is going to ignore it and the masses will continue to follow.
It should, but will those who believe in the current scientific dogma let it go? How many will admit they were wrong / fooled?
@@lindabirmingham603 Ironic though - the "dogma" is not all that "scientific".
At 65 years of age and a LMHR I am happily living my life free from the spell of fear that Dr Attia has cast over his many devotees. All i know is that after enjoying a low carb lifestyle for the past 9 years and feeling super healthy and fit and with a 0 CAC score, this is all the proof I personally need that this is the right lifestyle for me, I am beyond grateful to Dave Feldman, Nick Norwitz and team for their superlative work and it is my hope that other experts in the field will use this groundbrreaking research as a catalyst for immediate discussion and questioning of conventional thought.
Thank you very much.
ME, TOO.@@PrevMedHealth
you should get a CCTA because its going to show soft plaque build up, if any.
Having a 0 CAC score means nothing without knowing your soft plaque status, calcified plaque is relatively stable, soft plaque is the one to worry about!! And " low carb " Does not necessarily prevent insulin resistance or guarantee insulin sensitivity! Also, everyone's " work " should be up for questioning!... I find it amazing that it doesn't seem to matter what diet religion people are shackled by, every one seems to be able to provide scientific data to support it!..... Like pulling rabbits out of hats!!
When n = 1, people should realize what works for 1 may not work for all or any. I’d be surprised if there weren’t others who benefited from diet X but no certainty.
I dropped Peter…no nuanced capabilities…it’s ironic given his recent “enlightenment “ regarding his personality issues. 🤷♀️ Science is a conundrum for strong egos…it demands the constant humbling in the face of new findings!
I could not agree more about the constant need to check egos at the door
I dropped him a long time ago
He just decided not to be keto because he said he "had children" huh?!
@@ninawildr4207I know, weird. That's exactly his excuse.
-bg4dw Same here
I've been on a no carbohydrate high fat/carnivore diet for two years. My BMI is 22 and since i found this video now know my phenotype. i'm a LMHR , my problem is that the VA administers health care via protocols. This diet has enabled me to enjoy the highest quality of life that food can provide. At 75 I would like to volunteer ....4 stents TOT CHO 315, LDL 226, HDL 72, TGL 87......
Yep. Looks like it. Come see us if you like -859-721-1414.
What about the glucose and A1c, I’m similar BMI except half of ldl, tgl 56, glucose 102, A1c 5.3. Just wondering where the glucose should be for an LHMR
Good question. The hospital only gave me my lipid panel, ..I don't imagine you're having any major metabolic issues with a BMI of 22... I just performed Dr. Brewer's home plaque test {ankle-arm systolic blood pressure ratio) fortunately, my ratios were close to his example...1.17 average..that was test for peripheral artery disease. The upside is Dr. Brewers numbers indicated a 57yo circulatory system. After my 'stent' with metabolic disease I immediately went keto/carnivore/intermittent fasting... OMAD @@dossegundos7145
I have 25-30 data points of my A1C and lipid data -since 2005. I was diabetic. I then went on a low carb healthy fat (keto) data and improved everything including being medication free. My analysis clearly shows a strong correlation between low carb diet and low A1C.
My doctors were skeptical but I proved them wrong. I stopped Lipitor for a few months and saw my ldl go up.
I plotted my ldl and A1C and found no link. The link between TG and A1C is very strong. Granted this is just a one person data.
My doctors became very adament and insisted that I should take Lipitor or risk heart attack. I tried to reason as to why ldl is not the best marker to focus but could not get my point across. I showed them my other excellent lipid numbers -high HDL and low TG. Could not budge them. In any case, I would love to look at your data if this publicly available. Let me know.
Have you had a CT Angiogram?
@@jan_ellison_baszucki I did calcium score to track my calcification -under control.
So just don't eat junk? Seems like we get improvements without being dogmatically against carbs.
He said low carb (keto)@@dallysinghson5569
Appears the root cause of CVD is insulin resistance and high insulin. At some point pancreas cannot produce high enough insulin. Insulin is inflammatory. Insulin can no longer keep triglycerides stuffed in the fat cells or cannot push more glucose in the muscle cells. Glucose rises. High glucose damages glycocalyx lining blood vessels.
Ascorbic acid (vitamin C) uptake is inhibited instantly by high glucose. Low Vitamin C causes bleeding. Cholesterol increases to patch the damaged vessel walls.
High insulin also negatively impacts Vitamin D pathway.
High cholesterol appears to be a symptom or repair mechanism , not causal for CVD.
Blood metric that correlates the best with CVD is Triglycerides/HDL ratio. (Not LDL)
Body measurement that correlates the best with insulin resistance is waist/height ratio. (Abdominal fat)
Some good points. Thank you. The proposed Lipid Energy model States that LDL is increasing to carry those triglycerides from the liver to the muscle cells (in forms like VLDL. You don’t see high Remnant cholesterol because the TG component is being split off & burned for fuel, leaving LDL & HDL).
@@PrevMedHealth
Yep.
Dave is awesome. I donated a little to help fund his study.
The LMHR’s, by definition, will have low Triglycerides/HDL ratio. My hypothesis is the LMHR will not be at higher risk for CVD. And it will be another clue that LDL is not causal.
If this is proven true, the statin sellers will be very upset. Billions of dollars in profits at risk.
As a person who has been brainwashed my entire life because I have “hereditary” high bad cholesterol and my Dad has been using a statin for more than 30 years. I can say I have always refused to take statins and I’m thankful for the studies being put forth. I am still working through the scared feelings but my LDL is at 180. My HDL is at 36 which is low, I am working to raise my HDL by various methods. I’ve been eating carnivore for 5 months lost 26 pounds and at 48 years old I’m so pleased with this result. I had blood work done about a week ago. I am having it done again in June. My doctor still keeps pushing me to statins, she is a vegan or vegetarian type who herself looks unhealthy to me. So she will never agree with how I’m treating my body because she seems to base her personal beliefs as a diagnosis vs actual practice. I think I need to seek a new doctor
I so appreciate this conversation. Love the honesty.
In 1973 the public embraced the lipid hypothesis. Beef, bacon and eggs, and butter were the villains. So everyone switched to Chiffon margarine. "It's not nice to fool mother nature" but it's also not nice to fool the public. Chiffon was nothing more than Hydrogenated oils. Today 50 years later the lipid hypothesis has become an intense debate.
Spoiler alert - Peter Attia is not actually a participating guest in this discussion. Glad this new info is getting in front of subscribers to this channel but I've already seen it a couple times now. Would love to see a response from some of the more hardline/mainstream longevity influencers like Dr. Attia at some point. I'm sure it hasn't escaped his notice. Great content!
Great discussion. Very interesting.
My wife and I having eating keto style diet for several years and feel all the better for it which we are reminded of when slip back to old eating habits. We both have moderately elevated HDL and LDL levels that our GP's raise with us but not yet talked about prescribing statins.
The data discussed here is encouraging I look forward to seeing the studies conclusions.
Hey guys. I am so excited about what you are doing. All my adult life, 40 yrs now, my cholesterol has been borderline high. I have maintained my weight in the 120s at 5'4" by controlling carbs (not counting pregnancy). In 2012, I started dropping carbs more, as my body was getting older, to control my weight. And the LDL has gone up and up and up. I am at ldl 258 hdl 78 tri 101 slightly off your cutoffs. I considered eating oreos for a couple of weeks before my last blood draw last week, but passed. :) I have refused the statins much to several doctors' chagrin.
I went keto in 2012-2014 and was so glad to see Dave come along. My labs made no sense and the goofy engineer taking pics of his hand next to his food was beautiful art to me.
Looking at the subject as an engineer, causal atherosclerosis would appear to be broken glycocalyx. If glycocalyx is intact and healthy nothing sticks to arteries. Which type of diet is the best for repairing the glycocalyx would be a research project to see if keto or vegetarian works best. Great work Dave and Nick and teams, keep it up, facinating!
There are some very interesting supplements that focus on the glycocalyx. The two that I take are arterosil hp & endocalyx pro.
Yep.
I had a Glycocheck in October of 22 with a health score of 2.8. That's pretty low according to them. Should be at least 6.
Have taken two cacs now and they were both at zero.
Have taken Endocaylx on and off for a year.
Will be doing a CIMT along with another Glycocheck near the end of January 2024, then off to the Metabolic Heath Summit in Florida. Live in WI!!!
The stuff is exciting, thank you Dr Brewer and Jesus for your excellent work and podcasts! Many excellent guests!
Also had a dexa scan with an A+ score. 0.7 visceral fat.
5.3 A1c.
Kraft insulin survey showed some insulin resistance.
@@paulbrown631 I will probably book myself a dexa scan next year as I seem to be good at collecting visceral fat. That said Keto reduced it drastically. Tried stomach vacuum exercise and previously stomach didnt retract at all! Now I can suck it in like a pro.
Amazing work! Causality of LDL/ApoB could still be there, except that LMHR and maybe metabolically healthy individuals might not develop soft plaque from it. Seems like such a small subset of modern population that it didn't show any signal in LDL causality studies. I'm myself 22 bmi endurance athlete, less than 10% body fat, 5.3% A1c, eat 0 saturated fat (WFPB), and have a 124 LDL, 133 LP(a), 85 apoB and it scares me. Tri 65, HDL 51. I had similar values 15 years ago eating a higher fat diet with 4 eggs a day.
Only true way to know is doing a CIMT or CT angiogram, but can't find were to do a CIMT in Quebec and the CT is super expensive here.
I suspect that sufficiency argument comes into play here. A study showing that no inflammation or other endothelial damage could cause atherosclerosis would need to be done to make a more definitive causality statement. Has such a study been done? If so, what is the mechanism?
You might like to look into Malcolm Kendrick's work. He wrote "The Clot Thickens" and reveals that heart disease/ atherosclerosis is caused by factors that damage the lining of the arteries, leading to clotting. The damage and clotting happens in where the pressure is higher, such as where arteries branch. The clotting keeps occurring, forming layers. I used to do medical autopsies and have seen this in coronary arteries and even more in the aorta where the arteries branch.
He explains how LP(a) has multiple functions in immunity and cellular repair. Perhaps it is the emergency responders and not the arsonist. He has some good RUclips videos as well. Also David Diamond has done some amazing work on the cholesterol heart disease hypothesis. He has peer reviewed papers and great videos out there.
I had fibromyalgia on a mostly plant based diet. Pretty sure it was the oxalates and my chocolate addiction. I have been ketovore for almost 2 years, have a zero coronary artery calcium score and feel better at 61 than I felt in my entire adult life.
Wishing you the best of health...
Is it normal to run these numbers on a regular basis in Canada? Or is it because of your sports involvement? I have to ask around, because as a "regular" American, I never had any of these blood tests done til relatively recently. I never even went in for routine check ups til my 50s. Really not sure how normal this is for folks in USA. Unfortunately , I never asked about my bloods beyond Dr saying they are Okay. In my 60s, I started asking to take a copy of test results. Now at 68, I have had my first A1c which is 5.5. concerning to me, but Dr doesn't address at all.
@@jellybeanvinkler4878 Yes, this is standard lipid panel they give us. However apoB and lp(a) are not standard, had to request them. A1c at 5.5 is fine. You can always pass a glucose stress test, that would be the real test about pre-diabetes, a1c misses a lot apparently.
When we overlay the Heart disease map of the US with the diabetes map, the southeastern US has a compelling match. The smoking map has an incredible correlation to the heart disease map that can't be ignored. Also the poverty map fits well. Last but not least Heart Disease has a tendency to follow air pollution maps on a world wide basis.
Diabetes, smoking, poverty and air pollution. Look closely as they are indeed related in that they all can cause vascular damage, triggering the heart disease process. For many areas on the heart disease map all 4 co-exist.
Lifestyle ties these risk factors together, and air pollution is smoking's first cousin. While dietary choices are vital, we must never dismiss the air we inhale into our lungs which ends up in our blood stream. The quality of that air is vital to our cardiovascular health.
Thank you. I'm a non-lean hyper responder. Thankfully I had a CTA with contrast year after starting low carb (score = 0) so I have a benchmark to compare a second CTA with. And no, I'm not on a statin, even though the cardio and GP want me on one. I'm metabolically healthy with a LDL of 300.
Lots of bro science out there. Also lots of anecdotal evidence. Mine is that I'm in my late 70s and had an angiogram which showed zero plaque. All this after a lifetime of very high cholesterol and triglycerides and no statins. I've been very active all my life so I put it down to this. So, who knows what the factors are ? My father was a non smoker who died of a heart attack at 62......but he was obese,had the dreaded metabolic syndrome and high suger levels in his blood. Also, the latest research from Sweden showed that high levels of LDL were related to LONGER life spans.
So, what is it, guys? And finally, why do smokers with "acceptable" levels of cholesterol get heart attacks?
Nicotine is a powerful vasoconstrictor 🤷🏻♀️
Had a 4-Hour conversation yesterday with a nurse practitioner and had to explain what the Kraft insulin survey is.
She couldn't believe that insulin responded quickly with glucose in a glucose load.
I had to basically use what I learned from Doctor Brewer to teach this nurse practitioner how insulin works😢
I thought maybe it was going crazy that I knew this and she didn't.?
That is too common.
A lot of medical professionals lean on their qualifications and really aren't well educated, they just did what they had to do to pass.
@@ryanwellington7493 50% of the doctors graduated in the bottom half of their class!!!
Thanks for doing this work and then explaining it so well. I fit the zero carb super high cholesterol profile. When I was heavy and eating sad, fast food and straight junk food. I had normal bloodwork.
Not that I only drink water and eat meat and eggs. I am going to have a heart attack my Dr. says. Less than 80g of protein per day, 250g-300g of fat.
They tested me after I ate bacon and eggs for breakfast.
Total 594
Tri 106
Hdl 108
Ldl 465
What is your BMI?
5'7" 175, 32" waist. I'm 10lbs overweight atm, Fairly heavy on build and muscle. @@parsonsenergy
I hear you after a double coronary bypass my cardiologist wants my ldl at lower than 1.8 I can’t take statins so he’s pushing the jab repatha l don’t want none of it. Last year l got my ldl to 3 without any drugs eating sensibly not much carbs but not keto. He was impressed but still insists on the Jab. I won’t be going back wasting my money talking to a brick wall.
I got older and found that my skin seemed to be getting thinner and I bruised easily. I experimented with my own food and started eating the opposite of what doctors have been recommending. I for many years. I ate lots of whole milk products and lots of marbled red meat. After a little more than a month, I noticed that my skin didn't bruise nearly as easily, and when my doctor did a blood test, she said..."Your cholesterol is perfect!"
Funny thing is that the "conservative" approach would have put the lower 50% of the people the graph (both cohorts) on statin therapy to lower cholesterol causing them absolutely no benefit considering the zero plaque they carry and who knows what harm from interference with the normal human metabolism. Who knows, what one big recommendation that studies like this show is that no one should be put on a statin until a scan like this positively indicates plaque buildup - similar to how we don't put people on diabetes medication because of the risk of getting diabetes until the blood tests show they have diabetes (or cancer or whatever)....
I don’t recommend statins until you have plaque. The AHA standards committee doesn’t either any more. Unfortunately most doctors aren't aware of that.
Prevention by risk management is fundamental to modern societies e.g. there are speed limits on vehicles, based on risk assessment, because it reduces accidents, injuries and death. Risk management improves long term outcomes. Same deal with cardiac events. We are beholden to intervene before plaque appears if it improves long term outcomes. We are beholden to use medication, for those it will probably help, if it improves outcomes. Tons of studies, and scores of experts, support pharmaceutical intervention before plaque appears. It's called prevention. The debate about the risks and the interventions is ongoing, as it should be. Science isn't perfect, sometimes it is wrong, but it is capable of correction and adaption. While it isn't perfect it's a long way ahead of what is in second place. Kudos to the Feldman team for tackling the risk issue, w.r.t hyper LDL in a subset of dieters, head on.
"An ounce of prevention is worth a pound of cure" Benjamin Franklin
Giving the LMHR study the benefit of the doubt, assuming that the cohort and methodology is valid and at follow up there is no significant plaque progression will not invalidate the current LH LIPID HYPOTHESIS or the prescribing of pharmaceuticals to reduce heart event risk, because , the current LH has changed to regard small dense LDL sdLDL as causative in atherosclerosis. It is likely the LMHR cohort will be found to have low sdLDL and hence low atherosclerosis progression. If this finding comes about it will strongly validate, rather than invalidate, the LH. At the same time it will do nothing to reassure us about other possible long term side effects of the profile.
e5087 I agree with you completely. Issue is that a lot of doctors are trained (or have trained themselves) to follow guidelines without question. This may be OK in an army when the general orders the charge of the light brigade, but may be questionable in the science context. A scientist should always be open to change regardless of what has been proven or observed before. And a lot of these risk factors for heart disease are correlated and not proven to be causative. As such, any one major factor should not be a trigger for prescribing drugs - especially if the trigger is misread. One of the biggest misreading is that of blood pressure. Ideal blood pressure measurement calls for making a patient relax in a dark room for at least 10 minutes before taking the blood pressure. Also, the tolerance to white coat syndrome should be calculated. I can say from personal experience that my doctor is ready to prescribe blood pressure medication without consideration of any other factors.
Why is cholesterol even considered a problem at? HDL lipid protein, travels around the body dropping of cholesterol. As it does the lipo protein shrinks in relation to how much cholesterol is left inside. It continues to shrink as it drops off the molecule. But why does it shrink? Why not stay the same size? I say its because it must shrink, to get into places the larger lipid cant get into. The cholesterol needs to get where its going to repair damage that is done. The damage cant be repaired without cholesterol. The lipid shrinks smaller and smaller to allow the cholesterol to reach areas HDL can not.
To use the fireman analogy, they have trucks to transport them to the fire. But the trucks cant enter most buildings, but the firemen can. They drag the hoses in and put out the fire from the inside. Just because we see firemen inside a building, doesn’t mean thats why the fire is there. The men are they to do a job. To bring to water to the fire. The trucks (HDL) cant get in but the firemen (LDL) can. They are not causing damage, just there after repairing the damage. Most likely the damage is being caused by other things like, Glucose, Insulin, Stressors of many kinds.
@@jsherrier1196 Have you viewed "The Clot Thickens" by Malcomb Kendrick? Do you know about immature progenitor endothelium cells manufactured in the bone marrow in response to glycocalyx and endothelium damage? How those cells circulate throughout the system and sense damage and attach themselves to cover over the blood clot with a new wall, isolating the damage and preventing a clot moving downstream? Are you aware LDL cannot enter any cell not having LDL receptors? How everything in the immediate vicinity of damage will end up on back side of the newly built endothelium wall? Any cholesterol found in the blood clot comes from the red blood cell walls that were damaged or covered over. Blood vessels, having a one-cell thick endothelium layer, cannot heal from below as your skin does. Healing comes from progenitor cells in the bloodstream. Blood clotting is the result of damage from any source, be it from the mechanical injury of high BP, or excess blood sugar and insulin, other hormones like cortisol in excess, smoking, air pollution, stress and anxiety, etc,etc, etc......The lipid theory of CVD is dying and new light is continually being shed on the series of events and causes leading to arterial damage and end results of stroke and heart attack.
Cholesterol is considered a problem because Seventh Day Adventists and processed food companies worked together to inject bias into "the science" to benefit themselves.
The Seventh Day Adventists literally believe they are "doing the Lord's work" in discouraging people from eating meat.
Processed food companies benefit by being able to sell more product the more cholesterol is demonized.
Cholesterol isn’t a problem. Nick will not come out and say it, but there is absolutely no need to monitor your cholesterol.
My biggest dilemma: which “scientific consensus” is more nefarious-high cholesterol causes heart disease, or human carbon dioxide emissions will cause catastrophic “climate change”.
@@stevedow9076 science has no consensus. Consensus is politics. Not science. Its strictly for the dumbasses
@@jsherrier1196 Academia is a leftist bubble where everyone follows the leftist herd. No actual science going on there.
I bet you got quadruple vaxxed and are still wearing a mask to avoid contracting COVID…
There is something confusing here.They keep calling LDL and HDl ,cholesterol.I was given to believe that that these two lipids are NOT cholesterol which I'd a very specific molecule.These two lipids are either markers of cholesterol or transporters of cholesterol they are not cholesterol per se.Why don't they say this instead of keep calling them cholesterol.Tell me I am wrong !.
FYI btw Cleveland Clinic is currently telling high BP patients to limit salt to forego bo meds! Somebody please explain to them that it's the insulin not the damn salt.
I am a text book example of this topic-no insulin resistance(glucose great insulin test excellent, bp 99/64, bmi 26.5, No fatty liver-alt/ast excellent, low vldl, low LPa, good tryglicerides 102, good HDL 70 ) BUT LDL 167 and ApoB 130. A preventative cardiologist didn’t care about any of the rest of my numbers but said “statin” which I ignored. My metabolic health is excellent my weight is good I eat whole food and I am a 67 year old woman who thinks she’s healthy if she can quit worrying about the ApoB/LDL. Really loved! the comment “ApoB is necessary but not sufficient for CVD”. Gonna hang my hat on those hopeful words for now. Thank you
Very good podcast focused on the truth behind ASCVD!
This issue is too often misrepresented as a dichotomy, as Dr Brewer did in the introduction: “is it LDL, or is it metabolic disease that drives ASCVD?” The dichotomy is false. Attia himself preaches incessantly about metabolic disease being “gasoline on the fire” of ASCVD. Of course it’s a driver-a very powerful one. And reversing metabolic disease in a patient may halt their plaque growth.
But it may not. I have several patients who, in spite of excellent metabolic health, grow plaque. The only way we’ve been able to stop it is to lower their apo B below a given threshold. Perhaps other interventions will prove useful in the future, but for now, apo B lowering works, and the evidence supports this approach.
The findings presented here add nuance, and I look forward to more. But they have not overturned the apo B theory. The danger in thinking it has is that some, like several who have commented here, assume that their high LDL is harmless. It may be, but it cannot be assumed. Get a CCTA (or CIMT, as Dr Brewer recommends) and look. You may not be the exception you think you are.
I’m 76. I started a keto diet with TRE about a year ago, currently fluctuate with low carb (about 40-50 net carbs per day). I lost about 40 lbs while on keto, my DXA scan showed optimal level of visceral fat (1.8 lbs), feel more energetic and clear-headed, lowered my fasting blood sugar and blood pressure, also my triglycerides have lowered, HDL has gone up but Total cholesterol is 296 and LDL is 205. They were within acceptable range before I lost weight. Basically, the LDL and total cholesterol are my only potential dangers for CVD/stroke. My doctor is upset with me because I have refused statins.
Have you tried taking Niacin?
Straight niacin at 500 mg at 4 x per day. A hot flush occurs every time. When I did that my HDL went from a stubborn 40-41 up to 75 ish and my ldl went down to a better number than it had been. My over 300 combined cholesterol went down to much lower two hundreds.
It might be worth an experiment. You might start off with 500 mg Niacin once a day to get used to it and see if anything budges. Then go to 2 times per day to get used to that, etc.
Where did I get 2000 mg from? A guy that did just that and got his cholesterol in line and avoided stents and such recommended by his doctor.
I have been off of it for a year or longer and my levels are bad again. I am going to start back up with one dose of 500 mg or two x 500 mg per day at first. I would like to see if that has an effect before going up to 2000 mg which I know will have a positive effect.
I had given up statins, Aldo. They were having no real effect on my cholesterol. The Niacin did.
The bottle must state “Niacin.”
No other kind will work.
If you do this I would be curious how it works out.
I would also like yo know how much Niacin that Dr. Ford uses.
Sounds interesting. I think it’s worth a try.
Wow Dave and Nick did raised the same point that I had in mind which is you have to be nuanced about the word 'causal' when you are talking about necessary conditions. Good job guys.
A savior for those with high LDL as the exclusive "bad" marker? Yes, this would be a game-changer. OMG
Thank you, all!
There is a swedish study where they followed 44000 above 65 years old for 35 years ! It seems everyone that reached 100 had higher cholesterol levels then the ones that did not reach 100. Plus if i do not remember wrong lower sugar values.
Your confusion between “than” and “then” makes me question your recall…
I would love to see the same diagrams with the participants sorted according to time on keto in the LMHR group and sorted according to age in the control group, to see whether time in relation to LDL level is important.
Also who has higher Lp(a) levels would be interesting.
I would as well. I think they are planning deeper analysis in this direction.
That peter attia was wrong about covid and wrong about the shot so this is not surprising. I like his consistency
The question I have is what’s the difference between a LMHR and a person with FH who is metabolically healthy? Are those with FH more prone to developing plaque and if they are why? If both phenotypes have a number of high LDL particles and they’re both healthy why does one develop plaque and the other doesn’t? There seems to be little discussion around LDL particle types like small, dense and oxidized particles which seem to be more inflammatory vs big fluffy ones that seem to be benign. Do people with FH have a genetic disorder where their livers can’t clear LDL particles or have faulty LDL receptors that also can’t clear the particles? And if this is so is plaque just to be expected because of this?
FH looks like it's bad LDL receptors whereas LMHR might be another mechanism where LDL-C are shuttled for some reason. Maybe FH causes inflammation and damage to arteries and not LMHR.
I think I recall Dr David Diamond saying many people with FH do not have heart attacks I believe he said the ones that do have a genetic predisposition to blood clotting
I suspect a couple of things: 1. These people are rare, since they require 2 unusual genetic variations in the same person; and 2. We have seen a few. Instead of their LDL reliably dropping when they reintroduce carbs, their LDL often remains high (> 180)
@@PrevMedHealth FH people?
According to Dr David Diamond and Dr Malcolm Kendrick, a subset of people with FH also have a gene that makes them overproduce fibrinogen - a clotting factor that produces fibrin clots.
Malcolm Kendrick wrote an excellent book "The Clot Thickens" explaining how atherosclerotic plaques are caused by various chemical, physical, or immune agents that damage the lining of the arteries in areas of higher pressure. The lining must be repaired instantly or you would bleed to death. Repeated insults cause layers of clots. Circulating stem cells form a new endothelium and cover over the clot(s) resulting in a layered appearance with clots under the lining. LDL's twin, LP(a), is one of the first responders to arrive and stabilize the clot. It becomes a part of the clot. matrix.
It was originally thought by Ansel Keys that the cholesterol in plaques was from dietary cholesterol. However, there is no free cholesterol in the blood. It is carried by lipoprotein submarines. The cholesterol in plaques was from the cholesterol- rich red blood cell membranes that were enmeshed in the clots.
You might underestimate the financial interests that are involved!?
How much are these influencers paid to promote the different drugs and the LDL/ApoB narrative?
The business in insulin, statins etc. is a multi 100 billion (perhaps trillion) business!
They will do EVERYTHING to protect their interests!
This is about “profitcare” NOT healthcare!
Take care!
Here is what I get paid to promote drugs. 0$
@@PrevMedHealth I believe you!
You would not say the things you say if you were paid!
I refer more to LDL centric influencers.
Loving this!
Keep up the good work!❤
Note in the chart at 39:00, on the right-hand side, mHeart data alone blows the LDL-CVD correlation out of the window.
Actually, CV event rates tend to do that as well. That’s why Paul Ridker & Gavin Blake started looking at CV inflammation 20 years ago.
this video is so rambling. in sure there is a point but its not well presented.
I agree.
Before 10,000 years ago it was no agriculture ppl just were eating meat, fish . Ppl didn't die of heart attack.
One of your best videos. Thank you.
Thank you very much.
Everyone should write their congressman and tell them we want this funded. If they can pay for russian treadmill cats they can pay for this!!!
That's a really good point! Thank you
The pharmaceutical companies might not like your idea seeing they are embedded in our 3 letter health agencies.
Why is there no discussion on HgbA1c or CRP levels and their response to IF and keto?
You have a great data -pre and post on both the control and treatment group. I am sure you have done this: You can incorporate both the time and cross-sectional elements into in one single regression analysis and look at the keto effect after controlling for all the confounding factors.
We are to Be Fede
It WAS the most ‘important’.. but that’s changing thanks to you all! And let’s not forget how much talk, press & funding is NOW behind Ozempic and the like…
Superb presentation. This goes to show that we must not let science morph into dogma and religion. Thank you all for asking the right questions and testing the theory.
ApoB is still just a good proxy for glycosylated and oxidized LDL particle level.
I think that is a practical view. I think of it as including VLDL & IDL (Remnant cholesterol)
@@PrevMedHealth My point is that if you reduce glycosylation and oxidation pressure with diet, ApoB value is less important, but what do you think?
I was put on a statin med because of my high cholesterol levels and high triglycerides. Side effects were many including looking like i was 5 months pregnant. I was switched to another statin and got inflammation of the liver and if touched was painful. I decided to stop statins. Not for me.
Thank you for sharing.
Maybe I missed something here but Peter advocates lowering ldl-p not ldl-c, your audience might not understand the difference
You have a good point about LDL-C vs LDL-p. & I’m sure that there are some out there missing that point. But to me this is a different issue; causation vs correlation. If it’s causation, then most feel justified if taking lipid-lowering drugs that they are doing the key things for prevention. It's harder than that; it's managing metabolism. Statins & other lipid-lowering agents may be important, but not the key to remaining healthy.
Most of us here, do get the difference. What’s ironic with Peter is, I found him from his TED talk, way back in 2013, wherein he was humbled by a diabetes diagnosis! Recently he had very open discussions with both Huberman and de Lauer, regarding working through his own mental health issues. That’s why his condescension and stubbornness is untenable…like I said, true scientists leave ego at the door when entering a lab or a discussion!
I agree. Dr Attia is not discounting LDL he is saying that since APO-b100 is attached to non-hdl, it is the best metric for atherosclerosis. Trust Attia more than what is being said here.
@@TracingRobots Attia has said that high ApoB is causative to atherosclerosis. But the LMHR study, under the lens/context of metabolic health and being insulin sensitive, throws that claim out entirely.
@@jsherrier1196 So, ASCVD stems from arterial plaque accumulation and encompasses conditions such as Coronary Heart Disease (CHD), encompassing myocardial infarction, angina, and coronary artery stenosis. This perspective focuses on individuals exhibiting metabolic health and insulin sensitivity. While I refrain from relying solely on a single study, considering the prevailing beliefs regarding LDL and its purported causality, this study's outcomes diverge from the anticipated narrative. If this hypothesis were true, the evidence would unequivocally support it, yet the study's findings present a different scenario. Regarding the comment on smokers, isolated incidents contrast starkly with the substantial presentation observed in this cohort of 80 individuals. Within this context, the observed association appears relatively feeble.
There's so much conflicting information about cholesterol and statin use that as an average patient you do not know what to believe anymore.
Peter is pro statin isn’t he?
@@jsherrier1196 err no thats incorrect!
Peter Attia clearly states in his book that metabolic disease, as in insulin resistance, ... is one of the main risk drivers for heart risk. So I think he is quite nuanced in his messaging. You just cherry picked one small part from an interview where he talks about ApoB as ALSO being one of the main drivers of risk.
Has line of inquiry factored in those who have high levels of LP(a)?
I have not see that included yet
My favourite part of this clip was the Gozney pizza oven advert halfway through and about ten tasty looking deep pan bases all steaming hot. Pizza releases all my happy neurotransmitters such that I'll never calcify
It's odd to think the creator made a molecular that was "bad".
Are we looking at foreign particles that create arterial wall inflammation from leaky gut?
Yes but not necessarily from leaky gut. High blood sugar is VERY inflammatory, and simply eating a high carb diet is sufficient to cause atherosclerosis. Other causes of inflammation are smoking, breathing in diesel fumes, heavy metals.. and so on. They all damage the endothelium.
@@jerome4276 I understand, but the toxic leakage causes irritation
@@MrRONFULLERif it causes irritation then it causes inflammation. It’s a popular belief in complimentary medicine that autoimmune disorders are caused by leaky gut. Notable is that a number of autoimmune disorders are associated with cardiovascular disease. As well, it goes along with seeing elevated CRP (c-reactive protein) as it goes hand in hand with autoimmune. CRP is an inflammatory marker.
I'm 62, reasonably fit, I don't fanatically watch my diet, I have historically had high cholesterol, on average 230. Triglyceride numbers usually in a good range. Over the past 10 years I've had two Cardiac Calcium Scans which were both zero. And last month had a CTA Scan and it was zero. At my age and historic high cholesterol I would have expected some calcification.
The fact is, doctors don't really know what is the PROCESS of atherosclerosis, what part each substance plays and most importantly WHY cholesterol cumulates in some arteries, HOW that starts and WHAT is the process. All the data doctors have is statistical, not medical.
Its like you do a statistic on car accidents and, if most car accidents happen with red cars, then red cars are more dangerous than other colors, and so if people stopped driving red cars there would be much less accidents. But why, what has the color of cars to do with the risk of accident? To answer this you have to know WHY most accidents happen with red cars....
@@Cobalt1520 Totally agree!
230 is not high. I'd say it's normal at 62. When it goes over 300 than the problems start.
And the lied about statins too.
This was a great video. It was just a pity we could not hear Ford clearly at times.
Just my opinion, but I think the REAL NORMAL range for cholesterol is 200 to 300. The problem with that range is it doesn't make big bucks. I believe that financial conflict of interest is why the published range today is so low. 200-300 was considered normal in the 1970's while heart disease death rates declined at a nice rate in the US and statins did not exist.
No medication or supplement will ever much lifestyle.
@@PrevMedHealth 100% agreed. I have lived in places where death rates are the lowest, and now living where death rates are the highest. Huge difference in lifestyle.
This is a fascinating look at a very specific group (the lmhr). I would be very interested to know what drives their ldl-c changes so dramatically. And am I right in thinking that this group doesn’t seem to be representative of the general population or even the general population on keto?? Is there something specific about them or their specific brand of keto that is protective? Obviously your data throws a spanner into the ldl causation hypothesis, but just wondering how else this group differs. Also, although you site that “in neither group does LDL cholesterol associate with plaque”, while true for the subgroups you looked at, (small numbers compared to the whole cohort), if you look at the Miami Heart Study data from 2022, in the whole cohort studied to date, they found “high LDL-C levels were associated with 48% to 52% higher adjusted odds of having the study outcomes”.
Everyone in this conversation already knows the background, so they tend to jump in at the middle of the story (Dave’s slide on LMHR not equal to FH) rather than setting up the research problem and the research question. Let’s back up and see if we can lay it out together.
Background: LDL cholesterol has long been associated with cardiovascular disease (CVD) risk. Great effort has been put into measurement and management to lower LDL. Studies of association have been mixed, with some indicating that the risk is due more to the size of individual LDL particles. Either way, this still comes down to “high LDL indicates probable disease onset and progression and should be lowered.”
Additional background: Adopting a ketogenic diet has been shown to have wide ranging health benefits both on disease and competitive athletic performance. Improvements are observed in redox status, inflammatory function, liver function, kidney function, pancreatic function, intestinal epithelial cell function, neurological function, retinal microvascular function, and more. All of this occurs in the context of sustained euglycemic euinsulinemia (stable, normal blood sugar causing stable, normal insulin levels) thanks to the near or complete exclusion of dietary sugars (carbohydrate). For many individuals who have adopted a ketogenic style of nutrition, the benefits have been life changing: for Crohn’s, for epilepsy, for Type 1 and Type 2 diabetes, for chronic kidney disease, for non-alcoholic fatty liver disease, and so many more, patients have achieved benefits far beyond any other therapy they have tried, with no negative side effects.
Problem: Certain individuals who have adopted keto, in spite of the many metabolic benefits that they enjoy, experience a large increase in LDL cholesterol. The question, then, is this: is it possible that the high LDL is somehow part of the overall metabolic improvements observed in ketogenic nutrition? Or is it instead the case that for these people, like everyone else, the high LDL is a valid indicator of CVD onset and progression?
The researchers are undertaking a series of trials to see if they can begin to sort out the answer.
How are these keto-high-LDL people different from others and similar to each other? It turns out they are quite distinct. They have more or less normal LDL on a standard diet. The LDL goes up specifically on keto. Second, keto drives their triglycerides very low (under 80) AND drives their HDL up (over 70, if I recall). Finally, people with this pattern (what Dave calls “the Triad”) also tend to have normal to low body fat.
The studies and the results on these people ONLY apply to people who share exactly these criteria: sustained ketogenic (not just low carb) diet for at least one year, high LDL, low triglycerides, high HDL, normal/low body fat.
“Yeah, but what if I have low HDL?” This study doesn’t apply to you, or to any other exceptions. We will need work on other metabolic profiles in order to address different types of people, so the focus now is strictly on people with keto+high LDL+high HDL+low TG+moderate to low BMI.
Is this group representative of the general population? Not at all. Only a percentage are keto, to begin with. What we DON’T know is what percentage of the population would fit this target profile if everyone were to go keto and reach a normal weight. That’s purely hypothetical, but helps give you an idea of the fact that this pattern might develop only among a few people or might develop across a wide swath of the entire population… we have no way of knowing.
Why do a study on a pattern observed in a few people? If a person has type 2 diabetes, say, and they go keto, and the diabetes goes away but the LDL goes up, we need to know whether that person is at risk from the high LDL or if they are not at risk.
There is also the possibility that the analysis of this group of people may reveal important new understandings of the underlying metabolism of lipids and the conditions under which that metabolism is either safe/beneficial or risky/pathological. That’s a much bigger question, though, than the current work can resolve. But it’s another good reason to continue this exploration in a systematic way.
I hope this helps clarify the background and objectives of the work. If anyone has any added clarifying remarks or corrections, please chime in. My goal, as always, is to figure out how to explain this to practitioners and students.
❤
@@ketolomics ❤ thanks very much, even though I didn’t pose the question directly, I absolutely love and benefited from your explanation 👍🏽.
I am Ketovore and have been for 8 months now. Lost 5" and 35 lbs. My LDL is very high and my Coronary Artery Score I had taken this month is ZERO. Carotid ultrasound showed slight soft plaque with low risk. So, I'm not so sure LDL is related to atherosclerosis either.
Ivor/ Cummins
Please compare Kraft insulin Assay Test with LDL in LMHR
What about cholesterol and stroke? After a cryptogenic stroke (no cause stroke probably linked to a PFO in the heart) my doctor ordered me a statin, having a TC on 220. I refused. I've now just got another drug called Ezetimibe which works differently than a statin, not addressing the receptors on the liver but instead inhibiting the smaller intestines from taking up cholesterol. Any thoughts? The next thing is that experts often talk only about CVD and seldom or ever about cholesterol and stroke. Do I need to lower my 220 mg/dl after a stroke, even if it is a cryptogenic stroke with no strong connection to the "usual" risk factors? Please, all of you reading this, feel free to share your thoughts! (I have never smoked, or fancied alcohol. Never had high blood pressure, no diabetes, and normal glucose levels. 55 years old but a few kilos too heavy but nothing exceptional 95 kg/180 cm).
A simple analogy: cars cause highway accidents as apoB does ASCVD (52:30). That can be proven by correlation and intervention.
the problem with this discussion is that it is extremely narrow. being focused on a strict definition of lean mass hyper-responders makes the information non-generalizable and therefore not that useful. what percentage of carnivores do not quite make it into the definition? the implication of the discussion is that there are two well-defined categories. there is a large apparent risk gap between lean mass hyper-responders and almost lean mass near hyper-responders. I speculate that the almost group represents a much higher percentage of carnivores than LMHR.
Consider: T = 139, so more than 70, HDL = 77, so less than 80, BMI = 25, LDL = 390, ApoB = 240. Zero carb induced. No FH. And no IR, though plenty ApoB, so not causal.
Logically that makes sense. But there are a couple of generalizable points. For example, if it’s not LDL or ApoB causing the damage, what is it? That leads to the biggest point. (maybe it's lifestyle, not drugs)
My LDLs are 292. Everything else looks good. The doc wants me on statins and I’m trying some lifestyle changes first. Have not done an ApoB test yet but my fasting remnant cholesterol is 27. Calcium scan is zero. I am 62 years old.
My husband has high Triglycerides too. He had a Tia & triple bypass 4 years ago.
Read the book body science by Dave champion it may help you out a lot also check out the book Lies my doctor told me by Ken D Berry MD and his book and his other book Common Sense labs
From my experience, triglycerides are much "easier" to lower than cholesterol.
I managed to lower it to half in just 6 months just by doing exercise (half hour of aerobic exercise 4x/week, with 3x/week of weight training most times in the same workout session), stopped eating cakes, cookies and sweets. I wasn't overweight. I don't know if your husband is able to exercise everyday or if it is advisable to do so, but if he can do walks, everyday, and cut the sugar as much as possible, I think it would make a huge difference.
Cholesterol, however, didn't change.
I knew someone with a blue car who needed a triple bypass. Hence, all my cars are red.
Nicholas says that the hyper responders have a marker that is a necessary risk factor risk marker for cardiovascular disease, namely the "Bad cholesterol" well who has proven that it's actually a marker for heart disease? People are worried because the levels are high. but yet these people are metabolically healthy. Because, the marker is not actually a marker for heart disease. the only people saying that is are the people fighting this study. The Peter Attia's. he would look at those markers, and assume that because the markers are high its proof that the person is unhealthy beucause he has high levels of "bad cholesterol"
He then says that when they hyper lean mass responders go to a doctor and the doctor does a double take and see numbers that high and say "this can't be real" so the risk question is distinct "based on the evidence available at the time I think its a reasonable thing to say or assume these people would be at very high risk" Why would that be a reasonable thing to assume? unless your assumption is that "bad cholesterol" is in fact a marker for athersclerosis.
it does no good to have people fighting to change this paradigm cede the point that some high cholesterol is a marker for heart disease when they say "no one is saying cholesterol plays no role in heart disease" Well what role does it play? what study proved this? was it controlled experiment or was it associated causally? Cede no points. Force the people who say cholesterol has some link to heart to disease to show you which study PROVED that there was an associated link between cholesterol and atherosclerosis. that's assumed but is has never been proven. and the reason its so hard to question this this beuase because refer to the science and say it PROVED the link between cholesterol and heart disease. it never did.
if people with this high level of cholesterol are not at risk of heart disease then it stands to reason that ppl with lower levels of choleseterol also are not at risk. so then why say " No is saying cholesterol plays not role in heart disease" Unless you force people who are saying that it does to prove that it does you are ceding the point to them. why would you do that?
I think you bring up good points & agree with many of them. I think Nick’s being more than gracious in terms of debate. However, there is a real point here; for most people, I think high LDL actually is a biomarker for failing carb metabolism. It's just the LMHR individual reacts in the opposite direction.
Thank you for your important videoS. I wonder if you ever spoke about this article "A Review of Mechanisms on the Beneficial Effect of Exercise on Atherosclerosis" which pretends alLowing plaque regression . And if you made a video about exerciSe effects on atheroma ? I wish you the best end of year vacations !
Why don't you debate Peter Attia if you don't agree.
And Nick: the Buddha was quoted as saying “Question EVERYTHING! Even if you heard it from me”
We already know that high cholesterol/ApoB are not necessary for coronary artery disease; heart attacks occur in people with 'optimal' cholesterol levels. This research indicates that high LDL may not be sufficient (by itself) to cause CAD, at least in certain populations.
This indicates that more research is needed. Statins have too many side effects to be doled out to people that won't benefit.
Let me run this past you. I speculate that the foundational problem is some kind of liver problem, either caused by genetics or diet. The liver processes lipids. If the liver is damaged, even if the numbers indicate it is normal, it may not have the capacity to process lipids, letting some go through that are atherogenic.
So quick question, isn't the fundamental premise...looking for the exception to disprove the rule. The analogy I would have is finding the people that smoked for decades but don't have lung cancer as evidence that smoking doesn't cause lung cancer? That premise seems flawed to me...
AM I missing something, LMHR are the heart of this debate? what about Joe plumber with a belly, how does any of this help the guy like me survive his next heart attack other than to prove keto is the way to suspend maybe increased plaque buildup?
I think it would be good to consider the next step to take people who are LMHR and have cardiovascular disease w low carb diet to track their disease progression....an also consider my offer to discuss an important missing piece to the cause of heart disease.
I am 50 years old. Slim/athletic. Eat healthy, mostly low carb, high fats (butter, tallow, olive extra, coconut), high protein. Regular exercise.
Latest lab results show very high cholesterol and LDL.
From what I understand, if the glucose and insulin is good, then the cholesterol is not an issue.
My recent fasting blood work results:
Total cholesterol 266
LDL 160
ApoB 133
HDL 93
Triglycerides, 67
Triglycerides to HDL ratio 0.76
A1C 5.7
Fasting glucose, 99 or 5.6 (I exercised before the blood extraction, and I think I got a higher reading due to this)
Insulin 4.8
Insulin index 1.19 (Homa IR)
My Doc freaked out on the LDL.
I was ok with the high LDL but the ApoB is high too.
Should I be focusing on cutting saturated fats? or reducing sugars/carbs further?
I’m in a dillema!
So .. why look at BMI... What about body fat percentage?
I did not understand the perspective. Can someone provide simplified summary to this discussion?
Think you need to listen to Malcolm Kendrick and Paul Mason. The Clot Thickens
Honest Question: You are focused on LMHR as I've seen in other videos of yours and I understand your hypothesis there. But you also show in this video no relationship in the MIHeart cohort between LDL-C and plaque. Do you believe this is accurate and can be generalized? Curious whether you reject LDL-C as a marker in all populations vs LMHR, and if it matters for non-LMHR then why is there no relationship with plaque in your data set? If you are arguing that LMHR deserve special recognition it seems your argument would be stronger if the LDL-C-> plaque relationship was different for that group than for MiHeart. Not an expert so maybe I'm missing something here - thanks!
Thanks for your interest. With the LMHR LDL value 1000X the average, having the same level of cv plaque makes the relationship 1/1,000x.
Thank you for replying! I think my question was poorly phrased. Is there a relationship between LDL-C and plaque in non-LMHR? Your data say no. But if LDL-C does matter for ASCVD, then logically either plaque doesn't matter for ASCVD, or your assay is poor at measuring plaque. I'm not asking about LMHR here but about the MiHeart cohort. I don't see any other logical options but that (a) LDL-C doesn't matter or (b) plaque doesn't matter or (c) your assay does a poor job measuring plaque. Which is it?@@PrevMedHealth
Thanks for fighting city hall guys. That chart is very interesting. LMHR, maybe we will finally get a handle on this puzzle.
I don't think it is a puzzle. The answers are in the science archives and have been for sometime. It's just that no one connected the dots.
That is the point. Last time he claimed the significance about the drug that lower CVD, that significance was 2% absolute risk reduction with 80%(wow) percent of relative RR. Being on some sort of strong and expensive drugs the whole life just to opt in 2%? That is the personal choice
How can dietary fat cause insulin resistance when it doesn’t induce an insulin response
Good question! Doesn't make any scientific or medical sense. The only possible way I see, is if a person consumes far more fat than the body can use, then it will be converted to sugar which then changes to body fat for storage. Makes sense why you should not overeat anything, and do intermittent fasting on a regular basis, then the body is not converting the fat to sugars. But I'm not a doctor, but I did stay at a Holiday Inn last night!
@@marksmith4627 Fasting combined with carnivore is definitely the way to go…in my humble opinion.
Did you measure the Apo(B) or lipo (A)?
How do the LDL and HDL fats react to anti-oxidants in test tube? What does it take to break down oxidized fat in the body? There is so much blather about hardening of the arteries on the inet.