Peter Attia on the INSANE Longevity Benefits of Low ApoB (how to lower ApoB with diet)
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- Опубліковано 7 лют 2025
- For reducing cardiovascular disease risk, Peter Attia recommends keeping ApoB (Apolipoprotein B) as low as possible. His argument? ApoB directly causes atherosclerosis. It makes no sense to "manage risk". Instead, eliminate it. In this video, expect to learn:
• How to lower ApoB with diet
• Why ApoB increases with age
• If there's an ApoB level low enough where it's impossible to develop atherosclerosis
• The ApoB levels babies are born with (and why there's no negative consequences of low levels)
• Saturated fat's effect on ApoB
• Why most species don't even have ApoB
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@@living4adrenaline
absolutely
- signed
Charles Darwin
She always looks miserable.
Here are some key bullet points and suggestions from the video:
- ApoB levels rise with age likely due to decreased LDL receptor clearance, not increased synthesis. Evolutionarily we make more than needed.
- Reference ranges for ApoB are based on population distributions, not health risk. We should ignore these.
- ApoB is causally linked to atherosclerosis. Like smoking and lung cancer, it should be eliminated entirely rather than managed.
- Children have ApoB levels below 20 mg/dL, showing low levels are safe and physiologic. Levels below 30 mg/dL may halt atherosclerosis.
- Consider lifetime ApoB exposure ("area under the curve"), not just current levels. Lower for longer is best.
- Other major causal CVD factors are insulin resistance, hypertension, smoking. Control those too.
- To lower ApoB through diet:
- Reduce insulin resistance by limiting carbohydrates, especially refined/starchy carbs
- Limit saturated fat quantity, as it increases cholesterol synthesis and reduces LDL receptors
- Individual response varies; monitor lipids on high fat diets. Avoid if ApoB/LDL increase markedly.
Suggestions:
- Get an ApoB test and aim for level below 30 mg/dL through diet and medication if needed
- Adopt very low carb diet to improve insulin sensitivity
- Limit saturated fat intake if needed to control ApoB levels
- Exercise, maintain normal BMI, don't smoke to control other CVD risk factors
- Re-test ApoB every 3-6 months and adjust diet/meds to keep levels very low lifelong
Hero
I'm gonna start following you! Love the summary. BTW, did Peter ever say what he considers his 'ok' range? (I realize other risk factors weigh in, but....)
Thank you
Great job! Even so, I will by watching thoroughly the video just to check if you missed something.
What meds are you referring to in order to control ApoB levels? Statins and other cholesterol lowering drugs? Something to keep in mind that wasn't mentioned in the video. That elevated LDL-C levels were inversely associated with all-cause mortality, and CV mortality was significantly higher in the lowest LDL-C quartile in older adults. Anyone care to reconcile those findings?
What a time to be alive!!! Information like this is FREE for everyone that has access to the internet
summary by Molly.cơm
00:03 ApoB reference ranges are population-based and don't reflect true risk levels
02:17 Eliminate causal factors for disease as soon as possible
04:30 Lowering ApoB may reduce the risk of atherosclerosis.
06:52 Aging process primarily impacts clearance level of ApoB.
08:51 Evolutionary prioritization of cholesterol production leads to high levels, but modern environment no longer requires it.
11:00 Maintaining ApoB level below 30 mg/dL may prevent atherosclerosis.
13:08 Maintaining low ApoB levels is crucial for longevity and health.
15:22 Lowering triglyceride levels is key to managing ApoB
17:28 Carbohydrate restriction is most effective for triglyceride reduction
19:34 Various individuals react differently to low carb, high fat diets.
You're the real MVP, thanks bro!!!
Thank you
Thank you!
thanks
Thanks
The contextual citing of literature on this channel is an excellent feature- thank you
epidemiological garbage literature.
Misrepresented but overly relied on bio marker reference ranges is a widespread issue that deserves more attention
A lot of it has to do with which measures were historically easiest to monitor. Until fairly recently cholesterol was a lot easier to measure.
My recent ApoB was the first one my clinician has ever ordered. They had to call a tech to add the test to their system. Hopefully, my requesting the test and being persistent will open accessibility for others in my community and help educate my Healthcare provider
Thanks for making sense and encouraging quality programs to prevent diseases BEFORE they ensue.
Great You Tube presentation. Reminds me of when Peter and Rhonda started putting out podcasts 4-5 years ago. Solid foundational information. Thank you!
I've been bugging my cardiologist about a ApoB test for 2 years. "We don't do that" is their response. I've been sandbagged by doctors my whole 62 year life.
You should be able to pay out of pocket at any local lab, right???
You have to pay for it yourself.
A lot of cardiologists are ignorant about apo-B impact. Find a new cardiologist
I have been treated pretty good by medical professionals up until Covid. Just before Covid I had a procedure at the VA hospital and they completely wrecked my health causing tremendous physical trauma! I am Caucasian with blue eyes so…….☠️
Yeah that’s most doctors straight up idiots
🎯 Key points for quick navigation:
00:00 *🧬 ApoB Reference Ranges*
- Reference ranges for ApoB are population-based.
- Labs set different thresholds for ApoB levels based on population distribution.
- Understanding the causality of ApoB is crucial in assessing cardiovascular disease risk.
05:03 *🧪 Factors Affecting ApoB Levels*
- ApoB levels rise with age.
- Aging impacts ApoB levels primarily at the clearance level.
- Evolutionary perspective on the necessity of ApoB for cholesterol transport.
11:00 *🍔 Influence of Diet on ApoB Levels*
- Triglyceride levels are directly related to ApoB burden.
- Carbohydrate restriction is effective in reducing triglycerides.
- Saturated fat consumption can impact cholesterol synthesis and LDL receptors.
Made with HARPA AI
Priceless. I've been appreciating these two for many years.
In the same way that i appreciate hemerrhoids
@@panflutetoth9395 Try more fibre and less straining when making poo poo.
@@kopers695 No, hemerrhoids disappeared when i went low carb. Almost zero fiber
Can we explain why those with lowest LDL have the highest all-cause mortality, and why those with higher LDL (not highest), have lowest all-cause mortality? If we're struggling to lower ApoB and it's about 80% the value of LDL, then we're talking lowering LDL. Yet that's part of our immune system and related to longevity. This seems contradictory.
Do a search. It’s been explained over and over again.
All interesting. My questions are as follows. Why not just avoid saturated fat via a mediterranean or plant-based diet? What's the downside, particularly for an endurance athlete of weekend warrior status? Certainly seems like plenty of upside. What about saturated fat inhibiting insulin sensitivity through cellular mechanisms?
Thing is they didn't mention the impact of Pufas and Mufas aka most plant and seed oils on Cholesterol, LDL and ApoB. And I'm guessing it's even worst than saturated fats.
My standard cholesterol panel (from Jan '25) is TC 121, LDL 76, HDL 52, TRI 40, TRI/HDL 0.8. My ApoB is 43. Mid-60s, fit and healthy, active every day. Zero prescription meds. I'm not carnivore/keto/fasting. Lots (10 plus portions of 80g) of fresh, whole fruit and veggies, almost no refined carbs. Lots (100g plus) of coarse-cut, wholegrain oats, almost no refined grains. Lots of oily fish, almost no meat. Lots of EVOO (70-80ml), almost no other fats/oils. Lots of eggs, healthy nuts/seeds, beans, full-fat dairy (Feta-type cheese, Greek yogurt). All fresh, good-quality ingredients prepared from scratch... zero fast food, ready meals/snacks, UPFs of any kind. This is a diet high in healthy carbs, high in healthy fats, and very high in fibre... a long, long way from the Standard American Diet.
To synthesize one molecule of cholesterol, a total of 36 ATP molecules are required. This energy is utilized throughout the various stages of cholesterol biosynthesis, including the condensation of acetyl-CoA to form mevalonate, the conversion of mevalonate to isopentenyl pyrophosphate, and the subsequent steps involving the formation of farnesyl pyrophosphate, squalene, and lanosterol.
Excellent 🎉 Information and explanation. Much appreciated!
There is a condition with extremely low ApoB, familial hypobetalipoproteinemia or even abetalipoproteinemia. Unfortunately these patients have some issues related to vitamin defficiency and some neurological symptoms. Even though, as a Cardiologist, I agree that most people should try to have the lowest possible ApoB levels, because it will protect against ASCVD development and they will never be that low as on that conditions.
I live in Toronto, and I asked my doctor to give me the apob test, I knew about it from Peter. I am 65 and have been consistently doing cardiovascular training, intervals, steady state, etc. 35 years, anyway, my Apob is 59. My doctor was shocked, and she tried to put me on a statin 10 years ago because my father died of heart disease at 56. He also smoked 2 packs of Pall Mall plain cigarettes and pot. I could help my doctor lose weight and get her much healthier. 😂
17:44 To that point, my triglycerides were at 0.9 mmol/l after 4 years of strict clean keto. When my doctor saw that, she told me that healthy levels were expected to be between 1.2 and 1.7 mmol/l with a big smile on her face. 👊
I would have liked to hear more about the dietary carbohydrate triglyceride connection
My trig levels dropped from 3.6 to 0.5 mmol/L on low carb diet. My Dr. was stunned...😮
Watch more of their interviews!
Info everywhere.
Love hearing “experts” give us their feelings on how things work👍
Notice that this conversation began under the context of "correlation" and immediately transferred into "causation." Who doesn't understand that these are not, and cannot be, the same things?
These people need to spend 10 minutes with Dr. Malcolm Kendrick.
There has to be a way of doing things without medications. Doctors have moral responsibility to prevent and show that they need to be respected
I’m glad he acknowledged and at least sort of emphasized that there are people who are sensitive to saturated fat. Yes there are genetic testings and I’m surprised he didn’t go into those specific genotypes because they’re known (I have one!). Recommending a keto diet to someone like this who’s ApoB and lipids go “haywire” is very dangerous so I’m glad he clarified this. When I tried keto back in 2018, still in my 30’s, my blood pressure was like 170/110 one day and when I reduce/abstain from saturated fat my blood pressure is 115/72.
Dr. Attia can you elaborate on how Lp(a) figures into this in terms of whether it contributes to ApoB or it’s a separate risk factor? It seems Lp(a) was also an evolutionary mechanism to help with wound healing, infection, etc. that is no longer needed… (yes, I have this one too!).
Whoa. I didnt know that about sat fat. I suspect i might be as well. I mean I've had that exact thought but figured, eh, prob not a thing.
the keto/carnivore world has tested this over and over, sat fat is not (usually) what makes their apob skyrocket, its carb restriction versus energy demand. Its weird that peter keeps saying sfa is the reason behind their whack lipids,
@@johnny7808 I appreciate your comment and I’m sure that’s what you’ve read and seen but, again that is dangerous advice that the keto community pushes IF one has the particular genotype that is sensitive to saturated fat. Other reasons to also avoid animal protein such as colorectal cancers.
@@enabl3r agreed if we're only talking about those with that gene, but peter's not. The presumptive keto narrative that both attia and dayspring push about sat fat is unfounded. They take known data that some genes predispose an ldl increase from sfa then leap to the assumption that the triple digit ldl increase by some keto people must therefore be due to that gene and their sfa intake. Nick Norwitz has researched this with actual cases, found attia/dayspring to be incorrect, but they refuse to engage with him because they are stuck on their narrative. This is not at all to say that high ldl on keto is good for you, its simply about not misrepresenting facts. Attia thinks he is the world's expert on every topic and its annoying despite being on-brand. He is simply not an expert on the low bmi keto people and is just way too cocky for his own good.
@@BT-dl8kq I agree I think it depends on your exact body and genetic make up. For me, I’m the best with fish. Then poultry esp chicken are fine and I can do just mostly white meat and no skin. I do the worst with beef and pork but noticeably worse with processed meats however even lean grass fed steak will still affect my resting BP if I eat it too often. Pork is in between for me. Eggs and a little dairy don’t seem to be an issue for me, maybe it’s cause they’re odd-chained saturated fats.
It would be extremely beneficial if a test or if a biomarker could be found to check ApoB levels over a previous amount of time, sort of like A1C.
However, if we look at the big picture, a mediterran diet is proven to be the best diet for longevity - over and over again. I've never seen a study in which the mediterran diet was not the winner.
Which Mediterranean diet?
@@stuwhite2337 are there different versions? Choose the most popular version then.
Some variants of a vegan diet appear to have similar or better health outcomes compared to certain variations of the Mediterranean diet when they are directly compared. Certainly the Mediterranean diet is mostly healthy, it is also one of the most studied diets and we don't have enough information to say with certainty if there is a single optimal diet for human health let alone if the Mediterranean diet is that specific diet. Limiting ultra processed foods and saturated fat in favor of vegetables, fruit, legumes, whole grains, and sources of unsaturated fat certainly is healthy and the Mediterranean diet does generally achieve this especially in the versions that appear to be the most healthy.
Be more specific please.
@@garethbaus5471 key word being appear
My cardiologist is virtual walking textbook. He says that if ApoB at 30 prevents CVD, then any reduction in ApoB should demonstrate some benefit. Yet, at his yearly cardiology conferences at which ApoB has been discussed for a decade, no one has data showing a relation between ApoB reduction and improved outcomes.
Nathan Pritikin warned about high triglyceride levels with respect to heart disease back in the late 1970s.
Pritikin had no medical background in anything so why takes his advice?
@@StanDupp6371 Your comment mirrors the medical profession’s reaction. Then and to this day. Did you see the 60 Minutes segment back in the 1970’s about his program?
He was proven correct in many of his conclusions.
Dr. Dean Ornish program is essentially the same. How to reverse heart disease.
@@Zane_Zaminsky None of them ever reversed anything in any human else they would have awards, honors or a Noble Prize and they have none except Pritikin died at 69 form his junk diet and Ornish Young wife of 48 has cancer from the Ornish junk diet. Ornish is not even a Cardiologist but a book salesman.
Sadly for Mr. Pritikin, his plant based very low fat diet did not protect him from cancer. Apparently his arteries looked good though.
Great video… 100% plant-based is a great road to go down for success in long life!
I'm Keto and watch my sat. fat intake because I'm a hyper-responder to dietary fat. Although my TG and HDL and VLDL are awesome, my LDL is > 300 and now I'm very concerned. I haven't had APO-B or CTA done, but CAC is zero. So, fixed insulin sensitive with Keto while at the same time increased CVD risk due to increased LDL.
Apparently, high LDL is meaningless in a LMHR. Go figure. But research it, don't just believe me.
Wiki says *Apolipoproteins are proteins that bind lipids (oil-soluble substances such as fats, cholesterol and fat soluble vitamins) to form lipoproteins. They transport lipids in blood, cerebrospinal fluid and lymph.*
And wiki says ....
*Apolipoprotein B is the primary apolipoprotein of chylomicrons, VLDL, Lp(a), IDL, and LDL particles (LDL-commonly known as "bad cholesterol" when in reference to both heart disease and vascular disease in general), which is responsible for carrying fat molecules (lipids), including cholesterol, around the body to all cells within all tissues. While all the functional roles of ApoB within the LDL (and all larger) particles remain somewhat unclear, it is the primary organizing protein (of the entire complex shell*
So, a very low tryglyceride (45) but a ApoB that is high, what then?
Me too. Looks like reduce saturated fat, see what happens. Then, drugs like Repatha. I'm just starting to look into this, haven't taken action yet.
47 year old male. Type 2 diabetic. Fit and very active. Don't smoke and I don't drink. Total cholesterol is 189, Triglycerides 97, HDL 52, LDL 118, non HDL 137.. Dr wants me to start microdosing Crestor at 5mg every other day. Why am I afraid to start the statin?! 😫
Crestor crushed me. Muscle and joint pain along with memory issues.
It's very interesting reading the comments from folks coming out CN, US or EU.
Apparently doctors in Brazil are much more flexible on having a broader blood screen test and a more preventive approach of medicine.
Socialized medicine doesn't work, but hyper private controlled one is also problematic.
In Brazil we have a mixed model.
Thank you this video clears up several questions I’ve had.
Having perfectionist tendencies reduces life expectancy by 7 to 9 years.
Really😢 I need to work on that if it's true, thanks for highlighting
@@reuelgreene8847 no, you don’t need to work on it, it was a joke.
I agree. My apoB is 120 and don't plan on doing a damned thing 😂
First world problems
@@gabymalembe well you caught me😅
I am not on the low LDL train at this point. I recently went low carb to see if I can lower triglycerides of 126 and ApoB of 104 down. Will have another NMR lipoprofile done as 12 years ago my LDL size was large but my LDL-P was high. A1c has been 5.0 for over a year, but I have atherosclerosis in my thoracic and abdominal aorta now. Will just have to see. 23andMe shows I have an rs5082 CC/GG gene abnormality as well, which apparently makes me more prone to obesity with saturated fats, so working on that as well. Apparently close to 50% of the population has this abnormality and I'm wondering if this may be why you have groups who are fine with saturated fats and others not so much. Personally, from everything I've learned over the past few months, I don't think an LDL below 70, let alone 30, is healthy.
I would love to see Peter Attia and Nicholas Norwitz discussing ApoB/LDL. (Nick is wating for you, Peter.)
definitely not going to happen, way way more downside than upside for attia
Attia wouldn’t want to be questioned
Major risk factors for atherosclerosis is metabolic dysfunction as well as exposure to environmental toxins such as smoking and air pollution. A recent study shows that 92% of the adult population has some metabolic dysfunction and the greater the degree of this dysfunction the greater is one’s risk for not only atherosclerosis but most of today’s chronic diseases such as obesity, diabetes, heart disease, many cancers, auto-immune disorders, and cognitive disorders including dementia and Alzheimer’s disease. Given that 60% of the modern diet is unhealthy ultra-processed foods this should not be surprising. Preliminary results of a presently ongoing study of metabolically healthy adults following a ketogenic diet has revealed that in this population even extremely high levels of ApoB particles and extremely high levels of LDL cholesterol are NOT correlated to atherosclerotic plaque progression.
Has anyone ever found a paper that shows elevated risk from high apoB in a setting of TGL/HDL less than 1.8?
I doubt it is there.
rationaloear; Has anyone had a high Apo B with TGL/HDL < 1.8 ??
Clip leaves me with questions.
First, there must be a selective advantage to our cholesterol transport system. It must be functional at least in ancestral environments. What could that be? Identifying functions might help us figure out what/when levels are a problem.
Second, what is the effect size on Apo-B and heart disease? What is the evidence for its causal effects? It was just asserted and not discussed. Given evidences that other predictors like LDL and total cholesterol have curvilinear effects on all cause mortality and that cholesterol is functional for humans, I suspect that Apo-b would also have a curvilinear effect on mortality.
Third, I'd be interested to see effects of Apo-B when other risk factors are in the equation--BP, blood sugar, CRP?
Fourth, I'm skeptical that saturated fat is causal for heart disease. Fat quality (e.g., omega 3 v. 6) is more likely the problem. We humans have clearly evolved to eat animal fat, so it doesn't make much sense that it would be a problem for us unless it has been corrupted (which it likely has by animals eating grains that they weren't evolved to eat)
High ApoB in the context of a lean mass hyper responder is not concerning at all. You have to look at it through 2 different lenses. If you are a carb burner, yes it MAY matter. If you are low carb or a fat burner, it carries no significant amount of risk. I know it goes against what Peter wrote in his book and he’s all in on the causality of apoB but he’s wrong. Not completely wrong but will need some re-tooling in the future when he finally recognizes LMHR. I don’t know why he’s so afraid to discuss with Nick Norwitz.
right
Is this some carnivore-era paul saladino bs ?
@@PaulRamen I think that Paul Saladino is an idiot. If you look at the LMHR study, most have high ApoB yet all little to no CVD and even regression. If you look at CVD in the lens of the standard American diet, yes ApoB can be causal. We need to differentiate between the two
@@markleblanc451long time it sounded strange to me but now I agree with the statement, that there are no human studies that inform on cause and effect i.e. on risk. Because it requires a well controlled experiment which doesn't exist.
Concerning the ApoB (this is a speculation on my side) I wouldn't say it is causal, I would say it could probably be a coefficient in a complex equation, but with the contribution like:
Risk of Death ~ ApoB*crappy_lifestyle + other_factors
So if one is on a SAD diet one presumably may get CVD faster if one's ApoB is high. What could possibly reduce variable crappy_lifestyle to zero is for another conversation :)
We have strayed soooooo far from what our ancestors ate (unprocessed food) And We didn't evolve...God fearfully and wonderfully made us.
17:41 Great retort to clarify for us all
My issue with massively crushing any number lower is that based on the history of medicine crushing any number or symptom especially with a medicine usually results in more death and problems not less.
Always remember it’s not about how long you live or longevity it’s about the quality of your life while you’re here.
can't it be both?
Would that not also be a similar philosophy to a heroin addict?
@@michaelkos8001 There's a balance... and a possible MI later in life, which doesn't need to result in death, possibly because someone chose to abstain from manufactured drugs, is not the same as being a life-long heroin addict.
I have healthy insulin sensitivity, low blood pressure, I'm super fit, I don't smoke and my triglycerides have always been optimal (below 1 mmol/L). And yet I have sky high ApoB (134 mg/dl last test).
My AppB is at 133. (My LDL 160)
All other markers are great. And I have done all the important ones.
I’m mostly keto and sat fat.
However I’m in a dilema about what to do regarding the LDL/apoB
Get on a statin - it isn't a dilemma
@@jimsturt thanks, but the potential side effects don’t look too good, not just that, but the studies used to justify statins have been adulterated somewhat by the manufacturers. if you look deeper and between the lines, the benefit of being on a statin is extremely marginal to say the least, and the side effects seem to outweigh the benefits. I will probably go down the diet route before any medication, and perhaps reduce saturated fats and be more strict on any sugars.
@@JayJay-un3rp nah you're being mislead by keto people. benefits may look marginal over 10 years, but how old are you? if you're 40 you need to compound than over 40 years. It becomes massively beneficial.
side effects are actually rare when you look at placebo controlled studies - but if you honestly do have them than you can get a PCSK9 inhibitor.
simply put, there should be no reason you let this stay the way it is. the science is not in question about how harmful high ldl/apob is
Don't EVER get on a fucking statin. They are 13:1 harmful vs helpful. They are USUALLY deadly. They reduce your ability to create cholesterol, which is the precursor to ALL of your hormones.
Most of the time, reducing your ability to produce cholesterol, therefore keeping your total cholesterol down, actually prevents hdl from recycling damaged ldl that causes heart disease. That makes sure that your ratio of deadly ldl vs good ldl goes very very bad and stays that way.
Maintain high total cholesterol. It will make your good to bad ldl ratios stay in the better side, just because the damage happens over time. The increased hdl will also recycle ldl at a much higher rate, further reducing harmful ldl.
@@JayJay-un3rp exactly! A metanalysis found the probability of potential benefits from taking statins are equal to the potential to develop diabetes. Lifestyle/diet changes to reduce oxidized LDL particles (as well decrease TG:HDL ratio) would be better than taking a statin - I am convinced.
You can't get a straight answer. Free radicles are the flame. Without free radicles, it's very hard for cholesterol to cause any harm unless your levels are extremely high for a long period of time.
I always listen to Peter Attia, but this clip strikes me as quizzical. Reduce insulin resistance by reducing carbs, but don't eat too much saturated fat..so low carb, low fat..how exactly do you power yourself through the day. I must be missing something here?
Low saturated fats, not low fat. So that means you can still eat lots of avocados and olive oil
Don't eat too much does not mean eliminate.
Yes the obvious answer is avoiding as much saturated fats as possible , and go vegan or vegetarian with a small amount of meat
@@Foxtrottangoabc Don't be ridiculous.
Vegan is thoroughly debunked.
@@fryertuck6496 alot of evidence , medical evidence that says its beneficial for the heart , cholesterol levels . Though granted it is hard to maintain , but the challenge of going vegan and doing a healthy varied vegan diet did get me eating a broader range of food which was good
I have PPAR Alpha C;G so my apoB goes crazy on keto as does my LDL-p. But all my other markers get better, TG go down and HDL goes up. So how do you figure which is worse? High apoB or High TG and Low HdL?
Since high apoB is causal of heart disease as well as high blood pressure, diabetes and smoking, it's definitely high ApoB that is the worse.
I wish Peter here and elsewhere got a little more specific about the actual types of foods - and the actual food, commonly consumed, that is bad for insulin resistance and increased saturated fat. He said “carbohydrates” but she had to clarify that he meant simple/processed carbs, not vegetables. This is important because the listener with think - oh so I shouldn’t eat ANY carbs, which is impossible and potentially terrible for you. So just say it- bread, crackers, processed food, beer, etc.
And for saturated fats- what food? Red Meat and dairy? Because it sure sounds like that’s what he’s saying without saying it.
He said no to starchy carbs.
My ApoB is 122. But I'm 50, an ultra runner, never smoked, eat super healthy. My LDL particle numbers are 3x off the high end though, but moderate LDL. Trying to find out if my ApoB is from poor recovery?
People in their 80s with APO B levels lower than 105 have a higher mortality. So perhaps the reason APO B rises as we get older is because we need more of it?
I have heard that also. I have also heard that reverse causality is the reason for that finding and that indeed the lower APO B is the better , which makes sense. But who really knows?
Thanks for the clip, Rhonda. A question: Are triglycerides and ApoB always proportional, unlike LDL-C and ApoB? (As we know, the relationship between LDLC and ApoB is not always proportional for about 20% of the population.) For example, one may have very low LDL-C but high ApoB. Based on what Peter Attia says, I'm assuming that a low triglyceride level would *always* mean a low ApoB level. Is that correct? Thanks for your precious time.
In the past, my total chol has gone up to 321 on a partially-raw beef, Carnivore diet and has come down to 180 on a Vegan diet (which is difficult for me to sustain).
Just curious. I don't know mine. Do u have decent muscle mass? (I'm not sure how you gauge that,) what's Ur body fat? (I bet body fat in pounds to muscle in pounds could be a useful number to know) do you do enough zone 2 training? Is cholesterol a fuel source? (Is that what ApoB is? Cholesterol in blood? (It would be great if could up muscle mass and cardio and suddenly the muscles just soak it up to store and use as muscle glycogen.
Going healthy vegan reduced my high cholesterol and high blood pressure down to normal and I lost 40 pounds and I'm now at a normal weight. I read Dr. Michael Gregers book How Not to Die.
Total cholesterol is better high.
Ldl has to be chemically damaged to cause heart disease. Higher total levels means higher rates of ldl cycling, so damaged ldl stays the lowest.
Try mostly plants with smaller amounts of varied animal protein. More fish and chicken. Red meat less but still in diet. The diet with the most positive studies atttributes is the Mediterranean diet. It doesn’t have to be complicated to work. Read the book Blue Zones. All those groups share similar attributes in what they eat and how they live.
Thing that might help:
- Increase Fiber in diet
- lose bodyfat
- try to lose visceral fat(organ fat) through water fasting and or fasting mimicking diet
- lose processed foods
At 7:57 he says we don’t really need APoB and that most other animals don’t synthesize it. I wonder if ApoB is linked to vitamin C intake like LP(a). If according to the great Dr. Linus Pauling and Dr. Matthias Rath, animals that do not synthesize their on vitamin c are the only ones that make LP(a). Could this be the same for ApoB or could there be any relationship?
What this video needs as an addendum is a KETO VS CARNIVORE discussion.
In my home, we don't do strict carnivore - we do a little vegetable and some fruit when we feel like it.
My husband was doing poorly on "keto". He was tired, his skin looked bad, he looked aged in the face. I believe it is a very unnatural way to eat. No ancestors would have guzzled mct oil or had keto snacks with all the chemical ingredients.
On a meat based diet we both looks and feel great.
When we feel a little sluggish we'll add some fruit in for a few weeks and then cut it out for a while.
Yes but how is the vaginal odor with excessive meats?
@@kidagave1I dated a keto maniac for six months. She was 4 years in. Her cooter was delicious…
It’s important to follow a “clean” version of keto, though. Not the keto snacks that flooded the market. Glad you found carnivore works better, though!
@@lorinichols9996 exactly! I knew a vegan that was absolutely committed. He admitted to eating processed vegan snacks regularly. His teeth enamel began to fail, along with other aspects of his overall health. He’s no longer vegan ;))
Nice! Listening to your body is so important 😊
Bill Walcott wrote a book on metabolic typing that really is about Genetics and how depending on the primary climate that a tribe lived in for many generations you will see people who can manage eating a lot of fat and need it versus people who get in big trouble with it. So people who live at high latitudes tend to eat a lot of fats and protein, whereas people who live at the equator, eat many more plants.
How can we say that normal apoB in a baby is a metric for an adult? Seems far fetched. Is testosterone in a baby the same as a 30 y.o.?
I understood his point to be that children would (in theory) have the most need for apo B and therefore might be a starting place to consider what might be reasonable. I'm not sure why though as apo B is necessary for embryonic development in mice but not humans. I think we can all agree that a 30 y.o. needs testosterone more than a baby does. Therefore we can presume that a baby's testosterone should be lower than a 30 y.o. Same theory in reverse: if a child has more need for apo B than a 30 y.o. then a 30 y.o. should have lower levels than a baby. Your argument supports his point.
Where can I get these test done? Because whenever I ask my primary care physician, he tells me that he can’t order labs unless I show symptoms.
Genetic test revealed “Near APOE 2” and I have been mostly in ketosis sometimes low ketone levels and sometimes high. I know I feel best, function better when eliminating processed foods and increasing grass fed products and saturated fats such as avacado and olive oil. This has been a fascinating interview, thank you!
I just bought attita’s book. Wish me luck in this.
How is it?
I wonder if, in addition to genetic factors, saturated fat impact on ApoB is mediated by dietary fiber intake.
Interesting. Apparently eating fiber before carbohydrate & saturated fat keeps the sugar level controlled.
Fascinating conversation guys 👍 Tq
Maybe I'm just a skeptic, but even without him actually saying it, the subtext here seems to be "pharmacological intervention GO GO GO". So my first question would be 'In what ways and to what degree is P.A. influenced by the Statin industry?"
Agree 100%
I've seen a video of him saying he thinks there are better alternatives
You realize that most statins are generic, right? Most of them aren't even produced by the big drug companies anymore. There's not much money in generic drugs so the "big pharma" conspiracy doesn't really work in this case.
I have heard him talk more about non-statin therapies, but the question might still remain.
Is he saying that a c16 fat is worse than a c19 ( whatever that is )? Because all i heard was it had an effect on APob , but i didn't get what effect it had, was it a good or bad effect. Also, i would have liked to hear what food falls into the c17 , c18, c19 categories and if they were also good or bad. I feel that part was left hanging for the viewer.
"I'm not in the camp that believes if you're on a low-carb, high fat diet, and your LDL-C and APO-B go through the roof, that that's not problematic." Okay...so I'd like to see Peter have that discussion, one-on-one, with someone from that camp. Rhonda can moderate.
why do you want youtube charlatans telling you what you want to heard. Apob drives athersclerosis. people can be ignorant of it at their own peril
This would be like asking Neil De Grasse Tyson to have a discussion with someone from the Flat Earth camp.
@@randikagunaratne1465Long Name Neil is not someone I trust. He’s very commercial, unnecessarily political and a darling of FAKE news and the bureaucracy pushing the climate hoax. He’s also a whiny twerp. Just my opinion, of course. 😊
@@randikagunaratne1465 I don't think the science on ApoB is as established as you may think. I have immense respect for Dr. Attia. He knows more on this subject than you or I will probably ever know. But there are other lipidologists who have studied it even more thoroughly, and hold a different view. There is still much to learn and a healthy, respectful, debate/discussion would be far from casting one's pearls before swine. The best minds offering various perspectives would benefit the entire field, and ultimately, the public.
@@Scurvous There will always be experts who hold contrarian views for different reasons. What's essential when trying to form an opinion in the scientific field is not listening to one or two experts but to consider what the majority of experts are saying. If it's a 50/50 or 60/40 split, there's room for discussion. But if 80%+ are saying one thing while just 20% are saying the opposite, it's a waste of time like in the case of ApoB. 80% is the very conservative figure by the way. It's more likely 90%+.
Just learned my Apo B is 123. I was stunned. 59 yr old female taking HRT, already eats low carb and primarily whole food diet. Might eat pizza six times a year. Drink alcohol once or twice a month. Lift weights twice a week and walk daily. Don’t smoke. Cardiac calcium baseline was a O. Like - what the heck else can I do?! 😢
❤ bless you. Has your Dr monitored sex hormones, homocysteine, B12, folate, Hba1c glucose, fasting insulin, triglycerides and cholesterol?
I hope you find some answers xxx
@ most of those but I don’t have a fasting insulin level yet.
The key is a low saturated fat and processed carb diet, and a high cholesterol diet = seafood / shellfish.
Why?
We have billions of cholesterol transporters in the GI endothelium that also trigger a feedback loop to stop endogenous cholesterol production.
This reduces ApoB, inflammation and reduces energy waste on manufacturing cholesterol which is very taxing.
So how do I lower my ApoB? Mine is 121, yet my fasting insulin is 3.5, A1C is 5.3, HDL is 76, trig are 64, I dont eat processed foods or seed oils, I weigh 117 lb at 5'2" and work out 5 days a week, blood pressure 115/70 and I dont smoke or do drugs. Why is it so high and what do I do about it?
Forgive me but am getting a bit sick of Mr Peter Attia. I can't wait for the moment when he comes out and says "I was wrong about LDL and APOB" as that marker on its own being elevated means absolutely nothing to CVD. And the other one is regarding Cancer, as he apparently does not believe cancer to be a metabolic problem. I can't wait to see how he changes his narrative.
Dr.*
Do you mean you cant wait for him to change his narrative to suit your diet choices? 🤦♂️😂
What a stupid comment..... @@888jucu
What are you talking about?
I had hdl at 110mg/dL.
Triglycerides 48.
My fasting insulin was 2.0.
But LDL-c was 320.
But apoB was 150.
Has the recent 1 year study by Feldman with Lean-Mass, Hyper-Responders (LMHR) shown that LDLs are not the major factor in plaque progression?
I predict that Feldman's recent "Lundquist" trial is just the beginning of putting the "Lipid-Heart" hypothesis "out to pasture." As we see more and more rock solid scientific studies (RCT's) performed, it will be proven that all this stuff about LDL-C, LDL-P and ApoB CAUSING ASCVD has been a "smoke and mirrors" distraction away from the real root cause of heart disease-INSULIN RESISTANCE/METABOLIC DYSFUNCTION!
No it has not
@@888jucu What was that study's conclusion? ua-cam.com/video/IMkDwtJVeB0/v-deo.html
@@888jucu I'm interested in what it did show, mind sharing if you know? thanks.
MVX is more important than AboB to test longevity and health.
My head hurts!
Going to reduce my applebee ´s consumption and live forever!!!
Palmitate is the fatty acid we make, from excess acetyl-CoA (from any source; glucose, amino or fatty acids), when insulin signaling has promoted (experimentally 4 fold) the transcription of acetyl-CoA carboxylase, and activated the enzyme by dephosphorylating it. And only once we've made palmitate, do we elongate it and desaturate some of it (or desaturate it and elongate it) into oleate for esterification and transport. Palmitate is endogenous to all well fed cells (4 fold more when insulin is elevated). The molecule can't be the specific cause of elevated circulating cholesterol, although it's accumulation still might.
So what is the sink of palmitate that can combat accumulation? Getting it across the mitochondrial membrane and into respiration. Which you are inhibited from doing when acetyl-CoA activity is elevated, when insulin is elevated.
hello, can someone explain to me please why butter raises cholesterol, especially LDL more than coconut oil even butter has way less saturated fat? what specific types of saturated fats have the most impact on LDL? Which saturated fats (for example myristic acid, palmitic acid etc.) raise LDL cholesterol the most? Thank you very much
@@helmutkrusemann9194 Coconut oil is 71% fatty acids shorter that 16 carbons long. Fats containing short and medium chained (ie: < 16 Carbons) fatty acids aren't as reliant for lipoprotein transport and most are miscible in circulation. Plus when they reach their terminal cell they are not subject to inhibition crossing the mitochondrial membrane. So they travel directly to the liver and can be burned pretty much immediately (certainly not subject to inhibition by insulin signaling).
Whereas only 17% of butter contains short and medium chained fatty acids.
Fats burned immediately are not subject to being used to make phospholipids, and more saturated fatty acids contributing to more saturated phospholipids requires more uptake of cholesterol from circulation and into membranes to homeostatically regulate membrane viscosity (ie: long chained saturated fats being used to make membranes need less cholesterol; ∴ more can circulate).
At the end he seems to be throwing shade at Dave Feldmans efforts lol
my ApoB is 116 and I was told to use statins.Afterntaking crestor for 3 weeks I stopped because nausea and headaches were horrible
I think our bodies makes what it needs when it needs it and when we just focus on lowering these numbers without seeing what the body is telling us we are smacking down our body's intellegence.
I agree.. I feel just eating earthly food (what roams & grows on earth), not touched by factories & chemicals, and exercising well, sleeping well, is the answer to all this.!
@@eddiegarciajr6653 Agree
right.. you think human science is as intelligent as evolved human DNA? I'm not saying drugs won't help someone or even some percentage of folks...
Couldn't understand the hypertension point, no details 😢
I know many people who have had cardiovascular problems, all had low cholesterol levels, some smoked 10%, others were obese 10%, many work in stressful jobs 80%. I don't understand how stress isn't included among the risk factors?
That the acceptable ranges for ApoB are determined by percentiles rather than event risk is a huge relevation for me. I guess this applies to other biomarkers. Wow.
Please explain very high LDL-C, very high ApoB and very low triglycerides. That doesn't correspond to the "load" concept stated
Rhonda I have been trying so hard to ask you this question, if you see this, please reply! Does taking a beta blocker (in my case atenolol), that "artificially" lowers your heart rate prevent you from getting the insane benefits of vigorous, zone 3/4 cardio exercises? On atenolol, I can't get my heart rate much above 130-140 MAX, no matter how hard I work on the elliptical (and I work hard). Am I going to miss out on all the benefits of vigorous cardio due to being on a beta blocker?
I can only speak for myself I chose not to take a beta blocker because I have concert that it will inhibit the growth of collateral arteries after having stents. My blood pressure is normal and my ejection fraction is still good despite two mi you really need to be your own advocate
The training zones aren't so much about heart rate as systemic requirement for oxygen and waste product clearance... Thus just because your heart tops out at 140 doesn't mean the rest of the cells aren't still acting like the heart needs to be at 180... Does that make sense?
Atenolol has an extreme effect on HR, I used another type of BB before coming to the US, and I had to use it for a month. I changed it back to the original one, exactly because it altered my HR too much compared to the original one. even if I must pay a much higher price as it's not covered by my plan. (I don't want to promote a medicine here, so I won't disclose the name. I take it for my high blood pressure)
HR is just a proxy for your effort. Those calculators won't work for you anymore (and they did not work before, btw.).Peter has videos about z2/z5, use those.
I started a side project for runners on beta blockers, but it's still in the infancy stage.
I think it would be great if all these people making conflicting claims about cholesterol and heart disease would go on podcasts with *each other*, rather than with a bunch of people who haven't studied the subject deeply. I haven't seen Attia or Paul Saladino or David Diamond or any of these other people show much interest in talking to each other. I haven't looked very hard though, maybe it's out there. But if they really want to discover the truth, and convince people of it, then they ought to be interested in talking to each other.
My apob and triglycerides were great on a keto diet. Then I almost died from covid (2 months in the hospital) and got tested 6 months after I got out and those markers were very, very high. Triglycerides went from 60 to 160, for example. My apob was 135 (not sure what it was before covid) Still not sure why but my diet stayed the same. At least my cardiologist said I had no plague that he could see from the multitude of ct scans, mri's and xrays I had done. (Not sure which of those could show plague build up)
Did you get the CVax?
Concerning. A prospective large scale nurse study in the BMJ showed a strong association of poor COVID outcomes and Keto.
I wonder if this explains some of the excess deaths? If having got COVID badly leaves Triglycerides etc very high. Wish more research was being done. If they funded the research with only a fraction of what they spent vaccinating very young very low risk people?
@@mikekarr2920 No.
@@andrewnorris5415 I got my cholesterol back to normal (although not as good as prior to covid) but for some reason I haven't had my apob tested yet so I don't know the full story.
I smoke when I drink - is the world that great we live in? I mitigate the damage with other things most people don't do. Look at all the people smoking weed. What's that do to your lungs?
LDL goes up when children become teenagers because they need it to make hormones.
Is Apo b produced in the Mevalonate pathway?
8:55 If cholesterol is partially an energy conservation system, how does the body recover energy from it?
When you burn off your fat, it is aerobic energy...
.
Carbohydrates restriction is unnecessary, I've eaten a lot of pasta all my life and my triglycerides are in the 40-50. It may be useful to some people, but it is not necessary once your caloric balance, weight and exercise are on point.
Pharmacological intervention for everyone! Attia thinks it’s so important to get a colonoscopy twice a year to look for colon cancer so why not use direct measurement of atherosclerosis in our coronary arteries to directly measure the problem rather than measuring for a normal human protein, ApoB? Tests such as CAC, CIMT or CT Angiogram would make sense before going to pharmaceuticals. Plenty of people have so called high LDL-C, same as ApoB and don’t have CAD.
twice a year colonoscopy is ridiculously unwarrented, but don't take my word for it, check out the most recent you tube by Dr V Prasad about what colon tests are even useful
Has Peter looked at BRI as a superior indicator than BMI of risk of disease? This may partly explain why “normal” people in the BMI scale are 60% fatty liver while overweight people are 80% likely.
So I see lots of blood work . And I have lots of blood work on myself.
Just did echo cardiogram pre and post Bruce protocol. I’m in the exceptional category for heart function and calculated VO2.
History 3 years ago , my blood sugar averaged 6.0 my insulin was between 2 and 2.5 fasted and body fat measured less than 10% on dexa. My cholesterol looked in optimal range. But I felt tired and my hormones took a dive
All this to say I went keto
Now my LDLs are 130 -150. My HDLs are 70-80 my triglycerides are 60-70.
And I feel amazing! I did the echocardiogram pre and post stress test a few weeks ago --just to know!
Yes. I also had super positive results on keto with marvellous improvements, kidney, liver, & trigs down from 3.6mmol/L to 0.5mmol/L 😊
@@zenden6564Ditto. My LDL is 199. ApoB is 128. But low Hcrp, Trig, Glucose, Hb1Ac, Fasting Insulin, HDL is 58. Calcium score is O. I am 74. What a misunderstood science where cholesterol theories remain a mystery!
How do I get my health insurance to pay for an APOB test? I had a heart attack 2.5 years ago. My hdl, ldl, and combined all look good but I am a numbers person and I would like to know more to know if I need to change anything up. I am on 20mg rosuvastatin. Otherwise, if I have to pay out of pocket is there a lab that will do the test and not charge a liver and a spleen for it?
Thank you!
Apparently it’s an $18 test…just pay
Mine ordered it as soon as I asked
Remember, the more you obsess and worry the longer you live. Also if your lab numbers aren't perfect cut back on sleep. You need the extra time to analyze your healthy life-style failures.
lol
oh please Tony tell the way to longevity because you clearly have all the answers
What about the effect of chronic _you know?_ Higher levels of _you know_ seem to increase HISF (human irritation stress factor.) _In the, you know, listener._ 😣
This is the first time i've heard of ApoB. Eight minutes into this video, and they haven't even described what it is.
Yes I feel like this is a clip?
ApoB are simply non-HDL lipoproteins - LDL, VLDL, IDL, Lp(a), etc.
ApoB is used to transfer LDL cholesterol in the blood stream. But it can get caught in the endothelial wall of your arteries leading to stiffness and plaques. It's the bad actor in almost all cases of atherosclerosis.
This is typical when they don't have a clue what they talk about, just the same with the colesterol number of LDL, they have told pasients over 50 year, it's dangerous with a number over 150, your about to have a heart attack. Just bullshit, is your metabolic health that counts, colesterol is there to help in a normal functioning body!
@@Kjuken69 Cholesterol is definitely required for normal bodily function but you do not need excess amounts circulating in the blood stream. Particularly not LDL as this raises apoB.