Why Low Cholesterol & ApoB Levels Are Critical for Longevity | Dr. Peter Attia & Dr. Andrew Huberman

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Dr. Peter Attia and Dr. Andrew Huberman discuss the concept of causality in medicine, specifically focusing on the causal relationship between smoking and lung cancer, and LDL cholesterol or ApoB and atherosclerosis. They explore the current approach in medicine, the importance of understanding and mitigating risks, and question if methods could be more proactive rather than reactive.

Dr. Peter Attia is the host of The Drive podcast and is a world expert on behavioral approaches, nutritional interventions, supplementation and pharmacological techniques to improve lifespan, healthspan and athletic performance. Dr. Andrew Huberman is a tenured professor of neurobiology and ophthalmology at Stanford University School of Medicine and host of the Huberman Lab podcast.

#HubermanLab #PeterAttia #Alzheimers

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The Huberman Lab podcast is for general informational purposes only and does not constitute the practice of medicine, nursing or other professional health care services, including the giving of medical advice, and no doctor/patient relationship is formed. The use of information on this podcast or materials linked from this podcast is at the user’s own risk. The content of this podcast is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard or delay in obtaining medical advice for any medical condition they may have and should seek the assistance of their health care professionals for any such conditions.
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I am about to be 82. I have been on statins for many years and always think I want to get off them. I have moderately high blood pressure which is controlled with diuretics. I have no other risk factors other than my age. My total cholesterol is around 160 and my LDL is extremely low I believe due to the statins. Watching this I am convinced by Dr. Attia to forget about getting off of statins and continue doing what I do. Eat well, get regular exercise, take my meds and get as much enjoyment out of life as I can. Thanks for these conversations.

pbziegler
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Why is it that I could listen to these two all day long speak while in a meditative state? You both are mesmerizing. 🎉

lorimcintoshrealtor
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Such a Privilege to listen and learn from these two amazing gentlemen.

bludog
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¡Hola Profe!Going to relisten the episode! The shorter format is doing a good job to remind, what episodes to rewatch or relisten Thank You, for all You are doing .

olgazavilohhina
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I find it a bit curious that Dr. Attia calls himself "obsessive" with causality, when LDL is not the cause per se. Oxidized LDL that gets within arterial walls causes plaque, not standard LDL. The causes for atherosclerosis, then, are related to the inflammation that promotes that oxidation. We should be looking at lowering that instead of waging war on an essential molecule.

fabioriato
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So much conflicting info out there. I have seen several studies that show; higher cholesterol is associated with longevity, a Korean study showed that those with very low levels (sub 150) had higher mortality than those from 200-250, more than 50% of those admitted for heart attacks have levels in the 'normal' range. With advances in medicine, stents, statins and the war on smoking, heart disease is still the number 1 killer. I just don't think we have this figured out yet.

jimk
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I’m glad that you are keeping science at the forefront. Cardiovascular disease kills an American every 12 seconds and hypercholesterolemia is a profound - and eminently treatable -risk factor

nanduthalange
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Just went to the doctor in the Netherlands, she didn't know what apoB was 😂
She was looking in the system and was not able to test me on that.
When I go to a blood test site I can buy a ApoB test for 30 euro, so I will do that

nielsvdv
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Love how they boil it down to its essential essence.

jelizabethpetrie
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I get conflicting information on whether I am ok or not.

My current numbers are: Total Cholesterol 244, Triglycerides 58, HDL 106, LDL 128, ApoB 105, ApoA-1 222 mgdL. These have roughly been my numbers for years.
Originally I was told not to worry about my high LDL because my HDL is high and will protect me. Now my HDL is considered too high and is not good any more.
I then had my particle size tested, and the test showed low risk pattern with larger particle size and low insulin resistance. So I was considered good - no treatment necessary.
Now the most important indicator appears to be ApoB. My ApoB is too high so I need treatment.
I have also seen elsewhere that the most important indicator is the ratio ApoB / ApoA-1. This number is good for me due to my high ApoA-1 so I don't need treatment.

My doctor is now focusing on the ApoB only and wants me on crestor. This seems to agree with what you are saying. It just seems like the parameters keep changing.
I am 60, female, BMI 21, moderate exercise and eat healthy. (healthy fats, veges, some carbs, low sugar).
I prefer to avoid statins.

Mmmmmmmm
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It is the right time to step in PRECISION MEDICINE based on deep understanding rather than basics models which are most of the time non relevant and wrong. Thanks for this sharing and experience. Thumb up Dr 's.

GeraldTUR
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I have low LDL and low ApoB but still rather significant atherosclerosis. How come Type2 diabetes inflammation is not discussed here? No MD ever warned me about Type2 and atherosclerosis either.

maesc
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Peter Attia needs to have a debate with James Mason. The two are diametrically opposed in their claims and both extensively cite studies and resources.

utarian
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Since the war on cholesterol, dementia and Alzheimer's have skyrocketed.
I'm not gonna sacrifice my operating system for my motor.
And if I'm wrong I'll die young eating the foods that make me feel the most well.

sir_nicks_allot_
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Its a good argument and a good analogy, but there is a fundamental problem. Smoking is a negative intervention. Not smoking is a non-intervention. You dont have to weigh the risk of not smoking against the risk of smoking.
Statins use is an active intervention, which while it does lower cholesterol, has risk of diabetes and dementia, muscle pains. In this case it does make sense to evaluate when the risk of high cholesterol becomes substantial enough to make an active intervention known to cause negative effects

wmrajput
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I've watched a ton of YouTube doctors. Attia is the best. I always feel like I'm getting a modern, nuanced, agnostic take on how to increase my odds of remaining healthy.

scotey
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But what if the lipoproteins that carry LDL to where its needed in the body are quite essential to life, and its what causes those lipoproteins to lay down as plaque that is the ultimate cause? Addressing the lipoproteins/ldl as the cause, instead of what causes them to enter the intima and form plaque, could be an attack on the firefighter instead of the fire just because the fireman is always present at the fire! Reducing LDL that is essential to cellular function would then be just as bad as the plaque risk. What must be addressed is not LDL, but rather what is causing it to lay down plaque in the artery walls. That cause is inflammation in the arteries. And that has a wide range of causes and none are LDL. Address the cause of inflammation, and LDL will not harm you. High insulin/glucose due to bad diet is the main CAUSE of vascular disease and not LDL and its lipoproteins. Reducing LDL to reduce plaque burden could be cutting off your nose to spite your face! Instead, reduce the inflammatory factors that cause an otherwise beneficial LDL from becoming an issue.

thEngineer
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when Attia asks a question, he can certainly elaborate

kev
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LOVE Dr A and Andrew as well I have learned much and continue to do so

Michiganman
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My mom died at 36 from a heart attack. Her death certificate said arteriosclerosis was the cause. She drank and smoke. My apo b is 80 but lipoprotein a is 180. I’m definitely worried.

AnniesALF