Dr. Peter Attia on Bulletproof Radio


  • Check out these Podcast Notes with Dr. Peter Attia on Joe Rogan
  • Dave plans to live until he is 180 years old, he’s 45 now
    • We have examples of people who have lived to 120 with the current state of affairs
    • Centenarians make up 0.4% of the population (so 4 in 1,000 people will live to be 100)
      • However – it’s mostly genetic. “Those centenarians, on average, are doing things worse than the rest of us. They’re more likely to smoke, less likely to exercise, and less likely to eat well. Their longevity is despite their lifestyle, not because of it.” 
        • “The single most important thing you can do, to live longer, is pick the right parents”
      • What do we see genetic wise in these centenarians?
        • Hypofunctioning apo-CIII genes
        • Hypofunctioning PCSK9  genes
        • More likely to have the ApoE2 form than the ApoE3 or ApoE4 form of the ApoE gene
          • ApoE is the gene that codes for how the brain metabolizes cholesterol
          • ApoE2 possessors have a a genetic protection against Alzheimer’s disease
          • ApoE4 possessors are genetically predisposed to Alzheimer’s disease
      • Centenarians get the same diseases the rest of us get, just they get them about 20 years later
  • “There have only been a handful of changes in our understanding of longevity that have led to step function increases in life span”
    • We haven’t had one since the introduction of germ theory
    • Peter thinks we’re due for one soon, but – “We are notoriously horrible at predicting the future.” Here’s what he thinks is possible…
      • He does think we will, at some point, be able to better manipulate the TOR pathway, with much more specific molecules than we can do today – “I view this as a very plausible step towards longevity”
      • Another possible step point – being able to reprogram senescent cells
        • These are are cells in the body programmed to do bad things.
        • The more we age, the more senescents cells we get
      • Some form of addressing atherosclerosis – “If you want to live to 180, we absolutely have to fundamentally change the way your coronary arteries and other arteries interface with lipoproteins and oxidized cholesterol”
        • Nanoparticles may be able to replicate the functionality of an HDL particle – entering the sub endothelial space and delipidating oxidized sterols, and then clean out foam cells – that’s a HUGE step function
        • To really understand this, read Peter’s series on cholesterol on his blog
  • “The science and art of longevity are an interdiscipline of engineering”
    • Just start from your end point and work backwards
      • “See where the iceberg is, see where you are, and ask – How far am I from the iceberg? How fast am I traveling, How much do I need to shift the direction of my ship? And what new iceberg will that put me in line with?”
      • A really comprehensive family history coupled with a good set of blood diagnostic tests is enough for people to see what that first iceberg is
  • Peter hates this word
  • Once again – really check out Peter’s series of blog posts on cholesterol
  • When evaluating a patient for risk, Peter looks at 4 lipoproteins in the following order
    • Lp(a) aka Lipoprotein(a) – calculated through NMR (this gives you the number of Lp(a) in nanomols/liter)
      • 8% of the population have genetically inherited elevated Lp(a)
    • LDL Particle Number – this is highly important
      • “I am more interested in their eye color than their LDL cholesterol number” – LDL particle number is much more important
    • Small LDL Particle Number
      • Small LDL particles are generally riskier
    • VLDL Remnant – estimated with VLDL cholesterol
      • VLDL Cholesterol = LDL Cholesterol – Non-LDL Cholesterol
      • VLDL Remnants are problematic if you have enough of them
  • Given this – you can see why your cholesterol number alone, really doesn’t matter
  • Peter also looks to understand 4 things when examining a patient
    • Volume of triglycerides
      • Lipoproteins (like the above) traffic cholesterol, but they also traffic triglycerides
      • “You want your serum triglycerides as low as possible”
    • How much cholesterol you make
      • Every cell in the body makes cholesterol – usually enough to meet your own needs
      • If you’re sick, the adrenal glands probably need more cholesterol than they can make – lipoproteins would then traffic needed cholesterol to the adrenal glands
    • How your body recirculates cholesterol
      • When cholesterol is made, it’s trafficked throughout the body, and ends up back at the liver. The LDL particle gets brought into the liver through the LDL receptor, and the process then results in the cholesterol being put into bile, and partially reabsorbed in the gut – which we can measure
    • How well the liver clears lipoproteins out of circulation – which we can’t measure, but we can infer
  • As a general rule, Peter recommends not taking exogenous phytosterols as a tool to lower cholesterol
    • Phytosterols are a group of naturally occurring compounds found in plant cell membranes.
    • 8-12% of the population have defective or sub optimally working ATP binding cassettes – these people have a much harder time getting phytosterols out of their system
      • Cholesterol is the sterol from an animal
      • Phytosterol is the cholesterol equivalent from a plant
    • Taking high does of phytosterols can lower your cholesterol levels
      • The problem is that phytosterols are more atherogenic than cholesterol
  • ApoE is the gene that codes for how the brain metabolizes cholesterol
    • ApoE exists in three forms (ApoE2, ApoE3, ApoE4)
      • ApoE3 developed 200,000 years ago and ApoE2 developed 50,000 years ago
      • ApoE2 and ApoE3 cause you to be less resistant to parasitic infections in the brain
        • ApoE4 protects your brain from parasite infections
      • ApoE2 people have a a genetic protection against Alzheimer’s disease and athlerosclerosis
        • ApoE4 possessors are genetically predisposed to Alzheimer’s disease
data and the Microbiome
  • “The availability of data in the future, is going to out pace our ability of what to do with it on a large order”
  • As time goes on, the signal to noise ratio is going down, not up
  • “In general, we are much more confident than we should be”
  • “I just think the gut microbiome is a complete shit show” – no pun intended
    • There’s just so much data and we don’t know what to do with it
    • The data does not provide us with actionable insights and it’s not clear whether the findings are associative or causative to the things we care about
    • The process of getting your gut sequenced is really slow (it takes around 12 weeks to get results) – so it’s a slow feedback loop
Alzheimer’s Disease, Brain Function, and Ketones
  • What is Peter doing for himself and his patients to protect memory and brain function?
    • “Whatever things that are necessary to delay cognitive impairment in people who are susceptible, should also provide a benefit to those who are perfectly functional”
    • What can we impact?
      • Metabolism
      • Vascular health
      • Exposure to Toxins
    • “Anything you do that maximizes insulin sensitivity and reduces the risk of cardiovascular disease, is almost certainly reducing your risk of neurodegenerative disease”
  • Low hanging fruit things we can do to maximize cognitive function
    • Nutrition matters – The less you can create glucose fluctuations, the less you create insulin surges, and as a result – the steadier the influx of energy to your brain 
    • Sleep – The Oura Ring is the most accurate tool out there which measures sleep quality
      • Peter DEFINITELY notices a huge boost in cognitive function when he gets a good night sleep
    • “The biggest epidemic facing all of us is distraction”
      • We are all highly distracted and this hurts our cognitive function. processing speed, and short term memory
  • When it doubt look to evolution
    • Our ancestors probably didn’t walk around in a constant state of ketosis
      • Peter thinks we’re wired to go back and forth between utilizing carbs and ketones for energy quite easily
    • “It’s probably not an entirely unreasonable state to be walking around with a flux of intermittent ketosis”
    • There are some ketone salts on the market, where you take them (even if you are consuming carbohydrates) and you’ll instantly be in a state of ketosis
      • Blood ketone levels rise from 0 to 6 milimoles/liter for a few hours
      • Peter has noticed, when taking these ketone salts while already in a state of ketosis, he doesn’t get  much of a cognitive benefit
      • Tim Ferriss has brought up a good point on this –  The only place a high level of blood glucose+ketone levels is exhibited in nature is in a state of ketoacidosis. It’s an unatural state.
3 tips for performing better
  • Change the way you eat, sleep, and move
  • “If you optimize those three things, you’re getting 60-70% of the possible benefit that exists out there”

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