Tom's Diet & Supplements


Who wants to hear Tom rant about diet? Obviously. That's why I put all this in here: My bet, my insurance, what I'm mad about, and what I think I'm learning. You can take it or leave it, I don't mind. But you can't say I didn't tell you, I didn't share what I learned. So here you go.

Why? It started with a lifetime of nightmares (I just thought I deserved them), and gets worse. Yes, I'm motivated.

A Diet Bet

You can't not bet, pal. Whatever you do, it's a bet.

My diet, such as it is, is: (keto × vegan) − simple carbs (for nighttime headaches) + anchovies (for brains).

See?: Little or no sugar, flour, rice, or corn. No meat, milk, or eggs. I know, it's eating to live, and barely. But just consider the alternative, realistically.

Supplements: cheap insurance.

Other fads I'm looking out for include

Diet Chickenshit

Is it people, or is it their doctors, that are the most gutless, when the doctors won't tell them to just eat falafel, oatmeal, stirfry, and salads, instead of batter fried meat on cheese plus dessert, so that they would maybe not die so much of cancer and everything else? I heard it's because the doctors think everyone will just ignore them. Fine, go ahead and frickin' die. That's what you prefer? Wow. Apparently you have to go to the non-idiot line at the doctors office and say No, you don't prefer McDonalds to Life Itself and you're actually willing to reconsider a couple diet choices. Then *Maybe* they'll break down out of their standard-American-diet-locked customer mode and tell you, Hey that's actually good because you'll probably not die so young of cancer and heart disease and stuff because of that. But SSHHHH, don't tell anyone because it's a secret, not because it's actually a secret, but because some of the people around here are chickenshit and so we seriously can't even talk about it, or we can't even talk seriously about it. Now you tell me, who is it, the people, or the doctors?

An evolutionary aside

Now, low-carb advocates (like Amber O'Hearn who says "headache, lassitude, vague discomfort, are symptoms of 'rabbit starvation'" (!My Symptoms!)) are arguing humans evolved as marrow scavengers, i.e., as fat eaters. So the first tool was just a rock, but with a rock an early human, like an australopithecus maybe, could scavenge otherwise inaccessible and preserved marrow and brain by breaking the big bones and intact skulls left at a kill after the vultures were finished. To this evolutionary phase we can attribute the development (as compared with chimps) of more acidic stomachs, a more ketotic metabolism, less chimp-like raw-fiber digestion, preference for fatter (large) prey. And we can infer it supported tool use, eclectic carnivory, fatter bodies, basically more of ye olde fat-based brain. If your metabolism is fat-burning, that's called ketosis; but did you know, most of the carbon atoms in the brain come into the brain as ketones? Fat = brain food. (Amber, Did I get it right?) If so, this evolutionary track helped us smarten up and get bigger brains, fatter bodies, and kickstart the whole human evolutionary cascade.

I'll assert that the marrow scavenging preceded the aquatic phase of human evolution when we lost body fur, got (even) more skin fat, became fully bipedal (according to Elaine Morgan, acquired voluntary breathing control (necessarily preceding speech), learned to love swimming. Because the marrow+brain fat consumption and a bit more of our own brains would tend to lead us toward safer feeding of just as plentiful fat in netted or group-herded fish. A puddle off a pond being as good as a net if you have twenty family members splashing in a line to chase the fish into it, and a log to roll across the neck. And nets themselves, a generalization, being slightly more complex than rocks (and logs and puddles), but not much, less so than cloth, for example, therefore the semi-aquatic phase should be after the marrow scavenging phase based on increasing tool complexity.

Also if you can tolerate picked over carcasses you can tolerate stinky fish smells too. I'm going to say that it was later that our smell preferences changed to become more fastidious.

Diet Suggestions!

Okay. So, well, milk is evolutionarily correct too, obviously, so I tried a cream and bacon type of keto diet, but after a year my cholesterol was 300 and shortly after that I had to have a stent installed in my heart in order to not die. So I'm good with healthy fat (if I could figure out what that might be). For the last couple years, it's keto + vegan - simple carbs + anchovies. Lots of olive oil. Kale, when I can find a way to tolerate it (baked into chips with balsamic and olive oil, yes! Or fresh in bits on falafel with some olives: it's tolerable. Plus balsamic.

Here: My nutritionist said to try intermittent fasting. No late night snacks, and a late breakfast, gives your system 14 hours to run in ketosis and clean out the day's bluck. Longevity, okay? Study up, friend, the science is actually starting to come in! And please educate me, too; I don't know everything (for sure), or anything, (possibly).

Below are notes from Dr. Peter Attia's talk, "Reverse engineered approach to human longevity", on youtube. To live longer means to delay chronic disease. Consider the genetic contributors to longevity; we have documented about dozen among centenarians. (Among the dozen longevity genes, only the thyroid mutation doesn't have an evident chronic disease relationship.) For some examples Attia mentions:
  • Hypoactive ApoC-III: which leads to lower triglycerides and ApoB which relates to CHD.
  • Hypoactive PCSK9; which leads to much more LDL receptors on the liver, they clear ApoB-bearing particles out of circulation with great precision, where ApoB is what you need to understand to assess cardiovascular disease risk.
  • ApoE2 > ApoE3 or ApoE4 genes; these being what regulate peripheral and central lipid metabolism and cholesterol
    ApoE4 is the evolutionarily ancient type and was best for parasitic infection.
    People who have the ApoE2 variant have much less Alzheimers (20x less than ApoE4 carriers)
  • Less GHR: which seems to protect from cancer.
  • Lower IGF1: which seems to protect from cancer.
See how all these are tied back to the main chronic diseases: cardiovascular, cancer, and neurological decline, which along with accidents cause 80-98% of deaths.

So perhaps the genotypes can be mimicked.

To control CVD we need to jointly target lipoproteins, inflammation, and endothelial function. E.g., low dose methotrexate reduced cardiac mortality.

Alzheimers: NIH will not even fund research including the word "prevention", but the Cornell Alzheimer's Prevention Clinic has got us on the track of managing it better for sure.

That's his argument for longevity as a focal point for science, medicine, and lifestyle.

II: Widely across species (1) caloric restriction (CR) and diet restriction (DR) makes yeast, flies, worms, mammals all live longer. The NIH vs U Wisconsin rhesus monkeys showed only that calorie restriction helped longevity only if you ate a crappy diet (the UW one). And (2) Rapamycin (mTOR) extends life across all these. It works on a protein called TOR, which has to do with growth/non-growth, Both of which related to nutrient sensing. Also DAF2 in C elegans can be tweaked to >2x longevity and also sharpen the decline at the end, and its job is something like IGF1 in humans.

III: Human nutrition density is an evolutionarily recent event. We likely have not evolved proper nutrient sensing for this new nutrient-dense context; autophagy is our friend; senescence needs to be understood as cells poison others to advance aging, though necessary against cancer; inflammation with its many causes needs regulated.

IV: Tactics: Nutrition should be optimized so that: carbohydrates make your average glucose low (85mg/dL) with a standard deviation of <15mg/dL, which leads to low insulin AUC (integral of insulin over time) proxied by continuously measureable blood glucose. I.e., aim for perfect glucose homeostasis. Agnostic w.r.t. paleo or vegan or whatever. Just keep glucose low and not very variable. For some people this is a high or a low number, and dependent on exercise and sleep. proteins aim for a barely positive nitrogen balance. Not protein wasted, for muscle mass matters, but not so much that it's too much with excess amino acids . We need homeostasis in muscular system. Too much and too little are bad. Fat is the balance by amount. Sat, Mono unsat, polyunsaturateds may differ. Exercise: Observe the lifespan impact of the metabolic advantage of exercise. We can put glucose (glycogen) away quickly into the liver (limited capacity) or into the muscle (potentially a large sink for glycogen), so muscle mass is very helpful. With insulin resistance in the lower body muscles it tends toward the diabetes. It's hard to have diabetes with a lot of muscle. Avoid exercise-preventing injuries. Lower back pain can bring morbidity. Do heavy strength training. Do heavy hip hinge exercises like squatting dead-lifting and rowing, even until your blind demented 90's. Get the II-B muscle fibers activated at the end of the effort scale. Interval train too next priority.

Sleep: underappreciated but key. Sleep is a highly conserved behavior, doesn't go away, evolved before neurons. E.g., Lack -> testosterone drops, perhaps because slow-wave (delta) sleep, where pituitary puts out FSH & LH which make testosterone. Hippocampus is sensitive to sleep disturbances which consolidate memories. Lack of sleep exacerbates effective glucose dispoal. So improve glucose disposal by correcting sleep.

Diet and supplments etc., it's empirical: you have to measure a lot and cycle through to find the right diet which for 80 people there will be 70 different optimized diets.

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Copyright © 2000-2020, Thomas C. Veatch. All rights reserved.
Modified: October 25, 2020.