re: That Meat and Cheese is Killing You, baws

For fricks sakes man. The soccer board is a couple tabs up

Get this shite out of here.

Next you're gonna tell us that taking 3x scoops of preworkout and a 5 month gear stack is bad for gainz.

quote:

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I do it strictly for health reasons. 

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Lol.

I have posted about this ad nauseam in the past

Speaking in absolutes is rarely helpful/correct. Most contemporary nutritional "science" is very myopic in it's approach (tunnel vision, neglecting the big picture). I would also argue that it has been corrupted by corporate influence/ $$$$$

The discussion is much more nuanced....

If you are eating meat or drinking milk from a "concentration camp" animal, then sure, you will be getting a heavy dose of inflammatory omega 6, grain fed animal profile

If you are eating meat from a grass fed animal, beneficial omega 3 fat (along with the most nutrient dense profile food) will be coming your way

Dan John Heuristic = Eat as close to the sun from a trophic level perspective

- Plants = good
- Animal/animal products that eat said plants = good

Human intervention/alduteration

-animals fed grains = bad
-processed foods = terrible


In summary:

The name of the health, longevity and quality of life game (in general) is to:

-maximize / optimize glucose partitioning
-optimize a low inflammation diet (well sourced natural fats/proteins)
-practice relative caloric restriction
-preserve healthy skeletal muscle mass (the metabolic site optimizing glucose partitioning) and bone density while not overpromoting IGF-1 pathway (tumor promoting at an extreme)
-optimizing the gut microbiome

In general:

A diet high in fat with moderate protein and relative carbohydrate restriction (think keto, paleo, primal) accomplishes the goals above while maintaining a robust quality of life. Strong hormonal satiety is invoked by a diet high in fat/protein. This allows for interval episodes of fasting (intermittent fasting) and less meals per day (if you believe in the limiting exposures to food additives sort of logic). Most would argue that this is the way the human species evolved to eat and manage food scarcity. In modern times it promotes compliance with a dietary lifestyle change.

Metrics such as grip strength, waist to hip ratio <0.9, and wether you can get up from a chair or the ground without assistance become very simple / practical predictors of longevity. Muscle preservation /strength set the tone for metabolic robustness and resilience

The goals above are very difficult if not impossible to accomplish strictly on a vegan and /or protein restricted diet.

Peter Attia has commented on this a bunch

youtube

Peter Attia on Longevity

Notes:

- would be great to measure mTOR in blood (currently none); pathway senses amino acid concentrations and involved in protein synthesis; decreased mTOR activity increases longevity
- mTOR driven by leucine sensing (a branched chain amino acid), especially in muscle; don’t want too much or too little
- IGF-1 increases mTOR activity and both regulated by amino acid intake; activators AKT signaling pathway for cell growth and proliferation
- debate whether IGF-1 is driven by protein alone or by carbohydrates by way of insulin
- methionine shown to be most active factor for driving IGF-1
- as insulin goes down, IGFBP3 (anti proliferative effect) goes up
- sex-hormone binding globulin goes up when insulin down, free testosterone goes down; produced by living and binds hormones in blood; only 1-2% of hormones are unbound/active; relative binding affinity: dihydrotestosterone > testosterone > androstenediol > estradiol > estrone; free testosterone drop when restrict carbohydrates
- IGF-1 doesn’t initiate cancer, but does fuel existing cancerous cells; carbohydrates can initiate cancer via many pathways
- those with longest lives die from same diseases as everyone else, but just get them later; hence need to delay the big three that causes 75% of deaths: cardiovascular, cancer, neurodegeneration
- diet recommendation: consume the least amount of protein to grow muscle mass, but no more; lower carbohydrate as much as possible; fat becomes fill
- mucin keeps gut from microbiota; when break down, causes endotoxins to enter blood stream; can measure endotoxin, but lots of false positives; fiber, short chain fatty acids, Tregs
- ApoE - amount of mutant ApoE expressed matters more than genotype; currently no CLIA lab test, but some experimental; ¾ (20%) gives 2-fold increased risk, 4/4 gives 5-10-fold; but majority of people with Alzheimer’s is ¾ or 4/4; what may be more predictive is serum levels; if can measure, perhaps can change diet to decrease serum levels; ApoE4 expression is lower in the brain which causes Alzheimer’s; literature today suggests that when correct for LDL particle number and ApoB, then ApoE genotype doesn’t matter; high levels of ApoB associated with higher LDL particle levels and primary driver for plaques and vascular disease; ¾ or 4/4 should have harder time clearing LDL from circulation; what are differences between clearance and cholesterol internalization, in brain vs liver; drinking with ApoE4 causes damage due to inhibition of repair; ApoE4 itself creates aggregates
- pyruvate dehydrogenase - limiting step that is activated by cofactor vitamin B; bridge between glycolysis and Kreb’s
- breast cancer account for 3% deaths in women; all cancers 20-21%; cardiac disease 22-23%
- biggest drivers of cardiac disease: smoking, hypotension, and elevated ApoB (more LDL and cholesterol in macrophages; can increase HDL to take cholesterol out of macrophages; ApoB is best biomarker for cardiovascular disease)
- Alzheimer’s has increased 2.5% per year, but longevity has been increasing 0.6% per year; therefore isn’t just natural response of getting old; think may be related to type II diabetes and hyperinsulinemia; ApoE may just be susceptibility; neuronal energy problem
- increase central IGF-1 in brain to decrease dementia, decrease peripheral IGF-1 in blood; some evidence that increased central IGF-1 may prevent against diabetes
- astrocytes are supporting cells for neurons; primarily uptake glucose and convert to lactic acid as feed for neurons; thermodynamically more favorable to shoot right into citric acid cycle
- monocarboxylate transporters 1 (MCT-1) carries lactate, pyruvate, ketones BHB and acetoacetate into cell; MCT-1 transport lactate out of muscle and take to Cori cycle in liver to make glucose
- ketosis blood concentration (mM):
< 0.2 not in ketosis
0.2-0.5 slight/mild ketosis
0.5-3.0 induced/nutritional ketosis
2.5-3.5 post-exercise ketosis
3.0-6.0 starvation ketosis
15-25 ketoacidosis
- Warburg effect - cancer cells produce energy by high rate of glycolysis and lactic acid fermentation vs normal cells that have low rate of glycolysis and oxidation of pyruvate in mitochondria; glycolysis faster for making building blocks; potentially because cancer cells make anti-death signals and mitrochronial causes reactive oxygen species that would tip the balance towards pro-death; may be that in cancer mitochondria is purposely bypassed; may be why activating pyruvate dehydrogenase kinase and ketosis diet can kill cancer cells
- dietary anti-oxidants when have cancer suppresses pro-death signaling