How much protein can your body really digest/absorb/use?
I have said, many times, that protein is not easily turned into fat, it’s simple biochemistry. The observation that AA carbon ends up in fats isn’t evidence of anything other than this can happen, but the extent to which it does is small.
But there has to be a limit to protein intake? Beyond a certain point, we can’t put AA into ‘storage’, we need to use them! I’ve read many times, incorrectly, that we can only digest 20g of protein. That’s wrong. We can digest a lot of protein, but we can (if it’s a large amount) only use a fraction of what’s digested and absorbed. If ingested AA aren’t used for protein synthesis then the amino N is taken off (nitrogen isn’t well tolerated in biological systems as it exists as ammonia which raises pH – not good), urea is formed, and the remaining carbon skeleton of the AA is burned for fuel, turned into glucose, some of it can end up in fat, or it ends up in other biochemical roles. Some people will say that AA are used for ‘many’ other things… like what? Neurotransmitter synthesis (yes, but tiny amounts), creatine synthesis (yes, about 1g per day), and ‘other things’ (yes, but very little of these other things). So in sum, AA are used for making proteins or they’re deaminated and become substrates. A tiny amount of AA are used for ‘other’ processes beyond protein synthesis.
So what you say… there’s nothing wrong with a little extra protein!? True, a little extra isn’t bad it doesn’t cause bones to dissolve (die acid-ash hypothesis), it doesn’t cause our kidneys to fail (die Brenner hypothesis). But what else? Does the emerging number of papers showing that protein is associated (note) with reduced longevity have any relevance for humans? The question’s not an easy one to answer and not an easy one to test. I would state that most experimental models used to test this thesis are very likely to be poor, as they are for other protein-related questions for which we have sought answers for humans, models. Why? Well simply, the ‘risk’ of eating ‘too much’ protein reported in most observational trials falls in that 1.1-1.3 RR range, which people need to know is really in the noise (despite ‘correcting’ or adjusting for confounders). Then to fall onto an animal model as support for your wobbly RR is problematic. Why? No human is as near to being as inbred as most [all] animal models used for this work and nor does it have its food supply controlled from birth to grave, nor does it spend its life in a hermetically sealed low infection risk, pollutant-free environment and… well, physiology aside there are obvious reasons why fruit flies, rabbits, or rodents might not be the best model systems. But, and this is important, the evidence of this protein longevity effect cannot be blithely ignored either. To roundly dismiss all animal work isn’t a good idea either. Neither, and this is also important, can animal models be used as a/the reason for creating policy on protein recommendations. Observational data are also unlikely to provide the ‘unlock’ for this conundrum although people are hard at work twisting data on this.
Bottom line: More protein than the RDA, absolutely, but how much? Twice the RDA is about as high as I’d go. I see no compelling reason to go higher. How you fill the rest of your energy needs is your concern, but piling on the protein beyond 2 times the RDA may also have its problems? And exercise is the forgiver of many sins… staying active as you age, perhaps more than any other thing will IMO do more for you than protein!
References
1. Stokes T, Hector AJ, Morton RW, McGlory C, Phillips SM. Recent Perspectives Regarding the Role of Dietary Protein for the Promotion of Muscle Hypertrophy with Resistance Exercise Training. Nutrients 2018;10(2). doi: 10.3390/nu10020180.
2. Devries MC, Sithamparapillai A, Brimble KS, Banfield L, Morton RW, Phillips SM. Changes in Kidney Function Do Not Differ between Healthy Adults Consuming Higher- Compared with Lower- or Normal-Protein Diets: A Systematic Review and Meta-Analysis. J Nutr 2018;148(11):1760-75. doi: 10.1093/jn/nxy197.
3. Shams-White MM, Chung M, Du M, Fu Z, Insogna KL, Karlsen MC, LeBoff MS, Shapses SA, Sackey J, Wallace TC, et al. Dietary protein and bone health: a systematic review and meta-analysis from the National Osteoporosis Foundation. Am J Clin Nutr 2017;105(6):1528-43. doi: 10.3945/ajcn.116.145110.
4. Simpson SJ, Le Couteur DG, Raubenheimer D, Solon-Biet SM, Cooney GJ, Cogger VC, Fontana L. Dietary protein, aging and nutritional geometry. Ageing Res Rev 2017;39:78-86. doi: 10.1016/j.arr.2017.03.001.
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4moJeff Layne
Practicing Chiropractor; Health Research; Nutrition; Strength & Conditioning Coach
4yGreat article Stu. Just on the section about RR at 1.1-1.3 and so I am understanding this correctly, you're outlining that in observational data to date - and on average - that there's a risk ratio of about 10-30%, all of which is relative and in this case relative to animal models that make direct comparison very hard to unpack? I'm hoping I have this concept somewhat in the ballpark.
InnerPath Nutrition
4yAs a longtime scientist tasked with selling protein powders (ex-Weider Nutrition & others) I would like to float a concept that is virtually ignored that I thinks has a role to play in this equation. Glutamine (Gln) conversion to glutamate by cooking, acidity. We all know how important Gln is. But because of the old-fashioned amino acid analysis methodology of boiling a protein in strong acid, the glutamine & asparagine aminos are converted to glutamate and aspartate, affectionately called Glutamine & Asparagine, which is inaccurate and misleading. How many of us know the Gln/Glutamate ratios of undenatured or cooked proteins? The few times that true Gln has been measured in proteins shows a high preponderance of Gln, not glutamate. I realized this was a disconnect during my doctoral work on HMG proteins, which really do have a very long stretch of glutamate/asparate residues, not glutamine or asparagine. And remember that in human bodily fluids, glutamate is really MSG (which brings up yet another wrinkle on high intakes of cooked proteins, which is the norm for almost all subjects in protein studies and in real life). And glutamine is a predominant amino acid in circulation and tissue pools. My point is that a lot of metabolic energy and metabolism of other amino acids is used to restore/mantain the glutamine levels our GI tract, immune system and liver like. And it is possible that our bodies are sending signals to eat more protein in order to obtain more amino acids to maintain glutamine levels? I have been out of this field for a while so perhaps there is some updated info on this topic?
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4yGreat article dr Philips. It also helps with the, in my opinion, conflicting information of on the one hand, less protein for longevity and the other hand muscle mass being an indicator for longevity and better life quality. I'll keep lifting weights regularly and eat higher protein. Thank you.
Prof Phillips, what do muscle-protein-synthesis curves look like when a bolus dose of 20, 30, 40 or 50 grams of quality protein is ingested, say in a 30 yr old and a 50 yr old person, regardless of exercise.