Recently an article got everyone's knickers in a twist about protein and CVD. Here's an easy to read summary of the paper with my pictorial essay medicalnewstoday.com/articles/eatin…
Note: this is a conclusion from mice only... it's translation to humans... 🧐
High protein diets may contribute (!!) but we should revise dietary guidelines (???) In our 2020 paper also in mice 🐭 🤨
We created diets in mice that mimicked what people are - at the highest end of intake...
Part I - 14 people! Part II - 9 people. Leucine - no reference or data 'cept for a 2020 paper in? You guessed it 🐁 😉
Activates a pathway in immune cells that's ASSociated with atherosclerosis... 🤔
Now we 'pin down' the reason - now it's causal (??) Leu is the 'bad actor' 🫤 (in mice anyway and 22% is the magic threshold)
2020 study in 🐁🐭
Another dude thinks this is not a big deal (I'd agree)
Takeaway... 23 people and acute immune cell signalling
Mice and 22% protein that 'mimics' the higher end of what humans ingest
It's only Leu...
Time to have a hard think about what the science is and the message being pushed. The data are mildly interesting and give some food for thought. I stop (well) short of seeing this as a smoking (protein-filled) fun and the reason to change dietary guidance OR to issue a per meal or dietary threshold advice to people.
I note the absence of a disease incidence, or risk or any causative data in humans...
Carry on folks: exercise, fuel to meet your needs, enjoy time with friends, lower your stress, have purpose in life and you will live well
Also, don't drink Boost with more protein on top... and stop feeding your mouse >22% protein! 😉
Just appreciate the limitations of the data and the model and the design and the ex-vivo outcomes and the murine model before we blow the horn for protein 'causes' CVD (or even increases risk). Also #Science
This was the original stated purpose "there are several innovative features of the proposed experiments that are expected to significantly advance the field and improve muscle regrowth and mobility, with the overall goal of reducing risk of disability among older adults.
The proposed work is expected to have a powerful impact, as we will be the first to determine whether metformin, in combination with resistance exercise designed to elicit muscle hypertrophy, will augment progressive resistance training-induced muscle gains
Pairwise meta-analyses compare one condition with another to determine which variable is best/better for an outcome. But what if you have multiple variables to manipulate? Like resistance exercise!
If resistance exercise (RE) is a drug and hypertrophy or strength is the outcome, then what if it’s not just the dose, but the frequency of how often you take the dose, how long you take the dose for, what if you take a big dose, a small dose, or you ramp up your dose
What is the ‘best’ prescription for resistance training (RT) a 🧵
Some folks think we’ve figured it all out, but have we? Others would say there are an infinite number of combinations, kind of like toppings and combinations,
at a famous sandwich shop! Does all or any of this really matter when it comes to developing strength and muscle growth (hypertrophy)?
In our recent work (), we attempted to define a prescription for resistance training (RT) instead of what’s done in abjsm.bmj.com/content/early/…
pairwise meta-analysis, which looks for the superiority of one condition versus another.
The network that gave us the greatest stability was obviously the comparison to control, and that comparison, as our networks show, is the most robust.
A key point that it seems even those that 'study' in this area is to recognize is that a requirement for a nutrient may not be a level at which optimal function is achieved. The processes of adaptation and accommodation pubmed.ncbi.nlm.nih.gov/3958814/
seem to have been forgotten or not taught at all. There is a fascination with the ‘elegance’ of balance studies with little-to-no appreciation of all the flaws. pubmed.ncbi.nlm.nih.gov/2750699/ Flaws that in other areas would render the data next to useless!
And yet, many persist in citing data that supports notions that are long since forgotten in terms of what the data mean or the physiology that underpins it.
At the same time, there are those who would read this and opine that optimal intakes require protein intakes that
@Theresa_Furey@maxlugavere@McgrawRhiannon Or if you’d prefer a Mendelian randomization study pubmed.ncbi.nlm.nih.gov/33564816/. A desirable macronutrient composition, including high relative protein intake and low relative fat intake, may causally reduce the risk of CKD in the general population.
Per meal protein doses to 'optimize' anabolism? Aka, "how much protein should I eat?" I think it's pretty clear that 20g does the job (1). The incremental rise in MPS from 20-40g was 14% (using egg protein in young men after an intense
leg workout). Witard et al. (2), once again, 20g gets the job done (whey protein and leg exercises only). In that study going from 20-40g gets you an extra 16% in MPS. MacNaughton et al. (3) say 40g > 20g for whole-body resistance exercise; the difference between MPS
from 20 to 40g was ~18% (see Figure below). Now we know acute measures of MPS (over h) don't align well with hypertrophy (4), yet some insist that 40g is 'better' than 20g. My bet, since only two doses were tested that 30g would have done just as good a job in stimulating MPS.