Weaknesses:

• Epidemiology
• • Association is not causation. Epidemiology cannot establish a causal relationship.
• Food Frequency Questionaries
• • It's unclearly how frequently the FFQ was administered, but probably 1-4 years.
• Healthy User Bias
• Weak Hazard Ratios
• • Epidemiology needs very strong signals to be useful, weak signals indicate we are lookinga t the wrong questions.
• Relative Risk reported instead of absolute risk
• • Speaks to the lack of clinical relevance.

Notes:

Medeterrian blue zone - One wonders about the effect of plant based proteins and their correlation with plant based fats (industrial oils) in their observation set.

observed an inverse association between plant protein intake and all-cause mortality among women but not in men. In men, animal protein was inversely associated with mortality. - High Protein Intake Is Associated with Lower Risk of All-Cause Mortality in Community-Dwelling Chinese Older Men and Women

To me this means the signal they are looking at is too noisy to be meaningful (i.e. they are not accounting for carbohydrate consumption in these surveys)

Table 1 is interesting in that it shows that at baseline the more animal protein population had lower rates of hypertension and diabetes then the plant protein population (see all the weaknesses listed above)

Even the high animal protein group is eating 46% dietary carbohydrates, with (3.7+17) 20.7% of dietary fats coming from industrial oils. I point this out to illustrate how noisy this dataset is, its not a clean signal to vilify any one thing as a ultimate evil.

For all-cause mortality, there was a statistically significant interaction between plant protein and hypertension (lower risk for all-cause mortality per 1% of total energy from plant protein in parti-cipants without baseline hypertension).

Look at this fucking gymnastic statement. In the people without hypertension at baseline they were less likely to develop hypertension on plant based... but it wasn't protective for the people with baseline hypertension, and it isn't expressed in the context of carbohydrate load. What else in their own table of related data was also correlated with this hypertensive decrease? Fucking alcohol (5%-1%).... I would argue its almost impossible to develop hypertension without carbohydrates.

Higher intakes of animal protein were associated with lower risk for all-cause and cardiovascular mortality in this study of community-dwelling older adults after 20 years of follow-up.

Increased animal protein intake may be inversely associated with mortality in older adults through its protective effects on muscle strength, frailty, sarcopenia, or immune responses, all of which merit further studies (21). Increased intake of total or animal protein was positively associated with muscle strength (22), which in turn was in- versely associated with all-cause mortality in a recent meta-analysisof studies in older adults (23). Moreover, chronic or acute inflamma-tory conditions may impair the direct relationship between proteinintake and muscle strength in older adults, increasing dietary protein requirements (1).

In this study, plant protein was mostly coming from cereals, and this fact could be related to the null association between plant protein and mortalit

Ah yes, cereals, classic protein source. They are confusing crude nitrogen estimates in food sources with bioavailable digestible amino acid scores (see the DIAAS posts). So this entire data is suspect because their protein isn't actually comparable

The strengths of the current study include a long follow-up in a well-established cohort of older adults, and the inclusion of repeated dietary assessments to reduce bias from measurement errors in dietary questionnaires.

Yeah, maybe one FFQ in 20 years isn't enough?1!??!

Our study also has limitations.

• The relatively small sample size and low incidence of cancer-related deaths could have compromised the statistical power.
• Medical advice could have affected the dietary choices.
• Indeed,higher plant protein intakes are encouraged within a DASH diet compared to a Western diet (25).
• Residual confounding may re-main, even though we adjusted the analyses by a Mediterranean diet adherence score.

Model adjustments are just guesswork and don't actually show a underlying truth, they offset confounders by estimation and dead-reckoning

• Last, our results may be affected by sur-vivor bias, the mean age at baseline was 75 years, and require validation in other studies with a longer follow-up and in non-Mediterranean populations

Overall a interesting paper, I must respect the authors for not p-hacking a signal they want to publish and dealing with the consequences of the data they found. This is somewhat rare in epidemiology. This paper is suggestive for actual interventional studies, but isn't enough to inform any dietary choice or recommendation by itself.