Well guys due to forum glitches I cannot include everything I wanted to type out, but at least I have a nice overall summary for myself. So here's a brief version of my thoughts, with conclusions/references in the next post:
1. We are born with a certain number of nephrons per kidney that filter blood. Initially our glomerular filtration rate (GFR) in young adulthood is ~120 (mL/min/1.73 m^2); after age 30 this declines ~10 per year. We are born with more than we need; if some nephrons die then others can work harder to make up for this and thus it is possible to incur a significant amount of kidney damage without having a large change in GFR. There are other measures of kidney function than just GFR (primarily the amount of protein that makes it through to the urine), but GFR is what the literature focuses on and a decrease is likely going to be an earlier sign than increased proteinuria of kidney damage from high protein. [1]
2. It is difficult to measure GFR accurately in larger studies and the estimating formulas typically use creatinine and cystatin c, both of which can be flawed. [2]
3. It is difficult to determine how much protein people eat. One nice compilation of 5 different validation studies found a correlation coefficient of reported and actual intake for total kcal and grams of protein to be <=0.4 (1 would be the best). [3]
4. During pregnancy blood volume increases a lot as does GFR and this remains elevated up to 3 months post-partum. This does not seem to lead to any pathology. After having one kidney removed the other one compensates and increases its GFR (hyperfiltration); this also does not seem to lead to pathology for at least 20 years. [4]
5. Amino acids seem to function as renal vasodilators thus allowing more bloodflow to the kidneys. Protein thus acutely increases GFR.
6. The question is does this matter in the long term. Unfortunately, pretty much all of the large long term studies compare high and low protein where the high protein group is <1.5 g/kg/d. There are mixed findings in these studies, and questionable methodology in many due to the issues alluded to above. [5]
7. There are shorter term studies that use higher amounts but the problem is they are shorter term. If we normally lose 10 GFR per decade and we eat a high protein diet and lose say 4 times that amount (hypothetically); we're going to have significant problems after a couple of decades. After a couple of years though there won't be much difference at all. [6] [7]
8. Jose Antonio has published several studies on really high protein intakes in athletes; all are <=2 years so it's too soon to see significant changes. In the one study he published that was 2 years, it includes 5 people, and while he concludes that there was no change in the average creatinine levels of the 5, looking at the individual data shows the BUN values don't really line up with the reported intakes and 2 of the 5 had significant jumps in reported creatinine from year 1 to 2, which is worrisome. [8] [9]
9. Animal studies show mixed results. Many studies in rats and dogs don't show scary effects of high protein diets but one study in pigs does. [10] [11]
1. We are born with a certain number of nephrons per kidney that filter blood. Initially our glomerular filtration rate (GFR) in young adulthood is ~120 (mL/min/1.73 m^2); after age 30 this declines ~10 per year. We are born with more than we need; if some nephrons die then others can work harder to make up for this and thus it is possible to incur a significant amount of kidney damage without having a large change in GFR. There are other measures of kidney function than just GFR (primarily the amount of protein that makes it through to the urine), but GFR is what the literature focuses on and a decrease is likely going to be an earlier sign than increased proteinuria of kidney damage from high protein. [1]
2. It is difficult to measure GFR accurately in larger studies and the estimating formulas typically use creatinine and cystatin c, both of which can be flawed. [2]
3. It is difficult to determine how much protein people eat. One nice compilation of 5 different validation studies found a correlation coefficient of reported and actual intake for total kcal and grams of protein to be <=0.4 (1 would be the best). [3]
4. During pregnancy blood volume increases a lot as does GFR and this remains elevated up to 3 months post-partum. This does not seem to lead to any pathology. After having one kidney removed the other one compensates and increases its GFR (hyperfiltration); this also does not seem to lead to pathology for at least 20 years. [4]
5. Amino acids seem to function as renal vasodilators thus allowing more bloodflow to the kidneys. Protein thus acutely increases GFR.
6. The question is does this matter in the long term. Unfortunately, pretty much all of the large long term studies compare high and low protein where the high protein group is <1.5 g/kg/d. There are mixed findings in these studies, and questionable methodology in many due to the issues alluded to above. [5]
7. There are shorter term studies that use higher amounts but the problem is they are shorter term. If we normally lose 10 GFR per decade and we eat a high protein diet and lose say 4 times that amount (hypothetically); we're going to have significant problems after a couple of decades. After a couple of years though there won't be much difference at all. [6] [7]
8. Jose Antonio has published several studies on really high protein intakes in athletes; all are <=2 years so it's too soon to see significant changes. In the one study he published that was 2 years, it includes 5 people, and while he concludes that there was no change in the average creatinine levels of the 5, looking at the individual data shows the BUN values don't really line up with the reported intakes and 2 of the 5 had significant jumps in reported creatinine from year 1 to 2, which is worrisome. [8] [9]
9. Animal studies show mixed results. Many studies in rats and dogs don't show scary effects of high protein diets but one study in pigs does. [10] [11]
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