This analysis is based on evidence from 35 scientific study references.
Proteins and kidneys
Don’t worry if you have healthy kidneys and monitor your protein intake or if you have damaged kidneys.
It may be wise to gradually increase your protein intake to higher levels rather than hopping on both feet at the same time, but there isn’t much on this topic.
In general, it is recommended to consume more water during periods when protein intake is increased. It is not known if this is biologically based, but it may be prudent to do so.
When observing active male athletes and measuring urinary creatinine , albumin and urea, no significant changes were observed in dosage ranges of 1.28-2.8 g / kg of body weight.
The previous study lasted 7 days, but survey research supports this lack of association (in postmenopausal women). Although ‘high protein’ was defined as 1.1 +/- 0.2 g / kg of body weight, it was associated with a better glomerular filtration rate.
The nurse study (survey) corroborates these results, but also suggests that this apparent lack of damage is not true for kidney failure (damage) and that non-dairy animal proteins are associated with damage to a greater degree than other proteins.
There appear to be functional changes in the kidneys related to protein intake.
As protein modulates kidney function, these interactions can cause damage if acutely imposed on mice (10-15% of the diet, up to 35-45% of the diet immediately).
But nevertheless. in a study in healthy humans that went from 1.2 g / kg to 2.4 g / kg (doubling) was associated with higher than normal blood levels of protein metabolites; a tendency to adaptation (increase in GFR) was observed but it was not sufficient to eliminate uric acid and BUN for 7 days.
These studies are likely to indicate ‘too, too fast’ satiety, as controlled changes do not lead to adverse changes in kidney function. Therefore, it would be wise to slowly change your protein intake over a moderate period of time.
Damaged or unhealthy kidneys
Protein restricted diets are recommended for those with kidney damage, as it slows the seemingly inevitable progression of kidney damage. If protein was not controlled in those with kidney damage, it would accelerate (or at least not reduce) the decline in function.
Proteins and the liver
In healthy people and rats, there is no evidence to suggest that a relatively normal style of protein intake is harmful to the liver when consumed routinely as part of the diet.
However, there is some preliminary evidence that a very high protein feed-back after prolonged fasting (> 48 hours) can cause acute liver damage.
When is the damage seen?
Current standards for the treatment of liver disease (cirrhosis) recommend a reduction in protein intake due to the possibility of ammonia accumulation in the blood that can contribute to encephalopathy.
At least one animal model suggests that damage can be observed when cycling periods (5 days) of sufficient protein intake and periods of protein malnutrition.
Similar effects were seen after 48 hours of fasting when fed a diet containing 40-50% casein.
The latest study found that the 35% and 50% casein groups had higher AST and ALT levels than the lower protein controls, effectively controlling refeeding syndromes and their adverse effects on liver enzymes.
The increases in liver enzymes observed in this study were concurrent with a decrease in the expression of the cytoprotective gene HSP72 and increases in c-Fos and nur77, which are up-regulated in response to injury.
Therefore, such an animal study is preliminary evidence that re-feeding of high protein (35-50%) after 48 hours of fasting can damage the liver. The shorter fasts were not examined.
Finally, aflatoxin (a toxic mold that is produced from some species of nuts and seeds) is known to be more carcinogenic (causes cancer) when the diet is very high in protein and subsequently less potent in low protein diets.
This is due to the toxin being bioactivated by the P450 enzyme system, which has its overall activity increased when dietary protein is increased.
This phenomenon also has effects on drugs metabolized by P450, where it may be necessary to increase the dose due to a faster metabolism.
The above is not an adverse effect of high protein diets per se (as it requires the ingestion of aflatoxins, which can be avoided), but should still be taken into account.
The only other relevant information on the subject is a 1974 study showing that a 35% casein diet led to increased ALT and AST levels in rats; This study does not appear to have been replicated.
Beyond the above situations, there are no more adverse interactions between dietary protein per se and the liver. Protein is generally considered safe to eat since you have a healthy liver.
Amino acids are acidic right?
What about heartburn?
The evidence is theoretically strong, but the acidity of excessive amino acids does not appear to be a clinical concern. It is not powerful enough to harm most people.
Bone mineral density
When considering large survey research, there appears to be no relationship between protein intake and risk of bone fracture (indicative of bone health), except when total calcium intake was less than 400 mg per 1000 kcal per day, although the relationship was quite weak (RR = 1.51 when compared to the highest quartile).
Other reviews are not similar: “lack of correlation despite logical relationships.”
An intervention study found that protein intake was actually positively associated with bone mineral density, but this correlation was only demonstrated when the acidic effects of sulfate (from sulfurized amino acids) were controlled for.
Soy protein itself appears to have additional protective effects on bone mass in postmenopausal women, which may be due to the isoflavone content. For more information, read our soy isoflavones FAQ page.
The role of the kidneys
The kidneys can sharply increase the glomerular filtration rate (GFR), or the filtration rate of the blood.
They do so in response to dietary protein intake, and the lack of this compensation in some forms of kidney damage is one reason why protein intake is controlled in the treatment of kidney disease.
In addition, the kidneys serve to regulate the acid-base balance in the body through the sodium and bicarbonate buffer system. Acid disorders: the base balance can promote the pathophysiology (symptoms and signs of the disease) of kidney complications.
These protective measures appear to be preserved in healthy kidneys, but begin to fail when the kidneys are damaged in other ways.
The role of resistance training
When rats are subjected to a sharp and drastic increase in dietary protein and experience decreased kidney function, resistance training can alleviate some of the adverse changes and exert a protective effect.