A low-protein diet is a diet in which people decrease their intake of protein, and is used as a therapy for inherited metabolic disorders, such as phenylketonuria and homocystinuria, and can also be used to treat kidney or liver disease.
Low protein consumption appears to reduce the risk of bone breakage, presumably through changes in calcium homeostasis.
The daily requirement for humans to remain in nitrogen balance is relatively small.
The median human adult requirement for good quality protein is approximately 0.65 gram per kilogram body weight per day and the 97.5 percentile is 0.83 grams per kilogram body weight per day.
Children require more protein, depending on the growth phase.
A 70 kg adult human who was in the middle of the range would require approximately 45 grams of protein per day to be in nitrogen balance,
representing less than 10% of kilocalories in a 2,200 kilocalorie ration.
For adults, the recommended minimum amounts of each essential amino acid varies from 4 to 39 milligrams per kilogram of body weight per day.
Good quality protein comes from a wide variety of foods; there is neither a need to mix animal and plant food together nor a need to complement specific plant foods, such as rice and beans.
Apart from rare examples, such as Taro, each plant provides an amount of all the essential amino acids.
The relative abundance of the essential amino acids is more variable in plants than that found in animals, which tend to be very similar in essential amino acid abundance.
Calorie restriction has been demonstrated to increase the life span and decrease the age-associated morbidity of many experimental animals.
Increases in longevity or reductions in age-associated morbidity have also been shown for systems where protein or specific amino acids have been reduced.
Effects of calorie restriction are on metabolic health, promoting leanness, decreasing blood sugar and increasing insulin sensitivity.
Low-protein diets mimic many of the effects of calorie restriction.
Restricting consumption of the three branched-chain amino acids leucine, isoleucine and valine is sufficient to promote leanness and improve regulation of blood glucose.
Protein restriction improves multiple markers of metabolic health, such as reducing adiposity and improving insulin sensitivity.
The diets of humans living in some of the Blue Zones, regions of enhanced numbers of centenarians and reduced age-associated morbidity, contain less than 10% of energy from protein.
While none of the diets in these regions is completely based on plants, but plants form the bulk of the food eaten.
A standard dietary treatment for those with liver disease or damage is a low protein, high carbohydrate, moderate fat and low salt diet.
Calcium loss from bone occurs at protein intake below requirement when individuals are in negative protein balance, suggesting that too little protein is dangerous for bone health.
IGF-1, which contributes to muscle growth, also contributes to bone growth, and IGF-1 is modulated by protein intake.
At high protein levels, a net loss of calcium may occur through the urine in neutralizing the acid formed from the deamination and subsequent metabolism of methionine and cysteine.
Sstudies have shown a slight increase in risk of bone fracture when the quintile of highest protein consumption is compared to the quintile of lowest protein consumption: the trend is also seen for animal protein but not plant protein.
As protein consumption increases, calcium uptake from the gut is enhanced.
Normal increases in calcium uptake occur with increased protein in the range 0.8 grams to 1.5 grams of protein per kilogram body weight per day.
Calcium uptake from the gut does not compensate for calcium loss in the urine at protein consumption of 2 grams of protein per kilogram of body weight.
Calcium is not the only ion that neutralizes the sulphate from protein metabolism, and overall buffering and renal acid load also includes anions such as bicarbonate, organic ions, phosphorus and chloride as well as cations such as ammonium, titrateable acid, magnesium, potassium and sodium.
Increased consumption of fruits, vegetables and cooked legumes increases the ability of the body to buffer acid from protein metabolism, contributing to a base forming potential in the body due to their relative concentrations of proteins and ions.
Not all plant material is base forming, for example, nuts, grains and grain products add to the acid load.
Guidelines for adults with stage 3 to stage 5 non-dialysis dependent chronic kidney disease who do not have diabetes recommend a low protein diet of 0.55 to 60 g per kilogram per day of a very low protein diet or 0.28 to 0.43 g per kilogram per day supplemented with essential or ketogenic amino acids to meet dietary protein intake requirements and reduce the risk of kidney failure, impaired quality of life, and death.
Most guidelines, recommend dietary protein intake of less than 0.8 g per kilogram per day in persons with chronic kidney disease.
Lowered dietary protein intake, leads to vasoconstriction of glomerular afferent arterioles, reducing intraglomerular pressure and damage, whereas high protein diets, cause dilation of afferent arterioles which leads to glomerular hyper filtration and progression of chronic kidney disease.
Therefore, lower dietary protein intake in patients with non-dialysis, dependent chronic kidney disease decreases the risk of metabolic complications, progressions of kidney failure, and death.
In older patients with advanced non-dialysis depending CKD with GFR of 5 to 7 mL per minute randomly assigned to supplemental vegan low protein diets or to initiation of dialysis without dietary interventions: the low protein diet group is able to delay the time of dialysis initiation by approximately one year, and had fewer hospitalizations than those in the dialysis group.
A diet protein intake of 0.6-0.8 g per kilogram per day is advised for patients with chronic non-dialysis dependent kidney disease who do not have diabetes.
However, Cochrane studies suggest that low protein diet and patients with advanced chronic kidney disease has little and no affect on the number of patients who reach endstage kidney failure.