scholarly journals High protein intake without concerns?

Critical Care ◽  
2017 ◽  
Vol 21 (1) ◽  
Author(s):  
Olav Rooyackers ◽  
Martin Sundström Rehal ◽  
Felix Liebau ◽  
Åke Norberg ◽  
Jan Wernerman
2009 ◽  
Vol 20 (8) ◽  
pp. 1797-1804 ◽  
Author(s):  
Nynke Halbesma ◽  
Stephan J.L. Bakker ◽  
Desiree F. Jansen ◽  
Ronald P. Stolk ◽  
Dick De Zeeuw ◽  
...  

Critical Care ◽  
2022 ◽  
Vol 26 (1) ◽  
Author(s):  
Wolfgang H. Hartl ◽  
Philipp Kopper ◽  
Andreas Bender ◽  
Fabian Scheipl ◽  
Andrew G. Day ◽  
...  

Abstract Background Proteins are an essential part of medical nutrition therapy in critically ill patients. Guidelines almost universally recommend a high protein intake without robust evidence supporting its use. Methods Using a large international database, we modelled associations between the hazard rate of in-hospital death and live hospital discharge (competing risks) and three categories of protein intake (low: < 0.8 g/kg per day, standard: 0.8–1.2 g/kg per day, high: > 1.2 g/kg per day) during the first 11 days after ICU admission (acute phase). Time-varying cause-specific hazard ratios (HR) were calculated from piece-wise exponential additive mixed models. We used the estimated model to compare five different hypothetical protein diets (an exclusively low protein diet, a standard protein diet administered early (day 1 to 4) or late (day 5 to 11) after ICU admission, and an early or late high protein diet). Results Of 21,100 critically ill patients in the database, 16,489 fulfilled inclusion criteria for the analysis. By day 60, 11,360 (68.9%) patients had been discharged from hospital, 4,192 patients (25.4%) had died in hospital, and 937 patients (5.7%) were still hospitalized. Median daily low protein intake was 0.49 g/kg [IQR 0.27–0.66], standard intake 0.99 g/kg [IQR 0.89– 1.09], and high intake 1.41 g/kg [IQR 1.29–1.60]. In comparison with an exclusively low protein diet, a late standard protein diet was associated with a lower hazard of in-hospital death: minimum 0.75 (95% CI 0.64, 0.87), and a higher hazard of live hospital discharge: maximum HR 1.98 (95% CI 1.72, 2.28). Results on hospital discharge, however, were qualitatively changed by a sensitivity analysis. There was no evidence that an early standard or a high protein intake during the acute phase was associated with a further improvement of outcome. Conclusions Provision of a standard protein intake during the late acute phase may improve outcome compared to an exclusively low protein diet. In unselected critically ill patients, clinical outcome may not be improved by a high protein intake during the acute phase. Study registration ID number ISRCTN17829198


2002 ◽  
Vol 25 (4) ◽  
pp. 261-268 ◽  
Author(s):  
R. Bellomo ◽  
H. K. Tan ◽  
S. Bhonagiri ◽  
I. Gopal ◽  
J. Seacombe ◽  
...  

Aims To study the effect of combined continuous veno-venous hemodiafiltration (CVVHDF) and high (2.5 g/kg/day) parenteral amino acid supplementation on nitrogen balance, amino acid losses and azotemic control in a cohort of patients with severe acute renal failure (ARF). Methods We administered 2.5 grams/kg/day of amino acids intravenously to seven critically ill patients with ARF. We obtained paired blood and ultrafiltrate (UF) samples (n=20) and calculated amino acid clearances and losses, nitrogen balance, protein catabolic rate and total nitrogen losses. Results The median total serum amino acid concentration was high at 5.2 mmol/L with particularly high concentrations of ornithine, lysine, and phenylalanine, but a low level of histidine. The median overall amino acid clearance was 18.6 ml/min (range: 12 to 29 ml/min). UF losses as percentage of administered dose were high for tyrosine (53.6 %) but low for methionine (3.0 %) and arginine (2.3 %). A positive nitrogen balance was achieved in 7 (35%) of the 20 study days with an overall median nitrogen balance of -1.8 g/day. Urea levels were maintained at a median of 26.6 mmol/L. Conclusions High protein intake increases the serum concentrations of most amino acids. Such protein supplementation, when coupled with CVVHDF, achieves a slightly negative overall nitrogen balance in extremely catabolic patients while still allowing adequate azotemic control.


2020 ◽  
Vol 39 (7) ◽  
pp. 2192-2201 ◽  
Author(s):  
Wilhelmus G.P.M. Looijaard ◽  
Ingeborg M. Dekker ◽  
Albertus Beishuizen ◽  
Armand R.J. Girbes ◽  
Heleen M. Oudemans-van Straaten ◽  
...  

2006 ◽  
Vol 291 (2) ◽  
pp. F368-F374 ◽  
Author(s):  
Bing Yao ◽  
Jie Xu ◽  
Zhonghua Qi ◽  
Raymond C. Harris ◽  
Ming-Zhi Zhang

Renal cortical cyclooxygenase-2 (COX-2) is restricted to the macula densa and adjacent cortical thick ascending limbs (MD/cTALH). Renal cortical COX-2 increases in response to diabetes and renal ablation, both of which are characterized by hyperfiltration and reduced NaCl delivery to the MD due to increased proximal NaCl reabsorption. High-protein intake also induces hyperfiltration and decreases NaCl delivery to the MD due to increased NaCl reabsorption proximally. We investigated whether high protein induces cortical COX-2 and whether cortical COX-2 contributes to high protein-induced hyperfiltration and increased intrarenal renin biosynthesis. Cortical COX-2 increased after protein loading but decreased after protein restriction. COX-2 inhibition attenuated high protein-induced hyperfiltration but had no effect on high protein-induced intrarenal renin elevation. Therefore, induction of cortical COX-2 contributed to high protein-induced hyperfiltration but not intrarenal renin elevation. In the kidney cortex, neuronal nitric oxide synthase (nNOS) is also localized to the MD, and interactions between intrarenal nNOS and COX-2 systems have been proposed. Cortical COX-2 elevation seen in salt restriction was blocked by nNOS inhibiton. Cortical nNOS expression also increased after protein loading, and inhibition of nNOS activity completely reversed high protein-induced cortical COX-2 elevation and hyperfiltration. These results indicate that NO is a mediator of high protein-induced cortical COX-2 elevation and suggest that both intrarenal nNOS and COX-2 systems appear to regulate afferent arteriolar tone and subsequent hyperfiltration seen in high-protein intake.


2011 ◽  
Vol 70 (2) ◽  
pp. 205-214 ◽  
Author(s):  
Kevin D. Tipton

Athletes and exercisers have utilised high-protein diets for centuries. The objective of this review is to examine the evidence for the efficacy and potential dangers of high-protein diets. One important factor to consider is the definition of a ‘high-protein diet’. There are several ways to consider protein content of a diet. The composition of the diet can be determined as the absolute amount of the protein (or other nutrient of interest), the % of total energy (calories) as protein and the amount of protein ingested per kg of body weight. Many athletes consume very high amounts of protein. High-protein diets most often are associated with muscle hypertrophy and strength, but now also are advocated for weight loss and recovery from intense exercise or injuries. Prolonged intake of a large amount of protein has been associated with potential dangers, such as bone mineral loss and kidney damage. In otherwise healthy individuals, there is little evidence that high protein intake is dangerous. However, kidney damage may be an issue for individuals with already existing kidney dysfunction. Increased protein intake necessarily means that overall energy intake must increase or consumption of either carbohydrate or fat must decrease. In conclusion, high protein intake may be appropriate for some athletes, but there are potential negative consequences that must be carefully considered before adopting such a diet. In particular, care must be taken to ensure that there is sufficient intake of other nutrients to support the training load.


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