Introduction
In recent decades, trends in diets tailored to promote weight loss have resulted in a significant increase in the intake of protein, particular in people with overweight and obesity issues. Accordingly, researchers have questioned the benefits or risks linked to the habitual consumption of “dietary protein in excess of recommended intakes” (Martin et al., 2005). In general, the primary concern has involved the possibility that diets rich in protein may increase hyperfiltration and, hence, exacerbate renal damage. Nevertheless, the potential link between protein-rich diets and renal damage has also been questioned due to an absence of adequate clinical evidence. In fact, studies have suggested that hyperfiltration, which is the purported renal damage mechanism, is a common adaptive response to various physiological conditions (Martin et al., 2005). Although nutritionists may recommend the intake of a high-protein diet (HPD) during the treatment of a kidney disease, decades of research have not yielded substantial evidence for the detrimental consequences of consuming protein-rich diets in healthy individuals. As a result, the lay media continues to increasingly popularize the intake of HPDs as an effective strategy for reducing obesity due to its potential for minimizing fat mass and increasing satiety (Pesta & Samuel, 2014). HPDs’ mechanisms that ameliorate weight loss include the “increased secretion of satiety hormones (GIP, GLP-1), reduced orexigenic hormone secretion (ghrelin), the increased thermic effect of food, and protein-induced alterations in gluconeogenesis” that enhance glucose homeostasis (Pesta & Samuel, 2014). Hence, HPDs have the potential to exert beneficial impacts on various metabolic processes of the human body.
Protein content in every diet is often calculated in relation to protein amounts per body weight, energy intake proportions, and the absolute protein amounts consumed by an individual. Typically, nutritionists recommend the use of protein-rich diets in programs designed to ameliorate post-exercise recovery, weight loss, muscle hypertrophy, and weight maintenance (Clark & Clark, 2007). Although the optimal intake of dietary protein has been investigated for several decades, the issue has remained controversial with contradictory studies highlighting the benefits and drawbacks of HPDs. For example, some publications have suggested a link between the long-term intake of HPDs and clinical conditions like renal dysfunction and bone mass loss (Bernstein et al., 2007). Nonetheless, although researchers have noted that HPDs may have detrimental impacts on persons suffering from kidney dysfunction, current studies have failed to conclusively demonstrate that HPDs consumed by healthy individuals are harmful (Cuenca-Sanchez et al., 2015). For instance, Clifton (2012) pointed out that HPDs cause greater satiety and weight loss than diets rich in carbohydrates. In particular, the impact of HPDs on satiety modulation involves several metabolic pathways. First, consumption of HPDs stimulates signals that promote the release of peptide hormones from GI (gastrointestinal) tract, as well as the release of derived metabolites into blood (Cuenca-Sanchez et al., 2015). Secondly, protein intake induces metabolic hormones to transmit energy status information to the central nervous system. Consequently, long-term consumption of HPDs tends to decrease body adiposity, body weight, and food intake (Pesta & Samuel, 2014). Diets rich in protein also reduce blood pressure and plasma triglyceride (Clifton, 2012). Thus, most investigations have demonstrated that HPDs lack harmful consequences for renal function and bone density. As such, the goal of this paper is to explore contemporary primary research articles that have reported HPDs’ efficacy in weight management and human health. In addition, the investigation hypothesizes that the consumption of HPDs does not pose any harm to a healthy person.
Review of Research
In various clinical trials and observational studies, the influences of protein consumption on the progression or development of chronic kidney diseases (CKDs) have remained inconsistent. Nonetheless, short-term investigations involving humans and laboratory animals have shown that HPDs can trigger the development of glomerular hyperfiltration and hypertrophy (Juraschek et al., 2013). In most cases, the two conditions are the initial maladaptive reactions to adverse renal hemodynamics. Moreover, they function as antecedents to kidney injuries and the progression of a kidney disease. However, the effect of a prolonged intake of dietary protein on the function of kidneys in healthy persons is relatively less clear. The difficulty associated with identifying such effects is often intensified by trials’ dependence “on creatinine-based equations for estimated glomerular filtration rate (eGFR)” (Juraschek et al., 2013). Typically, the consumption of dietary protein increases the level of serum creatinine through the catabolism of protein. As a result, serum creatinine is seldom reliable for approximating GFR or the response of glomerular hyperfiltration in studies involving the manipulation of dietary protein (Juraschek et al., 2013). Alternative kidney function biomarkers include β2-microglobulin and cystatin C, which often remain unaffected when exposed to alterations in the level of creatinine due to the intake of HPDs.
In an ancillary investigation “of the OmniHeart (Optimal Macro-Nutrient Intake) trial,” Juraschek et al. (2013) used β2-microglobulin and cystatin C to determine the impacts of replacing carbohydrate-rich diets with HPDs on kidney functions in disease-free adults. During the research, the investigators utilized an estimating equation based on cystatin C to assess the effects of HPDs on the glomerular filtration process. The study design involved “a randomized 3-period crossover feeding trial” that tested the impacts of replacing a carbohydrate-rich diet with an HPD on the function of kidneys (Juraschek et al., 2013). A hundred and sixty-four healthy adults with stage-one hypertension or prehypertension were selected for the trial, which was carried out at a research clinic. In the study, each of the participants was fed three diets for six weeks. Two- to four-week washout duration was used to separate the periods of feeding. Additionally, the three diets emphasized unsaturated fat, protein, or carbohydrate. In particular, the energy intake of the dietary protein comprised either fifteen percent unsaturated fat and carbohydrate diets or a twenty-five percent protein diet (Juraschek et al., 2013). Next, the researchers collected β2-microglobulin, cystatin C, and serum creatinine at the termination of each of the feeding periods. The study results found that the “baseline cystatin C-based eGFR was 92.0±16.3 (SD) mL/min/1.73 m2” (Juraschek et al., 2013). When the investigators compared the results with the unsaturated fat and carbohydrate diets, they found that the protein-rich diet had increased the “cystatin C-based eGFR by ~4 mL/min/1.73 m2 (P < 0.001)” (Juraschek et al., 2013). Moreover, blood pressure changes failed to influence the protein diet’s effects on the function of kidneys. Also, no substantial difference between unsaturated fat and carbohydrate diets was noted. Although the participants’ lack of a kidney disorder at the baseline contributed to the study limitations, Juraschek et al., (2013) determined that an HPD intensified the eGFR. However, the researchers failed to conclusively identify a link between the long-term intake of a protein-rich diet and the development of kidney disease.
Krebs et al. (2010) reported similar observations in a study aimed at evaluating the safety and efficacy of low-carbohydrate versus low-fat diets on cardiac function, body composition, metabolic markers, and weight loss in obese adolescents. The researchers randomized subjects “to one of two diets: a high protein, low carbohydrate (20 g/day) diet (HPLC) or low fat (30% of calories) (LF) regimen for 13 weeks” (Krebs et al., 2010, p.252). During the study, the investigators maintained close monitoring to assess the safety of each diet. The results showed a significant decrease in the BMI-Z score of both groups with a greater reduction of the score in HPLC subjects. Accordingly, Krebs et al. (2010) concluded that an “HPLC diet is a safe and effective option for medically supervised weight loss in severely obese adolescents” (p.252).
In a related study, Stepien et al. (2011) observed that the consumption of HPDs can serve as an excellent strategy against overweight and obesity because it provokes changes in the pathways of energy metabolism. The researchers, however, suggested that such alterations varied with dietary adaptations. Thus, Stepien et al. (2011) conducted a parallel study of enzymatic gene expressions associated with energy and protein metabolism, as well as nutrient oxidation profiles, in order to elucidate the HPD mechanisms. The investigators fed “eighty male Wistar rats” a typical “protein diet (NP, 14% of protein) for one week” (Stepien et al., 2011). Subsequently, they either maintained the NP diets or assigned the rats to an HPD (containing fifty percent protein) for the first, third, sixth, and fourteenth day. Next, Stepien et al. (2011) measured mRNA gene levels involved in lipid and carbohydrate metabolism in the rats’ muscles, kidney, adipose tissues, and liver using actual time PCR. In addition, indirect calorimetry helped to measure substrate oxidation and energy expenditure. Also, the researchers assayed hormones, blood glucose, and liver glycogen. In the liver, the HPD lowered “mRNA encoding glycolysis enzymes (GK, L-PK) and lipogenesis enzymes (ACC, FAS)” (Stepien et al., 2011). The protein-rich diet also “increased mRNA encoding gluconeogenesis enzymes (PEPCK)” (Stepien et al., 2011). In addition, the diet decreased and later “restored mRNA encoding glycogen synthesis enzyme (GS),” but induced no change on “mRNA encoding β-oxidation enzymes (CPT1, ACOX1, βHAD)” (Stepien et al., 2011). Nonetheless, other organs revealed minimal changes following the HPD feeding. In parallel, the use of indirect calorimetry affirmed that the HPD reduced glucose oxidation and stabilized fat oxidation, although an increase in lipid oxidation was noted during the first day of dietary adaptation. Lastly, the experiment revealed a significant decrease in plasma insulin and uptake of hepatic glucose. Taken together, the study results demonstrated that the intake of HPD augmented CHO utilization above the increases in carbohydrate consumption (Stepien et al., 2011). However, it lowered lipogenesis, which explained the fat decreasing effect associated with HPDs.
Conclusion
This study has accomplished its goal of investigating primary research articles that support the primacy of HPDs in weight management and general health. In addition, the investigation has supported the hypothesis that the consumption of HPDs does not present any harm to a healthy person. Since recent trends in feeding regimens designed to increase weight loss have yielded a significant increase in protein consumption, researchers have begun to question the benefit or risk of excessive protein consumption (Martin et al., 2005). According to Juraschek et al. (2013), despite the fact that HPDs can intensify eGFR, no conclusive evidence has linked the long-term intake of a protein-rich diet to the development of kidney disease. Similarly, Krebs et al. (2010) reported that HPDs are effective and safe options for weight loss in medically supervised situations. Other studies have found that the intake of HPDs lowers lipogenesis and, hence, decreases body fat (Stepien et al., 2011). Thus, the consumption of HPDs is safe and serves as an effective strategy against overweight and obesity.
References
Bernstein, A. M., Treyzon, L., & Li, Z. (2007). Are high-protein, vegetable-based diets safe for kidney function? A review of the literature. Journal of the American Dietetic Association, 107(4), 644-650.
Clark, C. & Clark, M. (2007). The new high protein diet. London, UK: Vermilion.
Clifton, P. (2012). Effects of a high protein diet on body weight and comorbidities associated with obesity. British Journal of Nutrition, 108, Suppl 2, S122-S129.
Cuenca-Sanchez, M., Navas-Carrillo, D., & Orenes-Pinero, E. (2015). Controversies surrounding high-protein diet intake: Satiating effect and kidney and bone health. Advances in Nutrition, 6, 260-266. doi: 10.3945/an.114.007716
Juraschek, S. P., Appel, L. J., Anderson, C. A. M., & Miller, III, E. R. (2013). Effect of a high-protein diet on kidney function in healthy adults: Results from the OmniHeart trial. American Journal of Kidney Diseases, 61(4), 547–554. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3602135/
Krebs, N. F., Gao, D., Gralla, J., Collins, J. S., & Johnson, S. L. (2010). Efficacy and safety of a high protein, low carbohydrate diet for weight loss in severely obese adolescents. The Journal of Pediatrics, 157(2), 252–258. doi: 10.1016/j.jpeds.2010.02.010
Martin, W. F., Armstrong, L. E., & Rodriguez, N. R. (2005). Dietary protein intake and renal function. Nutrition & Metabolism (London), 2, 25. doi: 10.1186/1743-7075-2-25
Pesta, D. H. & Samuel, V. T. (2014). A high-protein diet for reducing body fat: mechanisms and possible caveats. Nutrition and Metabolism (London), 11, 53. doi: 10.1186/1743-7075-11-53.
Stepien, M., Gaudichon, C., Fromentin, G., Even, P., Tome, D., & Azzout-Marniche, D. (2011). Increasing protein at the expense of carbohydrate in the diet down-regulates glucose utilization as glucose sparing effect in rats. PLoS ONE, 6(2), e14664. doi: 10.1371/journal.pone.0014664.
