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group_5_presentation_2_-_high_protein_diets_and_kidney_function [2016/10/28 15:25] priyant |
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| - | **Multiple Sclerosis (MS)** is an autoimmune disease affecting the central nervous system. The disease specifically affects the myelin and as a result inflammation occurs and the myelin is damaged. Myelin performs the crucial role of nerve impulse through nerve fibers. If myelin is damaged then there will be a decrease in the transmission of nerve impulses. When the damage is significant then scar tissue will replace the myelin. The symptoms of MS vary for each individual, some include fatigue, pain, bladder problems, walking problems, cognitive difficulties and optic neuritis. Canada currently has the highest rate of MS with approximately 100,000 Canadians currently diagnosed (Multiple Sclerosis Society of Canada, 2016). | + | The Acceptable Macronutrient Distribution Ranges (AMDR) are the proportion of one’s caloric intake which should come from each macronutrient. It is recommended that 10-35% of daily energy intake should be provided by protein (Whitney, Rolfes, Hammond and Piche, 2013). In a typical Western diet, more than twice the recommended levels of protein are often consumed, and some research supports that this may be associated with the increased prevalence of chronic kidney disease in Western society (Hariharan, Vellanki and Kramer, 2015). Conversely, high protein diets are increasingly recommended for weight loss and weight management programs, and there is much controversy regarding the safety of such long-term diets. An article written by Kamal Patel, and featured on examine.com (2014), attempts to demystify the claim that high protein diets lead to increased glomerular filtration rate (GFR) which is a measure of the amount of blood that filters through the glomeruli every minute (mL/min). There is speculation that an increase in GFR leads to stress on the kidneys, resulting in kidney damage. |
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| - | **Jia and colleagues (2010)** tested the effects of a high protein diet on adult pigs. Pigs have very similar renal anatomy and physiology to that of humans, and thus are an appropriate test animal to use (Jia et al., 2010). Adult pigs were fed a diet consisting of either 15% of total calories from protein or 35% of total calories from protein for eight months. Protein came from a mixture of both plant and animal sources to closely resemble an average human diet. Between both the high and normal protein diets, lipid, fibre and micronutrient compositions were made equal to eliminate the presence of any confounding variables from diet. (Jia et al., 2010) After eight months, adult pigs fed the high protein diet had significantly higher kidney and glomerular volumes, however there was no significant difference in body mass between the high protein and normal protein groups. Additionally, after eight months, pigs fed the high protein diet exhibited more histological renal damage with 55% more fibrosis, and 30% more glomerulosclerosis in the kidney. There were also higher plasma homocysteine levels at 4 and 8 months. However, overall renal function as determined by inulin clearance, creatine clearance, or proteinuria was not affected by a high protein diet, as any increase in values at 4 months did not persist in the long term and differences overall were not statistically significant (Figure 1). Due to the similarity between pig and human renal physiology, this study presents evidence that suggests high protein diets may potentially be harmful to human renal function. (Jia et al., 2010) | + | **Jia and colleagues (2010)** tested the effects of a high protein diet on adult pigs. Pigs have very similar renal anatomy and physiology to that of humans, and thus are an appropriate test animal to use (Jia et al., 2010). Adult pigs were fed a diet consisting of either 15% of total calories from protein or 35% of total calories from protein for eight months. Protein came from a mixture of both plant and animal sources to closely resemble an average human diet. Between both the high and normal protein diets, lipid, fibre and micronutrient compositions were made equal to eliminate the presence of any confounding variables from diet. (Jia et al., 2010) After eight months, adult pigs fed the high protein diet had significantly higher kidney and glomerular volumes, however there was no significant difference in body mass between the high protein and normal protein groups. Additionally, after eight months, pigs fed the high protein diet exhibited more histological renal damage with 55% more fibrosis, and 30% more glomerulosclerosis in the kidney. There were also higher plasma homocysteine levels at 4 and 8 months. However, overall renal function as determined by inulin clearance, creatinine clearance, or proteinuria was not affected by a high protein diet, as any increase in values at 4 months did not persist in the long term and differences overall were not statistically significant (Figure 1). Due to the similarity between pig and human renal physiology, this study presents evidence that suggests high protein diets may potentially be harmful to human renal function. (Jia et al., 2010) |
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| Poortmans and Dellalieux (2000) investigated the relationship between high protein intake and renal function in both body-builders and athletes. The range of protein intake for the two groups was between 1.35 to 2.8 g/kg•b•wt. Through blood and urine analysis, they found no significant differences between the test groups regarding concentrations of plasma protein, creatinine and uric acid. High concentrations of these variables are indicative of protein absorption and potential renal impairment. Despite high plasma variables in both groups, there was no accumulation of urea, thus indicating that they were within the upper limit of normal. In addition, the GFR assessed by creatinine clearance suggested no sign of glomerular hyperfiltration. This supports that the high protein diet under 2.8 g/kg•b•wt does not adversely affect kidney physiology. | Poortmans and Dellalieux (2000) investigated the relationship between high protein intake and renal function in both body-builders and athletes. The range of protein intake for the two groups was between 1.35 to 2.8 g/kg•b•wt. Through blood and urine analysis, they found no significant differences between the test groups regarding concentrations of plasma protein, creatinine and uric acid. High concentrations of these variables are indicative of protein absorption and potential renal impairment. Despite high plasma variables in both groups, there was no accumulation of urea, thus indicating that they were within the upper limit of normal. In addition, the GFR assessed by creatinine clearance suggested no sign of glomerular hyperfiltration. This supports that the high protein diet under 2.8 g/kg•b•wt does not adversely affect kidney physiology. | ||
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| - | ====== References ====== | + | ====== Conclusion ====== |
| - | Amato, M. P. & Portaccio, E. (2012). Management options in multiple sclerosis-associated fatigue. Expert Opinion on Pharmacotherapy, 13(2), 207-216 | + | <style justify> |
| + | There is significant evidence presented in many scientific studies that recognizes high protein diets alter renal function in humans. However, there are inconsistencies between the results of short-term and long-term studies. Short term studies demonstrate an accompanied increase of GFR with high protein diets, whereas long-term studies lack statistical significance for a change in GFR, suggesting adapting renal physiology during chronic high protein intake. Additionally, source of protein and health status are important confounding variables that must be considered when evaluating the effects of kidney function of such diets. Despite the controversy surrounding the safety of high protein diets, there is no conclusive evidence supporting a direct causation between such diets and renal damage. | ||
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| - | Ascherio A, Munger KL (April 2007). "Environmental risk factors for multiple sclerosis. Part I: the role of infection". Annals of Neurology. 61 (4): 288–99. | ||
| - | Brosnan, C. F., & Raine, C. S. (1996). Mechanisms of immune injury in multiple sclerosis. Brain Pathology, 6(3), 243-257. | + | ====== References ====== |
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| - | Multiple Sclerosis Clinical Presentation. (2016). Retrieved September 18, 2016, from http://emedicine.medscape.com/article/1146199-clinical | + | |
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| - | Gilden DH (March 2005). "Infectious causes of multiple sclerosis". The Lancet Neurology. 4 (3): 195–202 | + | Aukema, H. M., Gauthier, J., Roy, M., Jia, Y., Li, H., & Aluko, R. E. (2011). Distinctive effects of plant protein sources on renal disease progression and associated cardiac hypertrophy in experimental kidney disease. Molecular nutrition & food research, 55(7), 1044-1051. |
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| - | Multiple Sclerosis Clinical Presentation. (2016). Retrieved September 18, 2016, from http://emedicine.medscape.com/article/1146199-clinical | + | Halbesma, N., Bakker, S. J., Jansen, D. F., Stolk, R. P., De Zeeuw, D., De Jong, P. E., & Gansevoort, R. T. (2009). High protein intake associates with cardiovascular events but not with loss of renal function. Journal of the American Society of Nephrology, 20(8), 1797-1804. |
| - | Multiple Sclerosis Society of Canada. (2016). Retrieved September 18, 2016, from https://mssociety.ca/about-ms/what-is-ms | + | Hariharan, D., Vellanki, K., & Kramer, H. (2015). The Western Diet and Chronic Kidney Disease. Current hypertension reports, 17(4), 1-9. |
| - | Rolak, L. A. (2003). Multiple Sclerosis: It's Not The Disease You Thought It Was.Clinical Medicine & Research, 1(1), 57-60. doi:10.3121/cmr.1.1.57 | + | Helal, I., Fick-Brosnahan, G. M., Reed-Gitomer, B., & Schrier, R. W. (2012). Glomerular hyperfiltration: definitions, mechanisms and clinical implications.Nature Reviews Nephrology, 8(5), 293-300. |
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| + | Poortmans, J. R., & Dellalieux, O. (2000). Do regular high protein diets have potential health risks on kidney function in athletes?. International Journal of Sport Nutrition, 10(1), 28-38. | ||
| + | Schwingshackl, L., & Hoffmann, G. (2014). Comparison of high vs. normal/low protein diets on renal function in subjects without chronic kidney disease: a systematic review and meta-analysis. | ||
| + | Wakefield, A. P., House, J. D., Ogborn, M. R., Weiler, H. A., & Aukema, H. M. (2011). A diet with 35% of energy from protein leads to kidney damage in female Sprague–Dawley rats. British journal of nutrition, 106(05), 656-663. | ||
| + | Whitney E., Rolfes, S. R., Hammond, G. and Piche, L. A. (2013). Understanding nutrition. Toronto: Nelson Education Ltd. | ||
