All Protein Things 3

Updated: May 6

In part 2, I made a case for why we should eat more protein, in part 3, I’d like to address some of the most common myths and misconceptions regarding high protein intake.

High protein & kidney damage


This seems to be the most common concern when discussing high protein diets. The misconception stems from old epidemiological studies that looked a bunch of obese individuals with co-morbidities and made an inference that high protein intake is a factor in causing kidney disease, diabetes, cancer, bone loss... [1] [2].

This is one of the reasons why epidemiological studies are garbage. Nothing is ever controlled as you can associated variables and interpret the results however you wish, then make a generalization about your population sample. That said, I think I’ll bash epidemiological studies in a separate post.


The results of said epidemiological studies couldn’t be further from the truth for a multitude of reasons. An increase in renal filtration rate is rather an adaptive physiologic mechanism, and is well documented the medical literature. For example in nephrectomy (surgical removal of 1 kidney) patients, the remaining kidney adapts by undergoing hypertrophy to accommodate the physiologic demands of the body. These adaptations are also seen in pregnancy where the mother’s kidneys develop renal vasodilation and increased filtration rates. We can also see some proteinuria (protein in urine) in people with long-hour standing jobs, and in athletes. The list goes on… None of that is pathologic, its all within the physiologic capacity of the human body.


Let us add more evidence to that. In this study [3], several bodybuilders were recruited and given 2.8g/kg of protein for 7 days as they were examined daily with relevant blood tests and urine analysis to look for pathologic increases in the values of albumin, proteinuria, urea production and creatinine. There was an increase in all parameters alright, but all within the normal limits. And none of the study subjects developed any kidney related problems.


That said, the study duration is extremely short so on its own it doesn’t provide much of evidence. However, I'd like to point out that bodybuilding has been around since the early 60s, so if high protein intakes did in fact cause any kind of kidney damage, we’d have lines and lines of bodybuilders and athletes queued up for a nephrology checkup every couple of months. Plot twist, we don’t.

Finally, This study here [4] suggests that higher protein intake may be of benefit. So, in the grand scheme of things, I think it is safe to say that high protein intake in individuals with normal kidney health is of no known consequence. And I say that because there is some evidence to support that high protein intake in individuals with diseased kidneys may cause further damage. That means that they already have a problem, and it wasn't created from said protein intake, it was rather aggravated. I think I've provided enough evidence to bust this myth. Should you want to read more on the topic, you can find that here.


High Protein intake, acidity & bone damage


About 25ish years ago, a couple of papers were published that studied protein intake and bone health. There appeared to be a negative relationship between them, where increased protein intake caused an increase in urinary calcium excretion [5], hence they concluded that high protein intake decreased bone mineral density and increases risk of fractures.

There were speculations as to why this happened. One hypothesis suggested that high protein intake creates an acidic environment which would increase bone resorption, hence explaining the increase in urinary losses of calcium, this modal was based on physio-chemistry studies done in-vitro and on dogs & rats, then extrapolated to human physiology [5].

Another hypothesis suggested that high protein intake causes low-grade metabolic acidosis, in which the blood pH and bicarb are at the lower limit of the normal range, hence its symptoms are not overt, but rather subclinical. This would decrease renal reabsorption of calcium, hence the increased urinary excretion.


Luckily, we have managed in the last 10 years to research the topic thoroughly, and a lot of the published work has been revisited and reevaluated. Physiology was much less understood 30 years ago than now, as was our understanding of human disease.


First of all, the systemic extra-vascular compartment is not in direct contact with the bone mineral tissue, as there is a barrier between those compartments. Meaning, there is no way that the acidic medium would reach the bone mineral [7]. So, the process must have been mediated by another pathway if it were to take place.


Second of all, the acid-base balance in the human body is tightly regulated. When a human has metabolic acidosis, their entire electrolyte equilibrium goes off. There is alteration in respiratory and kidney function, as well as a possible alteration in mental status.

To keep this short, you can die pretty quickly if you’re in metabolic acidosis. So, to claim that metabolic acidosis occurs with high protein intakes is absurd, even when its 'subclinical'. If there are alteration in blood pH and bicarb values, it'd only occur as a part of the normal homeostatic process.


Keeping that in mind, calcium control is mediated by 3 different tissues. Kidneys, bones and the intestines. These 3 manipulate absorption, resorption, mobilization and excretion. So when we look at only one, we'll be missing the whole picture. Whatever is lost in urine is made by for by increased absorption in the intestines to give a positive/neutral net effect [8].


That said, they always taught us in med school that lab ranges are there for reasons. That is not to say that there aren't subclinical diseases, rather we ought to pay attention to the slight variations in normal physiology, and to look at all elements involved therein.

I do want to mention that subclinical metabolic acidosis does exist in the realm of clinical medicine, but only in those with chronic kidney disease, and of no relevance to the topic at hand.


There are other refuted hypothesizes that I will not delve into. The metabolic acidosis hypothesis is the most prominent one. You can read further, or explore other claims here.


Since then we’ve come a long way in understanding the effect of protein intake on bone health. We now have enough evidence to suggest that high protein intakes do not negatively affect bone health, but may in fact improves it via IGF-1 secretion which promotes osteoblastic(bone building) activity, and by increasing intestinal calcium absorption [8]. That means the urinary calcium losses are compensated by increased intestinal absorption and increased modulation of IGF-1. This study however is done on postmenopausal women, thus, it is not sufficient on its own to broaden the scope of generalization, but at least is a human study.


The above mentioned effect can be further enhanced by increasing calcium intake with the high protein meals, thus having a net positive effect instead of a possible neutral one. This can be done by simply adding dairy or a straight up calcium pill.


I do want to dig deeper into the topic, but its taking too much time, as such, I might pick it back up at a further point in time and delve deeper therein. Overall, I hope I provided enough evidence for both cases.


This concludes part 3 of the series. In my next series, I have the intention of analyzing vegan diets and explain why they're not good for sports and performance. Talk soon...

References:


1. [1] Brenner, B. M., et al. “Dietary Protein Intake and the Progressive Nature of Kidney Disease: The Role of Hemodynamically Mediated Glomerular Injury in the Pathogenesis of Progressive Glomerular Sclerosis in Aging, Renal Ablation, and Intrinsic Renal Disease.” The New England Journal of Medicine, vol. 307, no. 11, 9 Sept. 1982, pp. 652–659, www.ncbi.nlm.nih.gov/pubmed/7050706, 10.1056/NEJM198209093071104. Accessed 12 Apr. 2020.


2. [2] Metges, Cornelia C., and Christian A. Barth. “Metabolic Consequences of a High Dietary-Protein Intake in Adulthood: Assessment of the Available Evidence.” The Journal of Nutrition, vol. 130, no. 4, 1 Apr. 2000, pp. 886–889, 10.1093/jn/130.4.886. Accessed 17 Mar. 2020.


3. [3] Millward, D. Joe. “Optimal Intakes of Protein in the Human Diet.” Proceedings of the Nutrition Society, vol. 58, no. 2, May 1999, pp. 403–413, 10.1017/s0029665199000531. Accessed 11 Mar. 2020.


4. [4] Poortmans, Jacques R., and Olivier Dellalieux. “Do Regular High Protein Diets Have Potential Health Risks on Kidney Function in Athletes?” International Journal of Sport Nutrition and Exercise Metabolism, vol. 10, no. 1, Mar. 2000, pp. 28–38, 10.1123/ijsnem.10.1.28.

5,6. [5] Bonjour, Jean-Philippe. “Dietary Protein: An Essential Nutrient For Bone Health.” Journal of the American College of Nutrition, vol. 24, no. sup6, Dec. 2005, pp. 526S-536S, 10.1080/07315724.2005.10719501. Accessed 7 Sept. 2019.



7. [7] Cao, Jay J., et al. “A Diet High in Meat Protein and Potential Renal Acid Load Increases Fractional Calcium Absorption and Urinary Calcium Excretion without Affecting Markers of Bone Resorption or Formation in Postmenopausal Women.” The Journal of Nutrition, vol. 141, no. 3, 1 Mar. 2011, pp. 391–397, www.ncbi.nlm.nih.gov/pubmed/21248199, 10.3945/jn.110.129361. Accessed 17 Apr. 2020.


8,9. [8] Dawson-Hughes, Bess. “Interaction of Dietary Calcium and Protein in Bone Health in Humans.” The Journal of Nutrition, vol. 133, no. 3, 1 Mar. 2003, pp. 852S-854S, 10.1093/jn/133.3.852s. Accessed 15 Dec. 2019.


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