In an interesting paper the question is asked what if the history of the development of our understanding of diabetes has it wrong? The paper (J. Denis McGarry. What If Minkowski Had Been Ageusic? An Alternative Angle on Diabetes. Science, Vol. 258, No. 5083 (Oct. 30, 1992), pp. 766-770).
Despite decades of intensive investigation, the basic pathophysiological mechanisms responsible for the metabolic derangements associated with diabetes mellitus have remained elusive. Explored here is the possibility that traditional concepts in this area might have carried the wrong emphasis. It is suggested that the phenomena of insulin resistance
and hyperglycemia might be more readily understood if viewed in the context of underlying abnormalities of lipid metabolism.
Some powerful food for thought in the paper. Another paper (Arius, Energy Metabolism
) summarizes the argument as:
The author considers the possibility that the hyperinsulinemia of early non-insulin—dependent diabetes is coincident with hyperamylinemia, since insulin and amylin are cosecreted. Amylin would cause an increase in plasma lactate (Cori cycle); and lactate, a better precursor than glucose for fatty acid synthesis, would indirectly promote the production of very-low-density lipoproteins (VLDL). There would follow an increased flux of triglycerides from liver to muscle (and adipose tissue) and, as proposed and elaborated on, an increase in insulin resistance and production of many of the metabolic disturbances occurring in diabetes.
The Randle cycle is a biochemical mechanism involving the competition between glucose and fatty acids for their oxidation and uptake in muscle
and adipose tissue
. The cycle controls fuel selection and adapts the substrate supply and demand in normal tissues. This cycle adds a nutrient-mediated fine tuning on top of the more coarse hormonal control on fuel metabolism. This adaptation to nutrient availability applies to the interaction between adipose tissue and muscle. Hormones that control adipose tissue lipolysis affect circulating concentrations of fatty acids, these in turn control the fuel selection in muscle. Mechanisms involved in the Randle Cycle include allosteric control, reversible phosphorylation and the expression of key enzymes. The energy balance from meals composed of differing macronutrient composition is identical, but the glucose and fat balances that contribute to the overall energy balance change reciprocally with meal composition.
Fatty acids may act directly upon the pancreatic β-cell to regulate glucose-stimulated insulin secretion. This effect is biphasic. Initially fatty acids potentiate the effects of glucose. After prolonged exposure to high fatty acid concentrations this changes to an inhibition. Randle suggested that the term fatty acid syndrome would be appropriate to apply to the biochemical syndrome resulting from the high concentration of fatty acids and the relationship to abnormalities of carbohydrate metabolism, including starvation, diabetes and Cushing’s syndrome.
My own weight had been in the 280 range for a long time. In the months before I was diagnosed as Type 2 Diabetic my weight dropped 50 lbs without any lifestyle changes. After I went on Metformin my weight was relatively lower for a while. When I eventually went on Insulin my weight went up 40+ lbs fairly quickly. It is well known that Insulin adds weight.
My own thought is that the Insulin is both the lock and the key. Increased levels of Insulin pushes glucose or fat into cells and decreased levels of Insulin allows fat to come out of cells. That’s why Intermittent Fasting is such a great bullet for Type 2 diabetics. It allows our fasting Insulin levels to drop. Add to that Low Carbohydrate diets and the perfect recipe for controlling Diabetes comes into play.
The problem never really was Insufficient Insulin. The problem was too much Insulin. And clearly it is a fat related problem.
I did a previous Protein Experiment where I compared the response of my Blood Sugar to 50 grams of Whey Protein vs 50 grams of Casein Protein. Since both of those were “pure” Protein with very little fat, I was curious how those results would compare to animal protein which had fat.
For this experiment I chose Chicken Drumsticks. I weighed them amount of mean (total minus bones left at the end) and the nutritional information shows them to have been close to 50g of Protein:
Here is the Blood Glucose numbers (smoothed) over several hours added to the data from the original Whey/Casein test. The chicken drumsticks are in yellow.
Accounting for Differences
- The drumsticks (in yellow) are lower overall because I have been on the PSMF longer and my blood sugar levels have dropped. This is evidence, at least to me, that the PSMF is doing good things for my metabolic health.
- There was a dip at the start of the chicken wing experiment which was due to exercise. In this case it was a particularly grueling Saturday morning routine with a lot of lifting and burpees, etc. That explains the drop from 72 down to 64 at the start.
- The highest number was very comparable to the Whey and Casein numbers in terms of rise from the minimum. The max rise in Blood Sugar in all of these cases was no more than 20 units.
- The slope down with the animal Protein is longer and slower. That may explain less feelings of hunger as the consumption of the Protein ends.
- The curve is longer than either of the “pure” Proteins. The fat may extend that longer than the pure proteins. I’d like to repeat the experiment with low fat chicken breasts and see if it’s the fat or if it is the animal Protein vs Milk Protein of the Whey/Casein choices that makes a difference.
50 grams of Protein is a decent serving size. It is more than enough to stimulate Protein Muscle Synthesis.
All in all, I see nothing to worry about with eating Protein even for Type 2 Diabetics like myself. With all of the “Protein turns into candy bars” fear mongering out there, some sanity needs to be applied to the subject.
Of course, I would encourage any diabetic to test to see where they are with this same test. At least this way they know what effect Protein would have on their body. If they are a Type 1 Diabetic this information could be helpful to determine what amount of Insulin they should add for Protein.
Here are some of the scientific studies concerning Protein Sparing Modified Fasts (PSMF) and high protein diets.
- A Palgi, J L Read, I Greenberg, M A Hoefer, B R Bistrian, and G L Blackburn Multidisciplinary treatment of obesity with a protein-sparing modified fast: results in 668 outpatients. American Journal of Public Health, October 1985
- Bistrian DR, Winterer J, Blackburn GL, Young V, Sherman M.. Effect of a protein-sparing diet and brief fast on nitrogen metabolism in mildly obese subjects, J Lab Clin Med. 1977 May;89(5):1030-5.
- Van Gaal LF, Snyders D, De Leeuw IH, Bekaert JL. Anthropometric and calorimetric evidence for the protein sparing effects of a new protein supplemented low calorie preparation. Am J Clin Nutr. 1985; 41:410-540.
- Curr Opin Endocrinol Diabetes Obes. 2008 Oct;15(5):416-21. Benefits of high-protein weight loss diets: enough evidence for practice? Brehm BJ, D’Alessio DA.
- Am J Clin Nutr. 2005 Jun;81(6):1298-306. Effect of an energy-restricted, high-protein, low-fat diet relative to a conventional high-carbohydrate, low-fat diet on weight loss, body composition, nutritional status, and markers of cardiovascular health in obese women. Noakes M, Keogh JB, Foster PR, Clifton PM.
- Eur J Nutr. 2013 Feb;52(1):317-25. Comparison of the effects of weight loss from a high-protein versus standard-protein energy-restricted diet on strength and aerobic capacity in overweight and obese men. Wycherley TP, Buckley JD, Noakes M, Clifton PM, Brinkworth GD.
- Schoeller DA1, Buchholz AC. Energetics of obesity and weight control: does diet composition matter?J Am Diet Assoc. 2005 May;105(5 Suppl 1):S24-8.
- Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, Christou DD. A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women. J Nutr. 2003 Feb;133(2):411-7.
- Halton TL, Hu FB. The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr. 2004 Oct;23(5):373-85.
- Brehm BJ, D’Alessio DA. Benefits of high-protein weight loss diets: enough evidence for practice? Curr Opin Endocrinol Diabetes Obes. 2008 Oct;15(5):416-21.
- de Luis, et.al. Effects of a high-protein/low carbohydrate versus a standard hypocaloric diet on adipocytokine levels and insulin resistance in obese patients along 9 months. Journal of Diabetes and its Complications. Volume 29, Issue 7, September–October 2015, Pages 950-954.
Muscle Protein Synthesis
- Satoshi Fujita,et.al. Effect of insulin on human skeletal muscle protein synthesis is modulated by insulin-induced changes in muscle blood flow and amino acid availability Am J Physiol Endocrinol Metab. 2006 Oct; 291(4): E745–E754.
- Buse, M. G. & Reid, S. S. (1975) Leucine. A possible regulator of protein turnover in muscle. J. Clin. Invest. 56:1250–1261.
- Hong, S. C. & Layman, D. K. (1984) Effects of leucine on in vitro protein synthesis and degradation in rat skeletal muscle. J. Nutr. 114:1204–1212.
- Li, J. B. & Jefferson, L. S. (1978) Influence of amino acid availability on protein turnover in perfused skeletal muscle. Biochim. Biophys. Acta 544:351–359.
- Lundholm K, Edström S, Ekman L, Karlberg I, Walker P, Scherstén T. Protein Degradation in Human Skeletal Muscle Tissue: The Effect of Insulin, Leucine, Amino Acids. Clin Sci (Lond). 1981 Mar;60(3):319-26.
Studies on Protein and Diabetes
- Donald K. Layman, Jamie I. Baum. Dietary Protein Impact on Glycemic Control during Weight Loss. The Journal of Nutrition, Volume 134, Issue 4, 1 April 2004, Pages 968S–973S.
- Judith Farrés, Albert Pujol, Mireia Coma, Jose Luis Ruiz, Jordi Naval, José Manuel Mas, Agustí Molins, Joan Fondevila and Patrick Aloy. Revealing the molecular relationship between type 2 diabetes and the metabolic changes induced by a very-low-carbohydrate low-fat ketogenic diet. Nutrition & Metabolism 2010 7:88.
- Chang J, Kashyap SR. The protein-sparing modified fast for obese patients with type 2 diabetes: what to expect. Cleveland Clinic J Med. 2014;81:557-565.
- Bruce R Bistrian, M.D., Ph.D., George L Blackburn, M.D., Ph.D., Jean-Pierre Flatt, Ph.D., Jack Sizer, M.D., Nevin S Scrimshaw, Ph.D., M.D. and Mindy Sherman, B.A. Nitrogen Metabolism and Insulin Requirements in Obese Diabetic Adults on a Protein-Sparing Modified Fast. Diabetes 1976 Jun; 25(6): 494-504.
- Mary C Gannon, Frank Q Nuttall, Asad Saeed, Kelly Jordan, and Heidi Hoover. An increase in dietary protein improves the blood glucose response in persons with type 2 diabetes. The American Journal of Clinical Nutrition October 2003 vol. 78 no. 4 pp 734-741.
- Diabetes 2004 Sep; 53(9): 2375-2382. Effect of a High-Protein, Low-Carbohydrate Diet on Blood Glucose Control in People With Type 2 Diabetes. Mary C. Gannon and Frank Q. Nuttall.
- Obes Facts. 2017 Jul; 10(3): 238–251. Effect of a High-Protein Diet versus Standard-Protein Diet on Weight Loss and Biomarkers of Metabolic Syndrome: A Randomized Clinical Trial. Ismael Campos-Nonato, Lucia Hernandez, and Simon Barquera.
Protein as a Macronutrient and Protein Requirements
- The American Journal of Clinical Nutrition, Volume 77, Issue 1, 1 January 2003, Pages 109–127. Meta-analysis of nitrogen balance studies for estimating protein requirements in healthy adults. William M Rand Peter L Pellett Vernon R Young.
- Jose Antonio, Corey A Peacock, Anya Ellerbroek, Brandon Fromhoff and Tobin Silver. The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals. Journal of the International Society of Sports Nutrition 2014:11:19.
- Am J Clin Nutr. 2016 Mar;103(3):738-46. doi: 10.3945/ajcn.115.119339. Epub 2016 Jan 27. Higher compared with lower dietary protein during an energy deficit combined with intense exercise promotes greater lean mass gain and fat mass loss: a randomized trial. Longland TM, Oikawa SY, Mitchell CJ, Devries MC, Phillips SM.