According to (Diabetes Care 1980 Mar; 3(2): 270-273. “Normal” Insulin Secretion: The Goal of Artificial Insulin Delivery Systems? R Philip Eaton, Richard C Allen, David S Schade and James C Standefer).
In the present study, we have determined prehepatic insulin production in six normal men throughout a day that included three typical 750-cal meals. Total insulin secretion for the 24 h was 45.4 ∪, secreted as 10.6 ∪ with breakfast, 13.4 ∪ with lunch, and 13.8 ∪ with dinner. The remaining 7.6 ∪ was secreted during the 9 h night at a rate of 0.85 ∪/h.
This may be why the transition down from 20 units a day to 8 units a day has been a more stressful one (with a couple of “higher” Blood Glucose levels) than any of the previous steps. I am now down into the range my body needs as a baseline.
If my LC-HF diet is keeping me from needing mealtime insulin then the remaining rate of approx .85 U/h would mean approx 20 U/day are needed for the background rate. I am far from a normal man (in so many ways) but I have to imagine that these were people substantially smaller than myself. Maybe 2/3 my weight so my requirements should be proportionately higher. Not a biologist so who knows?
An interesting additional factor is the question of gluconeogenesis during fasting. There was a study done on this as well (Metabolism
Volume 50, Issue 1, January 2001, Pages 47-52. Quantitative contributions of gluconeogenesis to glucose production during fasting in type 2 diabetes mellitus. Alexandre Wajngot, Visvanathan Chandramouli, William C. Schumann, Karin Ekberg, Paul K. Jones, Suad Efendic, Bernard R. Landau).
Contributions of gluconeogenesis to glucose production were determined between 14 to 22 hours into a fast in type 2 diabetics (n = 9) and age-weight-matched controls (n = 7); ages, 60.4 ± 2.3 versus 55.6 ± 1.2 years and body mass indices (BMI) 28.6 ± 2.3 versus 26.6 ± 0.8 kg/m2.
The results were interesting.
Thus, gluconeogenesis contributed more to glucose production in the diabetic than control subjects. Production and the contribution of gluconeogenesis declined more in the diabetic subjects during the fast.
Here’s where they are totally right and totally wrong at the same time. From the Mayo Clinic site (Avoid weight gain while taking insulin).
Take your insulin only as directed. Don’t skip or reduce your insulin dosages to ward off weight gain. Although you might shed pounds if you take less insulin than prescribed, the risks are serious. Without enough insulin, your blood sugar level will rise — and so will your risk of diabetes complications.
I get what they are saying. If you need insulin to regulate your blood sugar and you go off it then you’ve got serious problems up to death. The thing a diabetic should be watching isn’t the amount you were prescribed. It should be the amount needed to regulate your blood sugar. No more.
My doctor started me out by telling me that I needed to take 40 units of long-lasting insulin. When that led to a high HbA1C number he said that I needed to add meal-time insulin. I wish they would not call it that. So many false things there. He told me to use the 2nd Insulin and use 8 units before every meal. The diabetic nurse told me that was wrong and she had him fix the prescription.
They got me nutritional training and told me to count carbs. Not count as in limit, but to bolus for the amount of grams of carbs in what I was eating. Good advice for high carb meals. Not great when you consider gluconeogenesis. That all got me to a decent point of glucose control but was about 60 units a day (40 of basal and 20 of “meal-time” (fast acting) Insulin. In the last 5 years I have progressed to around 100 units a day (varies by my carb intake). It’s only now that I am getting lower than when I was diagnosed.
I am using less by doing LCHF (really mostly LC) and Intermittent Fasting (IF). Yesterday I used a total of 47 units of Insulin. I will lower my basal (constant) Insulin rate tomorrow to drive my Insulin levels even lower.
So if insulin causes weight gain then it would seem to logically follow that reducing insulin will result in weight loss. We know this is the case because if we just stopped taking our insulin we would lose a lot of weight fast*. However, getting rid of your need for external sources of Insulin is a great goal.
In my case, I lost 50+ lbs in six months before I was diagnosed with T2D. That was the body’s natural way of trying to handle the high blood sugar problem. Adding medications just pushed my weight up. That was true with just Metformin. Could this be because the study that the Metformin causes weight loss concept was built on a study of psychiatric patients not on diabetics? Other studies based on pre-T2Ds are equally questionable since their weight loss could be due to poorer control over their blood sugar levels.
This all makes the advice of the typical MD even more absurd when they tell you that “When you get your sugars in order you will be able to lose weight.” How is that even remotely possible when I have to use astronomical amounts of insulin to keep my sugar under control?
*Stopping your Insulin cold turkey can be bad and people die from doing this. I feel like I need to say this because there are dumb people out there. Don’t drop your Insulin alone for weight loss even if that weight loss itself is good for you. There are other ways. Make sure you monitor your blood sugar level closely no matter what treatment you use.
Time for the next paradox. (Science is: Relationships between changes in leptin and insulin resistance levels in obese individuals following weight loss).
Moderate weight reduction in obese participants over a short period significantly improved Insulin Resistance.
Maybe this isn’t really a paradox as much as it is a challenge. How do you possibly lose weight when you are on large doses of Insulin?
Next, which was the cause and which was the effect? Did what they do reduce the weight improve Insulin Resistance or did what they do reduce the insulin resistance result in weight loss?
Either way, we’ve now discovered at least one way to reduce Insulin Resistance – weight loss.
One Man’s Resistance is another man’s Sensitivity
Resistance and sensitivity are the inverse of each other. The goal is to improve our cells ability to deal with insulin. Saying it either way as Increase Insulin Sensitivity or Decrease Insulin Resistance is saying the same thing.
The connection between insulin and weight gain is well understood and acknowledged. From the Mayo Clinic website.
When you take insulin, glucose is able to enter your cells, and glucose levels in your blood drop. This is the desired therapeutic goal. But if you take in more calories than you need to maintain a healthy weight — given your level of activity — your cells will get more glucose than they need. Glucose that your cells don’t use accumulates as fat.
So what is their advice for avoiding this situation? Summarized as
- Count Calories
- Don’t skip meals
- Get aerobic activity
- See your doctor about getting on [more] medications
- Don’t skip taking your insulin
They pulled out the old tried-and-believed-to-be-true words. That don’t work at all. Nothing makes you feel deprived more than counting your calories. Skipping meals allows your insulin levels to drop. Exercise sounds good in theory but rarely ever gets put into practice. Get more meds which are going to push harder to get the glucose out of the blood into your cells? Sounds like the kind of advice you’d give someone for weight gain, not loss. Finally, don’t go off your insulin for weight loss purposes.
Most of what they say is well-intentioned but completely wrong. All of this explains why we got fat but doesn’t really help us get control of our insulin resistance. Why not tell people that they can skip meals as a way of getting their insulin resistance to improve? Are they so afraid someone will go too low that they don’t want to see people improve their core issue?
Here’s what the advice should be when targeted towards improving insulin resistance.
- Don’t count calories. Nothing makes you feel more deprived than counting calories and nothing sets you up for feeling more like a failure. Restricted calorie diets lower your metabolism and you will be worse off for years after the diet since your set point will then be lowered.
- Skip meals. At the very least don’t eat just because it’s time to eat. Eat because you are actually hungry. Understand that the fast you did from 7 PM to 7 AM could be stretched out till noon without harming you.
- Exercise is always good. If you fast you get more energy and more active naturally. Exercise has lasting effects on blood sugar levels.
- Find a doctor who is willing to work with you and explore options that he may not have learned about in medical school. At the very least one that understands what the meds she prescribes to you do and their effects on insulin resistance. At least find a doctor that acknowledges your problem is insulin resistance. (Added List of Low Carb Doctors).
- All other things being equal, you can only reduce your insulin needs by lowering your insulin resistance. The goal, therefore, is to figure out how to reduce your insulin usage. Don’t just stop taking insulin and let your insulin levels get really high. I’ve lost a friend recently to DKA so I take this very seriously. She was an undiagnosed T2D but in retrospect she had all of the external markers of a T2D adult.
It might be beneficial to do a post on each of the above treatment points but focus the points on the treatment I am doing now, 18/6 Intermittent Fasting.
Here are Studies specifically on the effects of diets on Diabetes (particularly low carbohydrate diets).
- Laura R Saslow, PhD, et.al. An Online Intervention Comparing a Very Low-Carbohydrate Ketogenic Diet and Lifestyle Recommendations Versus a Plate Method Diet in Overweight Individuals With Type 2 Diabetes: A Randomized Controlled Trial. J Med Internet Res. 2017 Feb; 19(2): e36.
- Guenther Boden. (2005). Effect of a Low-Carbohydrate Diet on Appetite, Blood Glucose Levels, and Insulin Resistance in Obese Patients with Type 2 Diabetes. Ann Intern Med. 2005; 142(6):403-411.
- Mary C. Gannon and Frank Q. Nuttall. Effect of a High-Protein, Low-Carbohydrate Diet on Blood Glucose Control in People With Type 2 Diabetes. Diabetes 2004 Sep; 53(9): 2375-2382.
- Jørgen Vesti, Nielsen, Eva Joensson. Low-carbohydrate diet in type 2 diabetes. Stable improvement of bodyweight and glycemic control during 22 months follow-up. Nutrition & Metabolism, December 2006, 3:22.
- Diabetes Care 2002 Apr; 25(4): 652-657. Effects of Energy-Restricted Diets Containing Increased Protein on Weight Loss, Resting Energy Expenditure, and the Thermic Effect of Feeding in Type 2 Diabetes. N.D. Luscombe, BSC HON1, P.M. Clifton, MD2, M. Noakes, MSC, PHD2, B. Parker, BSC HON1 and G. Wittert, MD.
- JAMA. 1994. Effects of Varying Carbohydrate Content of Diet in Patients With Non—Insulin-Dependent Diabetes Mellitus. Abhimanyu Garg, MBBS, MD; John P. Bantle, MD; Robert R. Henry, MD; et al Ann M. Coulston, RD; Kay A. Griver, RD; Susan K. Raatz, MS, RD; Linda Brinkley, RD; Y-D. Ida Chen, PhD; Scott M. Grundy, MD, PhD; Beverley A. Huet, MS; Gerald M. Reaven, MD.
- Lipids. 2009 Apr;44(4):297-309. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, Kraemer WJ, Bibus DM, Fernandez ML, Feinman RD.
- J Clin Invest. 1936 Nov; 15(6): 665–671. The Glycemic Response to Isoglucogenic Quantities of Protein and Carbohydrate. Jerome W. Conn and L. H. Newburgh.
- N Engl J Med 1988; 319:829-834. Comparison of a High-Carbohydrate Diet with a High-Monounsaturated-Fat Diet in Patients with Non-Insulin-Dependent Diabetes Mellitus. Abhimanyu Garg, M.B., B.S., M.D., Andrea Bonanome, M.D., Scott M. Grundy, M.D., Ph.D., Zu-Jun Zhang, M.D., and Roger H. Unger, M.D.
- Metabolism. Volume 41, Issue 12, December 1992, Pages 1373-1378 Metabolism. A high-monounsaturated-fat/low-carbohydrate diet improves peripheral insulin sensitivity in non-insulin-dependent diabetic patients. M. Parillo, A.A. Rivellese, A.V. Ciardullo, B. Capaldo, A. Giacco, S. Genovese, G. Riccardi.
- The Journal of Clinical Endocrinology & Metabolism, Volume 86, Issue 3, 1 March 2001, Pages 1040–1047, Effect of Protein Ingestion on the Glucose Appearance Rate in People with Type 2 Diabetes. M. C. Gannon J. A. Nuttall G. Damberg V. Gupta F. Q. Nuttall.
- Obesity (2016) 24, 79–86. Weight Loss on Low-Fat vs. Low-Carbohydrate Diets by Insulin Resistance Status Among Overweight Adults and Adults With Obesity: A Randomized Pilot Trial. Christopher D. Gardner, Lisa C. Offringa, Jennifer C. Hartle, Kris Kapphahn, and Rise Cherin.
- Bonnie J. Brehm, Randy J. Seeley, Stephen R. Daniels, David A. D’Alessio. A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 4, 1 April 2003, Pages 1617–1623.
- Nutr Metab (Lond). 2006 Jan 11;3:7. Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk. Noakes M, Foster PR, Keogh JB, James AP, Mamo JC, Clifton PM.
- Jeannie Tay B Nutr Diet (Hons), Grant D. Brinkworth PhD, Manny Noakes PhD, Jennifer Keogh M Sc, Peter M. Clifton PhD. Metabolic Effects of Weight Loss on a Very-Low-Carbohydrate Diet Compared With an Isocaloric High-Carbohydrate Diet in Abdominally Obese Subjects. Journal of the American College of Cardiology, Volume 51, Issue 1, 1–8 January 2008, Pages 59-67.
- JAMA. 1994 May 11;271(18):1421-8. Effects of varying carbohydrate content of diet in patients with non-insulin-dependent diabetes mellitus. Garg A, Bantle JP, Henry RR, Coulston AM, Griver KA, Raatz SK, Brinkley L, Chen YD, Grundy SM, Huet BA, et al.
- Nutrition & Metabolism2004 1:6. Metabolic response of people with type 2 diabetes to a high protein diet. Frank Q Nuttall, Mary C Gannon.
- 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.
- J Clin Invest. 1988 Feb; 81(2): 442–448. Twenty-four-hour profiles and pulsatile patterns of insulin secretion in normal and obese subjects. K S Polonsky, B D Given, and E Van Cauter.
- Nutrients. 2013 Jun; 5(6): 2019–2027. Body Fat Distribution and Insulin Resistance. Pavankumar Patel* and Nicola Abate.
- Connor WE, Prince MJ, Ullmann D, et al. The hypotriglyceridemic effect of fish oil in adult-onset diabetes without adverse glucose control. Ann N Y Acad Sci 1993;683:337–40.
- Fish Oil and Glycemic Control in Diabetes. DIABETES CARE, VOLUME 21, NUMBER 4, APRIL 1998. Frieberg, et.al.).
- Insulin Response to Glucose in Diabetic and Nondiabetic Subjects. John D. Bagdade, Edwin L. Bierman, and Daniel Porte Jr. Journal of Clinical Investigation. October 1, 1967.
These are studies related to diabetes in general:
- Diabetes Care 1991 Mar; 14(3): 173-194. Insulin Resistance: A Multifaceted Syndrome Responsible for NIDDM, Obesity, Hypertension, Dyslipidemia, and Atherosclerotic Cardiovascular Disease. Ralph A DeFronzo, MD and Eleuterio Ferrannini, MD.
- Diabetes 2017 Apr; 66(4): 815-822. Role of Adipose Tissue Insulin Resistance in the Natural History of Type 2 Diabetes: Results From the San Antonio Metabolism Study. Amalia Gastaldelli, Melania Gaggini and Ralph A. DeFronzo.
- J Clin Invest. 2000;106(4):473-481. Obesity and insulin resistance. Barbara B. Kahn, Jeffrey S. Flier.
- Diabetes. 2000 Dec; 49(12): 2063–2069. Mechanism by Which Metformin Reduces Glucose Production in Type 2 Diabetes. Ripudaman S. Hundal, Martin Krssak, Sylvie Dufour, Didier Laurent, Vincent Lebon, Visvanathan Chandramouli, Silvio E. Inzucchi, William C. Schumann, Kitt F. Petersen, Bernard R. Landau, and Gerald I. Shulman.
- BMC Endocr Disord. 2016. Efficacy and safety of insulin in type 2 diabetes: meta-analysis of randomised controlled trials. Erpeldinger S, et al.
- Diabetes Care 1980 Mar; 3(2): 270-273. “Normal” Insulin Secretion: The Goal of Artificial Insulin Delivery Systems? R Philip Eaton, Richard C Allen, David S Schade and James C Standefer.
- Metabolism Volume 50, Issue 1, January 2001, Pages 47-52. Quantitative contributions of gluconeogenesis to glucose production during fasting in type 2 diabetes mellitus. Alexandre Wajngot, Visvanathan Chandramouli, William C. Schumann, Karin Ekberg, Paul K. Jones, Suad Efendic, Bernard R. Landau.
- Clin Sci (Lond). 2016 Jun 1;130(12):1017-25. Impaired glucose tolerance after brief heat exposure: a randomized crossover study in healthy young men. Faure C, Charlot K, Henri S, Hardy-Dessources MD, Hue O, Antoine-Jonville S.
- Appetite. 2010 Aug; 55(1): 37–43. Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels. Stephen D. Anton, Ph.D., Corby K. Martin, Ph.D., Hongmei Han, M.S., Sandra Coulon, B.A., William T. Cefalu, M.D., Paula Geiselman, Ph.D., and Donald A. Williamson, Ph.D.
- Diabetes Care 2004 Jan; 27(1): 281-282. Vinegar Improves Insulin Sensitivity to a High-Carbohydrate Meal in Subjects With Insulin Resistance or Type 2 Diabetes. Carol S. Johnston, PHD, Cindy M. Kim, MS and Amanda J. Buller, MS.
- Nutrients. 2013 May; 5(5): 1544–1560. Non-Alcoholic Fatty Liver Disease (NAFLD) and Its Connection with Insulin Resistance, Dyslipidemia, Atherosclerosis and Coronary Heart Disease. Melania Gaggini, Mariangela Morelli, Emma Buzzigoli, Ralph A. DeFronzo, Elisabetta Bugianesi, and Amalia Gastaldelli.
- Michelle C Venables, Carl J Hulston, Hannah R Cox, Asker E Jeukendrup; Green tea extract ingestion, fat oxidation, and glucose tolerance in healthy humans, The American Journal of Clinical Nutrition, Volume 87, Issue 3, 1 March 2008, Pages 778–784.
- Br J Nutr. 2009 Mar;101(6):886-94. Effects of dietary supplementation with the green tea polyphenol epigallocatechin-3-gallate on insulin resistance and associated metabolic risk factors: randomized controlled trial. Brown AL, Lane J, Coverly J, Stocks J, Jackson S, Stephen A, Bluck L, Coward A, Hendrickx H.
- Ann Intern Med. 2017;167(6):365-374. Continuous Glucose Monitoring Versus Usual Care in Patients With Type 2 Diabetes Receiving Multiple Daily Insulin Injections: A Randomized Trial. Roy W. Beck, MD, PhD, et.al.
- Gisela Wilcox. Insulin and Insulin Resistance. Clin Biochem Rev. 2005 May; 26(2): 19–39.
- Proc Natl Acad Sci U S A. 2009 Sep 8; 106(36): 15430–15435. Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity. Elisa Fabbrini,et.al.
- Erion, K.A. & Corkey, B.E. (2017). Hyperinsulinemia: a Cause of Obesity? Curr Obes Rep (2017) 6: 178.
- Shanik MH1, Xu Y, Skrha J, Dankner R, Zick Y, Roth J. (2008). Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse? Diabetes Care. 2008 Feb;31 Suppl 2:S262-8.