Is Losing Weight the Cure for Your Diabetes?

Chances are you or someone you know has diabetes. In fact, over 30 million Americans have diabetes. What’s concerning is that diabetes remains the 7th highest cause of death in the United States.1 If the trend continues, doctors estimate that by 2050, 1 in 3 Americans will have diabetes.2 That statistic virtually guarantees that you or a close family member will be affected by diabetes. There is no doubt that diabetes is commonplace and a growing American epidemic. Obesity is closely tied to the rising number of diabetics. In fact, there is a term called diabesity that was created to encompass the twin conditions of obesity and diabetes.3 

That’s not surprising if you know that 90% of people with type 2 diabetes are overweight or obese.4 So, does having diabetes make people gain weight? Can losing weight ‘cure’ your diabetes? Can functional medicine help me? I get these questions a lot. First, you have to understand how your body processes sugar and find the root cause of your diabetes.

Blood Sugar Dysregulation

Diabetes is a blood sugar dysregulation disease. All forms of diabetes happen when the body doesn’t process blood sugar correctly. When you eat food, your body should digest it and extract nutrients, minerals, and convert carbs into glucose. The glucose level (blood sugar) immediately rises in your bloodstream.5 The more sugary your food is, the more glucose your body makes and puts into your bloodstream. That’s why you feel a burst of energy after you eat a sugary snack. When your glucose level is elevated, your pancreas sends out a hormone called insulin. Insulin tells cells to use blood sugar instead of burning fat to get energy. Some cells use the glucose right away for energy, and others store the blood sugar for later use.

Your blood sugar level drops after the insulin has done its job. Between meals, when blood sugar levels dip down, your pancreas reacts again. This time, it sends out a different hormone called glucagon that tells your body to use the blood sugar it stored earlier. The entire blood sugar system depends on the feedback loop between insulin and glucagon to keep your blood sugar level steady. When the cycle is interrupted, or your pancreas isn’t working correctly, you have blood sugar dysregulation or diabetes. There are different types of diabetes.

Type 1 Diabetes - often presents at a young age when someone has consistently high blood sugar levels, and their body isn’t making enough insulin. This is really an autoimmune condition where the body has created antibodies that attack the pancreas. It becomes damaged to the point where it cannot make enough insulin to participate in the feedback loop. So blood sugar remains high and cannot be used correctly.

Type 2 Diabetes - used to be called ‘adult-onset diabetes’ but younger people are being diagnosed as well. Type 2 diabetes is a condition where blood sugar levels are high, and the body isn’t able to correctly use glucose for cell energy. The cause of type 2 diabetes is insulin resistance.

Prediabetes - Some people also call this ‘borderline diabetes.’ Prediabetes is also caused by insulin resistance, but the blood sugar level isn’t high enough to yet to be called diabetes. If you have prediabetes, you are at a high risk of developing full-blown type 2 diabetes. We consider prediabetes as type 2 diabetes caught early.

What is Insulin Resistance?

Insulin resistance causes both type 2 diabetes and prediabetes. So what is it? And can insulin resistance be fixed? (Spoiler alert, it can be reversed.)

Insulin resistance is when cells can no longer use blood sugar correctly because they’ve become resistant to insulin. Remember, when blood sugar is high, the pancreas sends out insulin to remove blood sugar from the bloodstream and put it in the cells. Insulin is like the key that will unlock the door to let glucose inside the cell. Once inside, the cell uses glucose for energy. But with insulin resistance, the locks are worn out, and the insulin key doesn’t work. Without a working key, glucose can’t get inside the cells to be used for energy. The result is you feel tired, your immune system struggles to work, and your body can’t heal itself as well as it should. In the long term, your pancreas cranks out more and more insulin to try to reduce blood sugar and can eventually wear out the insulin-producing parts of the pancreas. Insulin resistance isn’t a lack of insulin. In fact, people typically have a rise in insulin levels, but the cells stop responding to the insulin, so lots of glucose remains in the bloodstream.

What Causes Insulin Resistance?

To break the cycle of insulin resistance and restore the normal feedback loop, we have to find the root cause for your condition. There are several ways your body can develop insulin resistance.

Gut Microbiota - In your digestive tract, you have a microbiota that is made up of bacteria, viruses, and fungi.6 All of these microbes help digest your food. Research has found that people who are obese have different proportions of bacterial microbes than leaner people.7 These additional bacterial microbes cause endotoxins to be absorbed through the digestive tract. Endotoxins cause inflammation and disrupt insulin receptors.8 The effect is like damaging the cell’s lock. The insulin key won’t work. 

Thyroid conditions - Your thyroid helps control many body functions like regulating body temperature, cholesterol levels, menstrual cycle, body weight, heart rate, and breathing.9 Thyroid hormones go to nearly every cell in the body since they manage your cells’ metabolism. Cells rely on thyroid hormones to make energy. With hyperthyroidism, the body makes too many thyroid hormones. This hormone overabundance speeds up the metabolism but disrupts the liver function.10 When the liver can’t store glucose well, too much blood sugar remains in the bloodstream. The excess of blood sugar leads to insulin resistance.  Hypothyroidism is when the body does not have enough thyroid hormones. In a hypothyroid condition, the body’s metabolism and organs are slow. Since metabolism isn’t running at the correct speed, enough blood sugar isn’t used by the cells and can build up in the bloodstream.11 This condition also leads to insulin resistance.

Leptin Resistance - Leptin is a hormone secreted by the liver that decreases our appetite and helps us lose weight.12 This hormone tells the brain we are no longer hungry. However, leptin resistance means that the body is not responding to the call to stop consuming calories. The result is weight gain. The extra calories consumed are digested and result in extra glucose in our blood. Over time, the excess glucose puts a strain on your pancreas, which must make additional insulin.13 Over time, excess insulin leads to insulin resistance.

Inflammation - Fat is an interesting body component. It pads our organs, stores energy and vitamins, insulates us, and is necessary for chemical reactions from reproduction to the immune system.14 However, fat also contains cytokines which, when released cause cell damage and inflammation.15 Excess fat means a large increase in cytokines and body-wide inflammation. Cytokines also cause insulin resistance.16

The Insulin Resistance/Fat Connection

Inflammation, leptin resistance, and gut microbiota are all causes of insulin resistance and linked with obesity. Each one of those causes stems from changes in the body’s chemistry or makeup as a result of excess weight gain. It’s easy to view excess weight is the primary cause of diabetes. But it’s not excess weight alone that is the issue. There’s also a connection and correlation with diabetes and where excess weight is stored on a person.

Visceral fat, also known as, ‘belly fat,’ is fat that is stored around a person’s abdomen, liver, pancreas, and intestines.17 Visceral fat isn’t the type of fat you can pinch with your fingers. Instead, it’s a fat that’s stored deeper inside behind your abdominal muscles and surrounding organs. What makes visceral fat dangerous is that it secretes a protein (RBP4) that causes insulin resistance. Since you can’t see your visceral fat, it’s harder to know if you have too much of it. Thankfully, checking your waist measurements can let you know if you might have an excess of this particular type of fat. For an accurate measurement, don’t suck in your belly and measure around your belly button. Women with waist measurements larger than 35 inches and men with measurements larger than 40 inches are at risk for excess visceral fat.18

Given that obesity and excess weight are linked with insulin resistance, it seems like significant weight loss would reverse insulin resistance. But it turns out that’s not necessarily the case. A study followed 15 obese women after liposuction to see if their metabolism and bloodwork reflected a huge fat reduction.19 The women lost 28-44% of their abdominal subcutaneous fat through liposuction. After three months, none of the women showed any improvement in their blood pressure, glucose, insulin, and lipid concentrations. Even though they had a huge amount of fat from the abdominal region removed, there was no change in the women’s insulin resistance. The type of fat removed was subcutaneous, pinchable fat just below the skin’s surface. Subcutaneous fat does not have the same effect on the body’s chemistry as visceral fat.

A ‘calories in, calories out’ plan or even liposuction doesn’t work to reverse insulin resistance because it doesn’t address if the body’s chemistry is working correctly or how it’s processing blood sugar. This also explains why some obese people do not have diabetes and some skinny people that have diabetes. Going back to the lock and key analogy, some obese people have excess fat that can contribute to altered gut microbiota and inflammation. Their body continues to crank out plenty of insulin keys, but their cell locks don’t wear out. On the other side, some thin people have consistently high blood sugar that leads to insulin resistance and diabetes. Instead of the weight gain normally seen in diabetics, these thin people have naturally high metabolisms that burn the extra glucose before it can be converted to fat. Thin or overweight, the path to begin reversing diabetes starts with addressing the root cause that began the cycle to insulin resistance and blood sugar dysregulation.

The Functional Medicine Approach

Conventional tests rely on testing blood sugar levels, but long before blood sugar rises, high insulin levels can indicate insulin resistance.20 Many people who are producing high amounts of insulin won’t have noticeable symptoms until blood sugar has started to rise as well. Weight gain can cause insulin resistance, and insulin resistance can cause extra fat to be stored. This cycle creates a revolving door of weight gain and diabetes which needs the initial cause to be changed to break the cycle.

Functional medicine takes a proactive approach to run the tests your history and exam indicate are needed to find the root cause for your blood sugar dysregulation. These advanced tests can unlock the underlying cause.

A1C test - This test measures the percentage of your red blood cells that are coated with sugar.21 It tells us your average blood sugar level for the last few months and predicts potential diabetic complications.

Lipid profiles - This test measures LDL, HDL, and triglyceride levels. These values can be used to look for inflammation and insulin resistance.

C-reactive protein test - This test measures the amount of c-reactive protein (CRP) in your blood.22 Elevated CRP indicates inflammation and can help uncover if systemic inflammation is fueling your diabetic condition.

There are additional tests to rule out liver dysfunction, thyroid problems, or gut bacteria imbalance. Without test results, you don’t have the cause driving your blood sugar dysregulation. The conventional approach is to lose weight alone. Reducing excess body fat is always a good idea, but weight loss alone doesn’t alter your blood chemistry. By finding the underlying cause, we can develop a personalized treatment plan to stop and begin reversing your blood sugar dysregulation.

Find us on Facebook for more information on our diabetic enhancement programs or our in-office health classes!


1 “Statistics About Diabetes.” ADA, 2019,

2 Bhupathiraju, S. N., & Hu, F. B. (2016). Epidemiology of Obesity and Diabetes and Their Cardiovascular Complications. Circulation research, 118(11), 1723–1735. doi:10.1161/CIRCRESAHA.115.306825

3 Kalra, Sanjay. “Journal Of Pakistan Medical Association.” JPMA, Apr. 2013,

4 “Type 2 Diabetes and Obesity: Twin Epidemics.” American Society for Metabolic and Bariatric Surgery, 30 Dec. 2014,

5 “How The Body Metabolizes Sugar.”, 16 Nov. 2016,

6 MacGill, Markus. “Gut Microbiota: Definition, Importance, and Medical Uses.” Medical News Today, MediLexicon International, 26 June 2018,

7 Caricilli, A. M., & Saad, M. J. (2013). The role of gut microbiota on insulin resistance. Nutrients, 5(3), 829–851. doi:10.3390/nu5030829

8 Zivot, JB, and WD Hoffman. “Pathogenic Effects of Endotoxin.” New Horiz., 3 May 1995, pp. 267–275.,

9 [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. How does the thyroid gland work? 2010 Nov 17 [Updated 2018 Apr 19]. Available from:

10 “Vol 11 Issue 1 P.7-8.” American Thyroid Association, 2019,

11 Gabriela Brenta, “Why Can Insulin Resistance Be a Natural Consequence of Thyroid Dysfunction?,” Journal of Thyroid Research, vol. 2011, Article ID 152850, 9 pages, 2011.

12 Gruzdeva, O., Borodkina, D., Uchasova, E., Dyleva, Y., & Barbarash, O. (2019). Leptin resistance: underlying mechanisms and diagnosis. Diabetes, metabolic syndrome and obesity : targets and therapy, 12, 191–198. doi:10.2147/DMSO.S182406

13 Paz-Filho, G., Mastronardi, C., Wong, M. L., & Licinio, J. (2012). Leptin therapy, insulin sensitivity, and glucose homeostasis. Indian journal of endocrinology and metabolism, 16(Suppl 3), S549–S555. doi:10.4103/2230-8210.105571

14 Rush University Medical Center. “Hypothyroidism Symptoms Linger despite Medication Use, Normal Blood Tests.” ScienceDaily, ScienceDaily, 12 Oct. 2016,

15 Zhang, J. M., & An, J. (2007). Cytokines, inflammation, and pain. International anesthesiology clinics, 45(2), 27–37. doi:10.1097/AIA.0b013e318034194e

16 Yu, Chunli, et al. “Mechanism by Which Fatty Acids Inhibit Insulin Activation of Insulin Receptor Substrate-1 (IRS-1)-Associated Phosphatidylinositol 3-Kinase Activity in Muscle.” Journal of Biological Chemistry, vol. 277, no. 52, 2002, pp. 50230–50236., doi:10.1074/jbc.m200958200.

17 “Visceral Fat (Active Fat).” Visceral Fat (Active Fat) - Types of Fat, Insulin Resistance & Health Risks, 2019,

18 Woodham, Chai. “You May Be Fat and Not Even Know It Why the Belly Fat We Can’t See Is More Dangerous than We Realize.” U.S. News and World Report, 30 Apr. 2012,

19 Klein, Samuel, et al. “Absence of an Effect of Liposuction on Insulin Action and Risk Factors for Coronary Heart Disease.” New England Journal of Medicine, vol. 350, no. 25, 2004, pp. 2549–2557., doi:10.1056/nejmoa033179.

20 “Insulin Resistance.” Insulin Resistance - Symptoms, Causes, Treatment, 2019,

21 “A1C Test.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 18 Dec. 2018,

22 “C-Reactive Protein Test.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 21 Nov. 2017,