By MYNDARO 11-12-2020

Over the last 200 years, the complexity and diversity of diabetes have been incrementally uncovered. Researchers have long known that those diagnosed with type 1 diabetes are predominantly young people with insulin deficiencies stemming from autoimmune pancreatic cell destruction. In contrast, patients with type 2 diabetes, which is much more common, are typically overweight. The most important factors attributed to the pervasiveness of type 2 diabetes include the general population’s increase in body weight, sedentary lifestyles, and high-calorie diets. While type 2 diabetes is still most common in older adults, in recent years the average age of this disease’s onset has fallen as it grows more common in young adults and even teenagers.

In 1936, Harold Himsworth was the first to distinguish between insulin deficiency and insulin resistance.1 Now, we understand that insulin resistance, together with beta cell dysfunction, are crucial to the development of type 2 diabetes. Metabolic syndrome, or syndrome X, is a collection of conditions that includes hypertension, excess fat around the waist, high blood sugar levels (insulin resistance), decreased levels of good cholesterol, or high-density lipoprotein (HDL), and elevated triglyceride levels. Together, these conditions indicate whether a person is at higher risk of developing diabetes, cardiovascular disease, and glucose intolerance. To avoid developing diabetes, those with metabolic syndrome conditions should immediately take preventative measures.2                              

The typical type 1 Diabetic is usually lean, insulin deficient, and diagnosed early on – from his first day of life to adolescence (or sometimes early adulthood). The insulin- producing beta cells of a type 1 diabetic’s pancreas are internally destroyed, and the disease requires management with insulin. Most often, he will end up on an insulin pump. But, with proper management, the type 1 diabetic can thrive long term. However, if uncontrolled, one can develop diabetic complications that include nerve, kidney, and eye damage.

For the type 2 diabetic, life is different. Type 2 diabetes is typically the result of a genetic predisposition compounded by poor environmental factors. Poor eating habits and a sedentary lifestyle don’t help matters much for the type 2 diabetic. The fast-food industry and society’s dependence on processed food rich in high fructose corn syrup burden the liver and make it fat. In response, it produces excess glucose. The type 2 diabetic’s muscles, which object to this glucose uptake, suffer too. Gut hormones called incretins diminish, leading to even more glucose spillover in the bloodstream. Burdened by the fat around them, the type 2 diabetic’s beta cells produce less insulin. Alpha cells in the pancreas produce excess glucagon, which in turn results in even higher blood glucose levels. The type 2 diabetic’s kidneys reabsorb glucose at a lower threshold, and their brain suffers from neurotransmitter dysfunction. The United Kingdom Prospective Diabetes Study (UKPDS) and other similar studies have found that by the time one is diagnosed, 50% to 75% of the type 2 diabetic’s pancreatic beta cells are lost.3 4

After diagnosis, the type 2 diabetic starts adjusting diet and exercise. The doctor prescribes oral medications or insulin injections depending on the disease’s severity. Some type 2 diabetics who lack control over their condition end up suffering kidney damage, neuropathy, stroke, heart attack and other complications.


  • 1 A. J. Krentz and G. A. Hitman, "Sir Harold Himsworth and insulin insensitivity 75 years on," Diabetic Medicine, vol. 28, no. 12, p. 1435-1435, 2011.

  • 2 S. O'Neill and L. O'Driscoll, "Metabolic syndrome: a closer look at the growing epidemic and its associated pathologies," Obesity Reviews, vol. 16, no. 1, p. 1-12, 2015.

  • 3 R. R. Holman, S. K. Paul, M. A. Bethel, D. R. Matthews, H. Andrew and W. Neil, "10-Year Follow-up of Intensive Glucose Control in Type 2 Diabetes," The New England Journal of Medicine, vol. 359, no. 15, pp. 1577-1589, 2008.

  • 4 J. Chalmers and M. E. Cooper, "UKPDS and the legacy effect," The New England Journal of Medicine, vol. 359, no. 15, p. 1618-1620, 2008.


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