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Why does obesity cause diabetes? You asked Google – here’s the answer

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Every day millions of internet users ask Google life’s most difficult questions, big and small. Our writers answer some of the commonest queries

Cause” is a strong word. It means that A results in B happening. Causality is also surprisingly difficult to prove. Most medical studies only show association between A and B, while causality often remains speculative and frustratingly elusive. Obesity and diabetes are no exception.

There are many types of diabetes. All are unified by elevated levels of blood sugar. Type 1 diabetes accounts for less than 10% of cases and results from autoimmune destruction of the beta cells in the pancreas, which produce and release insulin. (In an autoimmune process, antibodies that normally target and fight infection instead target one’s own cells). Type 3c (secondary) diabetes can occur when there has been destruction of the pancreatic beta cells through some other process, such as excessive alcohol, inflammation or surgical resection.

There are also many genetic forms of diabetes, each usually resulting from a single gene mutation that affects pancreatic function in some way. Finally, there is type 2 diabetes (T2D), which accounts for more than 90% of cases globally. Media reports of diabetes, particularly in the context of obesity, usually relate to T2D, the two terms often being used interchangeably.

Only T2D appears to be associated with obesity. Epidemiological studies across the world have shown that the greater one’s body mass index (BMI), the greater the chance of developing T2D. However, this is not the same as saying that obesity causes T2D. The majority of people who are obese will never develop T2D – a fact that exposes the statement “obesity causes diabetes” as absurd. Rather than referring to obesity as a cause of diabetes, it is more accurate to frame the issue as one of association between obesity and T2D (which is incontrovertibly true).

As we gain weight, the sensitivity of our tissues to the effects of insulin diminishes (so-called “insulin resistance”). In response, our pancreatic beta cells, which produce insulin, need to work harder to produce more of it.

Imagine driving a car up a hill: this is analogous to your body encountering insulin resistance following weight gain. To get up the hill, you change gear, step on the accelerator and make the engine work harder. In the same way, the pancreatic beta cells need to work harder to produce more insulin to compensate for insulin resistance. If you are lucky enough to drive a car with a good engine, you will make it up the hill, however steep, and never develop T2D regardless of how much weight you gain. If, however, your car’s engine has insufficient power to get up the hill, your car will eventually stop, and may roll back down.

The chance of this happening depends on the steepness of the hill (how much weight you gain) and the strength of your engine (or the strength of your beta cells and their ability to produce more insulin). The point at which your car stops (when your pancreatic beta cells are no longer able to produce enough insulin), is termed, aptly, “beta cell exhaustion”. From this point, there is usually an inexorable decline in the release of insulin from the beta cells, when blood sugar levels progressively increase and T2D eventually becomes manifest.

Our genetic makeup determines the strength of our pancreatic beta cells, and therefore influences which of us will make it up the hill and which of us will halt and roll back down. This is why T2D is in fact a genetic condition, and weight gain or obesity often contribute to its manifestation.

Why does insulin resistance occur with weight gain? To answer this, it is important to understand that abdominal (visceral) fat confers the greatest risk. Blood from visceral fat, laden with fatty acids, drains directly into the liver. Some of these fatty acids can spill over into the general circulation, where they can compete with glucose (sugar) uptake into more peripheral tissues, such as muscle. Given that glucose uptake is an insulin-mediated process, this competition promotes insulin resistance. Visceral fat also produces hormones called adipokines, some of which can further dampen the sensitivity of the insulin receptor to the effects of insulin.

Using our analogy, weight gain around the waist confers the steepest gradient up which to drive a car.

The development of T2D is complex. There are many processes implicated, ranging from excretion of glucose in the urine, appetite regulation, control of pancreatic hormonal function and the role of gut bacteria. However, weight gain and insulin resistance appear to be associated with many of these processes.

Currently, we cannot do much about the elements of our genetic makeup that influence pancreatic beta cell function, although this may change in the future. We can, however, improve our insulin sensitivity – and reduce the gradient of the hill ahead of us.

Aside from weight regulation, exercise and regular activity are important: exercise, in addition to numerous other benefits, improves our insulin sensitivity. Avoiding sleep deprivation, which can promote insulin resistance, is also important. On top of this, a varied diet – one that limits processed food and advanced glycation end-products (AGEs) – can help improve insulin sensitivity: preparation technique involving high moisture, short heating times and the use of acidic marinades (such as lemon juice and vinegar) are techniques that can reduce our consumption of AGEs.

Type 2 diabetes is a genetic condition – but there is plenty we can do to make our mountains into molehills.

 Thomas Barber is an associate clinical professor in endocrinology and diabetes based at the University of Warwick, and honorary consultant endocrinologist at University Hospitals Coventry and Warwickshire (UHCW) NHS trust, where he leads the obesity service