Diabetes is a long-term disease characterised by high blood glucose levels, which over time leads to damage of the heart, blood vessels, eyes, kidneys, and nerves.
There are two types of diabetes: type 1 and type 2. However, over 90% of diabetes cases are type 2.
Type 2 diabetes is a metabolic disorder that causes glucose and insulin levels in the blood to remain persistently high. It usually happens when the pancreas loses its ability to produce enough insulin, and tissues such as the muscles can’t respond to insulin appropriately.
According to the International Diabetes Federation (IDF), 463 million adults aged between 20 and 79 years old were living with type 2 diabetes in 2019. And without appropriate prevention services, that figure is projected to rise to 700 million by 2045.
This article describes the global burden of type 2 diabetes, its causes, and the factors that increase the risk of developing it.
The Global Burden of Type 2 Diabetes
According to the International Diabetes Federation (IDF), in 2021, 537 million adults aged between 20 and 79 worldwide live with type 2 diabetes, a number that is projected to rise to 700 million by 2045.
Diabetes has caused 6.7 million deaths in 2021 so far – one every five seconds.
Diabetes has caused at least $966 billion in health expenditure, a 316% rise over the last 15 years. However, the actual burden of the disease is likely higher. A total of 541 million adults have impaired glucose tolerance, placing them at increased risk of type 2 diabetes.
At least 80% of the diabetes cases are in low-to-middle income countries, but the incidence and prevalence of diabetes vary according to geographical region.
The Western Pacific region has the highest prevalence of diabetes (206 million), followed by South-East Asia (90 million) and the Middle East and North African regions (73 million). Africa currently has the lowest rate of diabetes at 24 million, with an estimated 2.7 million people now living with diabetes in Nigeria.
In the United Kingdom, 4.9 million people live with diabetes, 850,000 of which are yet to be diagnosed. More than 13.6 million people are at increased risk of type 2 diabetes, and Diabetes UK, a leading charity, predicts that 5.5 million people will have diabetes by 2030.
The National Health Service (NHS) spends at least £10 billion annually on diabetes, about 10% of its budget. And shockingly, 80% of the money spent on diabetes is for treating complications.
Needless but crucial to say, the current and projected situation is dire!
What Causes Type 2 Diabetes
There are irregularly shaped tissues within the pancreas called the Islet of Langerhans. These tissues contain alpha cells that produce the hormone glucagon and beta cells that produce insulin.
Insulin and glucagon work together to control blood sugar, but this section will focus on insulin.
Insulin regulates blood sugar by instructing the cells in the body to absorb glucose from the bloodstream after a meal. If there’s any excess glucose, insulin stimulates the liver and muscles to store it as glycogen or the adipose (fat) tissue to store it as fat. Insulin also encourages fat cells to store excess fat and protein as fat.
Type 2 diabetes occurs when two things happen (Glicia-Garcia et al., 2020):
- The beta cells in the pancreas stop producing enough insulin
- The liver, muscles and fat tissues stop being sensitive or responding to insulin
Now you may be asking, why do the beta cells stop producing enough insulin, and why do the liver, muscles and fat stop responding to insulin?
When a person eats excess fat, protein and carbohydrates for prolonged periods, the pancreas must produce insulin continuously to remove the nutrients from the blood and store them adequately. Continuous insulin production puts enormous stress on the pancreas, which gradually loses its ability to produce enough insulin.
At the same time, the liver, fat cells and muscles stop responding to insulin correctly. Insulin typically stimulates the liver to store excess glucose as glycogen or fat. But if the beta cells cannot produce insulin or the liver cells can’t respond to insulin, excess glucose remains in the bloodstream.
Similarly, without enough insulin or being able to respond to insulin, fat cells cannot store excess glucose or fat as fatty acids, and the muscles cannot store excess glucose as glycogen. And once again, excess glucose and fatty acids remain in the bloodstream.
While they’re able, the beta cells try to counter this by producing more insulin to take the nutrients out of the blood and into the liver, muscle, and fat cells. But they eventually wear out and ultimately lose their ability to produce insulin.
With excessive free fatty acids and glucose floating in the blood, cells release many inflammatory proteins causing damage to organs around the body, including the heart, eyes, kidneys. Left uncontrolled, diabetes can cause death.
Factors that Increase Type 2 Diabetes Risk
The risk factors for type 2 diabetes are split into modifiable risk factors and non-modifiable risk factors. Modifiable risk factors are those you can control, while non-modifiable factors are those you can’t control.
Modifiable Risk Factor
Excess fat, especially around the abdomen, is the strongest risk factor for type 2 diabetes (Neeland et al., 2012). Obesity can increase the risk of insulin resistance, a key component of type 2 diabetes. Obesity results from a lack of exercise and unhealthy diets, typically low in fibre and rich in vegetable oils, sugar and refined foods (Sami et al., 2017).
Cardiovascular risk factors such as hypertension and high blood triglycerides increase type 2 diabetes risk. Other modifiable risk factors that increase type 2 diabetes risk include:
- Medications: Drugs such as steroids, thiazides, beta-blockers and statins (Fathallah et al., 2015)
- Alcohol: while moderate drinking may be protective, heavy drinking increases risk.
- Smoking: smoking more than 20 cigarettes daily can double type 2 diabetes risk. It affects beta-cell function and reduces insulin sensitivity (Maddatu et al., 2017)
Non-modifiable Risk Factors
Diabetes is most common in middle-aged adults, although it is increasingly occurring in children. Caucasians are more at risk over the age of 40. However, the risk occurs at a much lower age for other ethnicities. The risk of type 2 diabetes is higher for Africans, African-Caribbeans and South Asians over 25 years.
Type 2 diabetes seems to be more common in men than women. But the reasons men are more affected than women are not clear. It may be because they are more likely to carry fat around their abdomen.
If you have a parent, brother, sister, or child with diabetes, you are two to six times more likely to get it. People of South Asian, African-Caribbean, or Black African descent are also two- to four-fold more likely to develop type 2 diabetes than Caucasians.
Your mother’s nutrition, while she was pregnant, might also influence your risk of type 2 diabetes. According to the thrifty gene hypothesis, if you were exposed to poor nutrition while in your mother’s womb, you are programmed to store more energy to ensure survival after birth.
This programming is beneficial if you continue to live in a famine-like environment because it increases your chance of survival. However, in an environment with excesses, such as the Western countries or urban areas in developing countries, the programming is detrimental. You are more likely to store fat quickly, become overweight or obese and dramatically increase your risk of metabolic conditions such as type 2 diabetes (Hales and Barker, 2001).
Having a history of gestational diabetes also increases the risk of type 2 diabetes. Women with gestational diabetes are seven-fold more likely than those without a gestational diabetes history to develop type 2 diabetes (Sheiner, 2020).
And there you have it, a simple explanation of the global burden, causes and risk factors for type 2 diabetes.
Type 2 diabetes is preventable with a healthy lifestyle: nutritious diet, exercise, moderate drinking, and no smoking.
Lifestyle changes can be challenging to make on your own. If you’ve tried without success, please get help from a registered professional.
- International Diabetes Federation. (2021) IDF Diabetes Atlas, 10th edition. Brussels, Belgium. Available from: https://diabetesatlas.org. Accessed: 06 November 2021.
- Glicia-Garcia, U., Benito-Vicente, A., Jebari, S., Larrea-Sebal, A., Siddiqi, H., Uribe, K.B., Ostolaza, H., and Cesar M. (2020) Pathophysiology of type 2 diabetes mellitus. International Journal of Molecular Sciences, 21: 6275.
- Neeland, I.J., Turer, A.T., Ayers, C.R., Powell-Wiley, T.M., Vega, G.L., Farzaneh-Far, R, et al. (2012) Dysfunctional adiposity and the risk of prediabetes and type 2 diabetes in obese adults. JAMA, 308: 1150-9.
- Sami, W., Ansari, T., Butt, N.B., ab Hamid, M.R. (2017) Effect of diet on type 2 diabetes mellitus: a review. International Journal of Health Sciences, 11(2): 65–71.
- Maddatu, J., Anderson-Baucum, E., Evans-Molina, C. (2017) Smoking and the risk of type 2 diabetes. Translational Research, 184: P101-107.
- Fathallah, N., Slim, R., Larif, S., Hmouda, H., Salem, C.B. (2015) Drug-induced hyperglycaemia and diabetes. Drug Safety, 38(12): 1153–68.
- Kolb, H., Martin, S. (2017) Environmental/lifestyle factors in the pathogenesis and prevention of type 2 diabetes. BMC Medicine, 15: 131.
- Hales, C.N., Barker, D.J. (2001) The thrifty phenotype hypothesis: type 2 diabetes. British Medical Bulletin, 60(1): 5–20.
- Sheiner, E. (2020) Gestational diabetes mellitus: long-term consequences for the mother and child grand challenge: how to move on towards. Frontiers in Clinical Diabetes and Healthcare, https://doi.org.10.3389/fcdhc.2020.546256.