Introduction Type 2 diabetes mellitus is a metabolic disease that is classified by an individual having chronic hyperglycaemia due to the pancreas losing its ability to produce insulin because pf a loss of pancreatic beta cells, and/or the body becoming insulin resistant (Hertado & Vella, 2019). This is a significant public health concern across the globe that is continually increasing in prevalence (Wilmot et al., 2011). According to the World Health Organisation (2016), diabetes affects 422 million people globally with most of these individuals being impacted by type 2 diabetes mellitus. Diabetes Australia (2015), suggest that Australian’s who are affected by diabetes spend approximately $14.6 billion per year on services related to diabetes, and an estimated 500,000 people in Australia have undiagnosed diabetes (more than 90% is type 2 diabetes). The common age bracket that individuals develop type 2 diabetes is over 40 (Chung et al., 2014). Although type 2 diabetes can be hard to detect due to the mild symptoms, some of these signs and symptoms include thirst (polydipsia), excessive urination (polyuria), fatigue, and a change in vision (World Health Organisation, 2018). Some medications may be used to lower blood glucose levels (i.e. biguanides, thiazolidnediones, and DPP-4 inhibitors), activate the pancreas to create more insulin (i.e. sulphonlureas), and slow down digestion (i.e. alpha glucosidase inhibitors) (Diabetes Australia, 2015). Due to the fact that type 2 diabetes is a common disease, it is possible that a healthy person can be affected by this disease. A healthy person can develop type 2 diabetes due to a combination of factors which predominantly include an individual’s genetic makeup, poor diet, and physical inactivity and a sedentary lifestyle.
Genetics The genetic makeup of an individual is a risk factor for developing type 2 diabetes mellitus. According to Li et al, (2018), genetics is one of the major contributors to the development of type 2 diabetes. In other words, if an individual’s parents or other immediate family members have type 2 diabetes mellitus, this could increase the risk of that individual developing the disease. If one parent has type 2 diabetes, the lifetime risk of developing the disease increases to 40%, and if both parents have type 2 diabetes the risk increases to approximately 70% (Prasad & Groop, 2015). This displays the remarkable increase in risk if family members have been affected by this disease. Although this is the case, which gene is responsible for this? There are multiple genes that can be associated with type 2 diabetes, however the most relevant risk related gene that has the strongest genetic link to developing type 2 diabetes is the transcription factor 7-like 2 gene, otherwise known as TCF7L2 (Dorajoo, Liu & Boehm, 2015). Genetic mutations of the TCF7L2 gene are linked to an increased risk of developing type 2 diabetes mellitus, as this has a negative effect on the secretion of insulin and the production of glucose in the body (Huang et al., 2018). A healthy individual may have an undesirable genetic makeup that can increase their risk of developing type 2 diabetes. Although this is the case, genetics alone isn’t the only risk factor for developing type 2 diabetes. A poor diet can possibly change a healthy individual into becoming a type 2 diabetic.
Diet A poor diet is another predominant contributor for developing type 2 diabetes mellitus. Individuals who don’t consume a balanced diet are more susceptible to developing type 2 diabetes when compared to individuals who undertake a balanced diet. A poor diet generally includes an over-consumption of foods that are calorie dense and high in fats, which will likely result in a calorie surplus. According to de Courten et al. (2016), foods that are rich in polyunsaturated fatty acids and high in fiber can decrease the risk of developing type 2 diabetes, on the other hand consuming a western diet that is high in trans fatty acids and a high glycaemic index is a predisposing factor for developing this disease. These nutrients are believed to lead to an increased Body Mass Index (BMI), and this added weight will most likely be in the form of adipose tissue which could lead to obesity (de Courten et al., 2016). Although obesity is heavily associated with lifestyle choices such as diet, it is also a major risk factor for individuals developing type 2 diabetes. There are many undesirable effects obesity has physically and mentally on an individual, however it’s physiological effect it has on insulin is why it is a major risk factor for type 2 diabetes. This is because the more obese or excess weight an individual has, the more insulin resistant their cells become due to the amount of non-esterified fatty acids, hormones, glycerol, cytokines and proinflammatory markers in the body (Al-Goblan, Al-Alfi & Khan, 2014). If the body is insulin resistant, it can’t efficiently utilise glucose in the blood which may make an individual hyperglycaemic, resulting in type 2 diabetes (Hertado & Vella, 2019). Even though a poor diet is a lifestyle choice that can have a negative impact on developing type 2 diabetes, individuals who choose to be physically inactive and live a sedentary lifestyle are also at risk of developing type 2 diabetes mellitus.
Physical Activity and Sedentary Behaviour Individuals that do not complete regular physical activity and live a sedentary lifestyle are at risk of becoming a type 2 diabetic. Nowadays, individuals are sitting down for longer periods of time due to technological changes in society. For example, sitting frequently occurs when individuals are on their computer, behind a desk at work, driving, watching TV, etc. The Australian physical activity and sedentary behaviour guidelines suggest that adults aged between 18-64 should complete 150-300 minutes of moderate intensity physical activity per week, or 75-150 minutes of vigorous intensity physical activity per week, or a combination of both (The Department of Health, 2019). The Department of Health (2019), also advise to minimise and break up long periods of sitting, which may help with reducing sedentary behaviour. Similar to a poor diet, if individuals don’t undertake regular physical activity, they are more likely to become obese which could increase their risk of developing type 2 diabetes. According to Hussey et al. (2012), completing exercise can increase the oxidative capacity and GLUT4 (the primary glucose transporter protein) volume in the muscles of type 2 diabetic individuals. These adaptations are important because they can assist with insulin sensitivity and muscle glycogen storage in type 2 diabetic patients (Hussey et al., 2012). In other words, individuals with type 2 diabetes have hyperglycaemia, and find it difficult to
remove this high blood glucose due to the body being insulin resistant. Exercise has a positive effect on this as it can aid in disposing this high blood glucose content and assist in utilising and storing glycogen (glucose converts into glycogen) in the muscle. This is important because a type 2 diabetic is unable/has difficulty removing this glucose if sedentary which will not aid in the treatment of this disease. Additionally, type 2 diabetic patients who don’t exercise are more prone to cardiovascular disease, as this is the leading cause of mortality and morbidity for type 2 diabetics (Smith et al., 2016). On the other hand, this risk can be significantly reduced if individuals undertake regular physical activity (Smith et al., 2016). A healthy individual could accumulate type 2 diabetes if they live a sedentary lifestyle and don’t participate in regular physical activity. However, undertaking regular exercise could decrease the risk of developing type 2 diabetes.
Conclusion Type 2 diabetes mellitus is a global epidemic that is growing rapidly. It is a disease that affects patients’ blood sugar levels and makes them hyperglycaemic due to the body becoming insulin resistant. Although it can be avoided, it is possible for a healthy individual to become a type 2 diabetic. This is primarily due to a combination of the genetic makeup of an individual, if an individual consumes a poor diet, and whether or not the individual is physically active and lives a sedentary lifestyle. All three of these major risk factors inter- relate with each other in regard to the prevalence of developing type 2 diabetes mellitus.
References Al-Goblan AS, Al-Alfi MA, & Khan MZ. (2014). Mechanism linking diabetes mellitus and obesity. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 2014, 587-591. doi: 10.2147/DMSO.S67400
Chung, J. O., Cho, D. H., Chung, D. J., & Chung, M. Y. (2014). An assessment of the impact of type 2 diabetes on the quality of life based on age at diabetes diagnosis. Acta Diabetologica, 51(6), 1065–1072. doi: 10.1007/s00592-014-0677-9
de Courten, B., de Courten, M., Soldatos, G., Dougherty, S., Straznicky, N., Schlaich, M., ... Forbes, J. (2016). Diet low in advanced glycation end products increases insulin sensitivity in healthy overweight individuals: a double-blind, randomized, crossover trial. doi:10.3945/ajcn.115.125427
Department of Health. (2019). Australia's Physical Activity and Sedentary Behaviour Guidelines and the Australian 24-Hour Movement Guidelines. Retrieved from https://www1.health.gov.au/internet/main/publishing.nsf/Content/health-pubhlth-strateg- phys-act-guidelines#npa1864
Diabetes Australia. (2015). Diabetes in Australia. Retrieved from https://www.diabetesaustralia.com.au/diabetes-in-australia
Diabetes Australia. (2015). Tablets. Retrieved from https://www.diabetesaustralia.com.au/tablets
Dorajoo, R., Liu, J., & Boehm, B.O. (2015). Genetics of Type 2 Diabetes and Clinical Utility. Genes, 6(2), 372-384. doi:10.3390/genes6020372
Huang, Z., Liao, Y., Huang, R. Chen, J., & Sun, H. (2018). Possible role of TCF7L2 in the pathogenesis of type 2 diabetes mellitus. Biotechnology & Biotechnological Equipment, 32(4), 830-834. doi: 10.1080/13102818.2018.1438211
Hurtado, M. D., & Vella, A. (2019). What is type 2 diabetes? Medicine, 47(1), 10–15. doi: 10.1016/j.mpmed.2018.10.010
Hussey, S. E., McGee, S. L., Garnham, A. P., McConell, G., & Hargreaves, M. (2012). Exercise increases skeletal muscle GLUT4 gene expression in patients with type 2 diabetes. Obesity and Metabolism, 14(8), 768-771. doi: 10.1111/j.1463-1326.2012.01585.x
Ley, S. H., Ardisson Korat, A. V., Qi Sun, Tobias, D. K., Cuilin Zhang, Lu Qi, ... Hu, F. B. (2016). Contribution of the Nurses’ Health Studies to Uncovering Risk Factors for Type 2 Diabetes: Diet, Lifestyle, Biomarkers, and Genetics. American Journal of Public Health, 106(9), 1624–1630. doi: 10.2105/AJPH.2016.303314
Li, S. X., Imamura, F., Schulze, M. B., Jusheng Zheng, Zheng Ye, Agudo, A., ... Wareham, N. J. (2018). Interplay between genetic predisposition, macronutrient intake and type 2 diabetes incidence: analysis within EPIC-InterAct across eight European countries. Diabetologia, 61(6), 1325–1332. doi: 10.1007/s00125-018-4586-2
Prasad, R.B., & Groop, L. (2015). Genetics of Type 2 Diabetes—Pitfalls and Possibilities. Genes, 6(1), 87-123. doi:10.3390/genes6010087
Smith, C., Ul Haq, M., Jerums, G., Hanson, E., Hayes, A., Allen, J., ... Levinger, I. (2016). Assessing the value of BMI and aerobic capacity as surrogate markers for the severity of left ventricular diastolic dysfunction in patients with type 2 diabetes who are obese. Clinical Medicine Insights: Cardiology. 10. 61-65. doi: 10.4137/CMC.S38116
Wilmot, E., Davies, M. J., Edwardson, C. L., Gorely, T., Khunti, K., Nimmo, M. A., ... Biddle, S. J. H. (2011). Rationale and study design for a randomised controlled trial to reduce sedentary time in adults at risk of type 2 diabetes mellitus: project STAND (Sedentary Time and diabetes). BMC Public Health, 11, 908. doi: 10.1186/1471-2458-11-908
World Health Organisation. (2018). Diabetes. Retrieved from https://www.who.int/news- room/fact-sheets/detail/diabetes
World Health Organisation. (2016). Global reports on diabetes. Retrieved from https://www.who.int/diabetes/publications/grd-2016/en/