Diabetes is a chronic disease in which a person has high levels of blood glucose due to impairment of insulin (a hormone) production or response.
When we take in food, it is broken down through the digestive process into its components, thus, fat, protein, carbohydrates, vitamins and minerals. The food component that affects blood glucose level is carbohydrate. When Carbohydrate is digested, it is converted into glucose and other monosaccharides which are then absorbed into the bloodstream. Blood glucose serves as the main source of energy for the cells in the body. Specialized cells in the human pancreas called beta cells produce the hormone insulin which is needed by the cells of the body to use up blood glucose. When there is excess glucose in the blood, it is converted and stored in the liver as glycogen.
In people with diabetes, the pancreas does not produce insulin or the quantity produced is inadequate, or the body cells do not respond to insulin or a combination of these factors (DRWF, 2012). This leads to accumulation of glucose in the blood, depriving body cells of their main energy source. The common symptoms associated with diabetes are excessive hunger (polyphagia), excessive thirst and fluid intake (polydipsia), and frequent urination (polyuria). Because of extensive research going on now a days, many types of diabetes have been discovered but the most common types are the type 1 and type 2 diabetes (WHO, 2010).
In type 1 diabetes, there is no production of insulin because the beta cells of the pancreas are under attack by the body’s own immune system which destroys the cells gradually (Zimmet, Tuomi et al., 1994). The rate at which the individual’s immune system fight and destroy the beta cells differs from person to person (Humphrey, McCarty et al., 1998). In children, the destruction of the beta cells occurs rapidly whiles the destruction occurs slowly in adults. People with this type of diabetes have to spend their entire life on exotic insulin for survival which comes in the form of insulin pumps and insulin shots (Willis, Scott et al., 1996).
People with type 2 diabetes are resistant to the action of insulin (DeFronzo, Bonadonna et al., 1997). They do not need any external insulin for survival because for them the pancreas is able to produce the right amount of insulin but their body cells do not respond to the action of the hormone (Papadakis, 2014). It is very difficult to detect this type of diabetes when earlier medical screening are not done because it takes years for the signs and symptoms of the disease to manifest (Mooy, Grootenhuis et al., 1995).
In 2004, the World Health Organization recorded 220 million deaths resulting from diabetes. It is predicted that between 2005 and 2030 diabetes-related deaths will double (WHO, 2010). Diabetes-related deaths often occur in adults below the age of 70 years and about 80% of these deaths occur in middle and low income countries (National Diabetes Data Group, 2005). The most prevalent type of diabetes is the type 2 (WHO, 2016).
So what are the risk factors for diabetes?
Aging is one of the non-modifiable risk factors for type 2 diabetes because our physical activity level reduces considerably and our muscle mass also reduces (Cantu-Brito, Mimenza-Alvarado et al., 2010). Physical activity helps the body cells to use glucose in the blood and make the cells more sensitive to insulin. Engaging in a physical activity for at least 60 minutes tends to break down fat to be used as energy. The more the fats are reduced the more sensitive the cells become (Manson, Stampfer et al., 2003).
Excessive body fat or obesity is the most common cause of diabetes worldwide. Also, having excess fat in the abdominal region predisposes one to getting type 2 diabetes (Ali, Earl et al., 2001).
Family history is another risk factor for type 2 diabetes. A grandparent or a parent who had diabetes in their early stages of life increases the chance of the members of the family getting diabetes in their life if their diet is not carefully chosen (Ann, Mark et al., 2002).
During pregnancy, the blood sugar goes up because certain hormones released during pregnancy hinders the work of insulin. This is known as gestational diabetes. Women who get this type of diabetes during pregnancy are at risk of getting diabetes later in life. Also, women who deliver a child weighing more than 4kg are at risk of getting diabetes later in life because gestational diabetes results in higher offspring adiposity (Debbie, Paul et al., 2011).
Another risk factor for diabetes is hypertension or high blood pressure. The World Health Organization (2010) define hypertension as “having a systolic blood pressure of greater or equal to 140 mmHg and a diastolic blood pressure of 90 mmHg or both”. Research has found that most people who are hypertensive also develop type 2 diabetes later in their life or vice versa (Ninh, John et al., 2008).
High cholesterol and triglyceride levels also increases ones risk of developing type 2 diabetes (Papadakis, 2014).
Research has found out that, Africans, Hispanics, American Indian and Asia Americans are at a high risk of getting diabetes (Lowrie, Liew et al., 1992)
What are the complications of diabetes?
When diabetes is not detected and treated early, it can lead to complicated issues such as cardiovascular diseases like coronary artery diseases with accompanying chest pain, heart attack, and narrowing of the blood arteries (Ninh, John et al., 2008). It could also lead to nerve damage because elevated levels of blood glucose can damage the blood vessels that supply oxygen and nutrients to the nerves. Impairment of the nerves can lead to loss of sensation or numbness, especially of the hands and arms, the legs and feet and tingling in the ears. It becomes difficult for a patient with numbness in the feet to detect cuts or wounds. Bacteria feed on wounds because the blood is rich in glucose and the rate of their growth doubles quickly and the wound becomes very difficult to heal which can lead to amputation (Peter, Eva et al., 2013).
Because the blood vessels get damaged by high blood sugar, the vessels that make up the glomeruli of the kidney and the vessels to the retina of the eye can get damaged which could lead to kidney and eye problems (Peter, Eva et al., 2013).
It is recommended that people visit health centres regularly for medical check-ups to monitor their blood glucose level, and allow early detection and treatment of diabetes. People must also adapt healthy lifestyles including regular exercise for at least 30 minutes daily, eating balanced diet and drinking plenty of clean water, and regular intake of fruit and vegetables.
For more information and better healthy eating habits to prevent diabetes in the future, kindly contact the author [email protected]
Ali, M. M., et al. (2001). “Prevalence of Obesity, diabetes, and obesity related health risk factors.” The Journal of the American Medical Association 289(1).
Ann, M. A., et al. (2002). “Family Historym Diabetes, and other Demographic and risk factors among participants of the National Health and Nutrition Examination survey 1999-2002.” ncbi 2(2).
Campbell, P. and M. Carlson (1993). ” Impact of obesity on insulin action in NIDDM.” 42: 405–410.
Cantu-Brito, C., et al. (2010). “Diabetes mellitus and aging as a risk factor for celebral vascular disease: epidemiology, pathophysiology and prevention.” PubMede 62(4): 333-342.
Debbie, A. L., et al. (2011). “Association of Maternal Diabetes Mellitus in Pregnancy with Offspring Adiposity into Early Childhood.” AHA.
DeFronzo, R., et al. (1997). Pathogenesis of NIDDM, International Textbook of Diabetes Mellitus.
DRWF, D. r. a. w. f. (2012). “What is Diabetes.” Retrieved 4th August, 2016, from www.diabeteswellness.net.
Humphrey, A., et al. (1998). ” Autoantibodies to glutamic acid decarboxylase and phenotypic features associated with early insulin treatment in individuals with adult–onset diabetes mellitus. .” Diabetic Med 15: 113.
Lowrie, E. G., et al. (1992). “Race and diabetes as death risk predictors in hemodialysis patients.” (38): 22-31.
Manson, J. E., et al. (2003). “Physical activity and incidence of non-insulin dependent diabetes mellitus in women.” ScienceDirect 338(8770).
Mooy, J., et al. (1995). “Prevalence and determinants of glucose intolerance in a Dutch population. .” The Hoorn Study. Diabetes Care 18.
National Diabetes Data Group (2005). “Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance.” 28: 1039–1057.
Ninh, T. N., et al. (2008). “Association of hypertension, diabetes, dyslipidemia and metabolic syndrome with obesity: findings from the Nationa Health and Nutrition Examination Survey.” Journal of the American College of Surgeon 207(6): 928-934.
Papadakis, M. (2014). Current Medical Diagnosis and treatment. New York, The McGraw Hill companies.
Peter, J. D., et al. (2013). “Nerve Damage (Diabetic Neuropathies).” Retrieved 08/08/2016, 2016.
Willis, J., et al. (1996). ” Islet cell antibodies and antibodies against glutamic acid decarboxylase in newly diagnosed adult–onset diabetes mellitus.” 33: 89 – 97.
World Health Organization (2010). “Diabetes fact sheet.” International Diabetes Federation 4th Edition
World Health Organization. WHO | Diabetes [Internet]. WHO. [cited 2016 Aug 10]. Available from: http://www.who.int/mediacentre/factsheets/fs312/en/
Zimmet, P., et al. (1994). ” Latent autoimmune diabetes mellitus in adults (LADA): the role of antibodies to glutamic acid decarboxylase in diagnosis and prediction of insulin dependency.” Diabetic Med 11: 299–303.
By: Dery Bede, Bachelor of Dietetics student at UHAS, Ho, Ghana
©2016 Scientect e-mag | Volume 1 (1): A10