Based from the interview and observation, the two most common diseases occurring in both sides of the family are: (1) diabetes, specifically NIDDM, and (2) heart disease, specifically atherosclerosis. These diseases are commonly known as lifestyle diseases mainly because of their non-curable characteristic.
It was found out that diabetes, in the family, might skip a generation because one of our grandparents had it, but none of their children or our parents was able to acquire diabetes. However, this is still only a theory and is not yet conclusive as we are yet to establish the prevalence among our (second) generation. Heart disease, on the other hand, was concluded mostly in the wider scale search as it is observed not to be prevalent among first degree relatives. This was mainly because of mild heart attacks occurring within first degree relatives suggesting a high probability of myocardial infarction and coronary artery diseases.
As previously mentioned, Diabetes Mellitus is a metabolic and chronic disease characterized by high levels of sugar or glucose in the blood due to deficiency in insulin, a hormone responsible for the breakdown of dietary glucose. Hyperglycemia, or high blood glucose, is usually presented with the triad of excessive urination, thirst, and hunger (i.e. polyuria, polydipsia, and polyphagia). If left untreated, diabetes may lead to major complications in other organs of the body such as the kidneys, blood vessels, and eyes, arising from the increase in viscosity due to excess blood glucose. (Khardori, 2012)
A recent study by Wheeler and colleagues has identified two loci, PPARG and KCNJ11, to be genetic determinants of Type 2 Diabetes/T2D (Wheeler & Barroso, 2011), or Non-Insulin Dependent Diabetes Mellitus (NIDDM). A 2012 study, on the other hand, specifically identified that occurrence in nucleotide polymorphisms of TCF7L2 as a T2D susceptibility gene (Ip, Chiang & Jin, 2012).
In 2011, Wei and colleagues have studied that prevalence of diabetes significantly varies between ethnic groups, specifically with African Americans and whites (Wei, et al., 2011). According to them, there is a much higher risk for the disease in African American than with whites. While it was concluded that an increased BMI, fasting glucose, triglyceride, and HDL cholesterol may contribute to the greater risk in African Americans, prehypertension and hypertension have been highly associated with greater risk of diabetes in whites.
In general, it is believed that the development of diabetes, specifically NIDDM, is mainly due to a defective pancreatic β-cell function, which is responsible for the production of insulin. While it is not officially classified as an autoimmune disease, NIDDM appears to be connected to disruptions in innate immunity such as decreased cytokine responses and decreased phagocytotic functions (Geerlings & Hoepelman, 2006). Lower immune functions support higher incidence of infections in diabetic patients. Also there are evidences that certain inflammation markers such as C-reactive protein and interleukin-6 can contribute to development of NIDDM later on. However, much research is still needed to confirm effects on innate immunity of NIDDM (Pickup, 2004).
Atherosclerosis and Heart Disease
Diseases of the heart encompass a variety of complications. However, one appears to affect all of them most. Atherosclerosis, the principal cause of coronary artery diseases (CAD), is a disease characterized by either: (1) inflammation of the arteries, or (2) a plaque build-up consisting mainly of lipids, cholesterol and calcium (Boudi, 2012). The disease is usually asymptomatic and only experienced through occurrence of a heart attack. Some clinical presentations include chest pain, shortness of breath and weakness/tiredness.
Atherosclerosis is commonly due to the presence of plaque in the vessels causing disruption of normal blood flow. The deficiency in oxygen due to lessened blood flow then produces a succession of clinical compensations, which may result to vascular remodeling or increase in size and vascularity of the vessels and the heart. A study by Moatti and colleagues in 2001 suggests that a certain chemokine receptor CX3CR1 I249 can be considered as a genetic risk factor for coronary artery disease. The specific receptor, which is located in monocytes, acts through chemotaxis or adhesion. Such allows accumulation of monocytes that have initially migrated in vessel walls due to presence of foreign bodies, and consequently leads to atherosclerosis (Moatti, et al. 2001).
What is most evident for atherosclerosis and heart diseases, however, is that risk factors are mainly environmental/lifestyle in nature. This includes hypertension, cigarette smoking, and the previously mentioned, diabetes mellitus. Lifestyle also greatly affects differences in prevalence among ethnic groups such as that of the United States and France and the Mediterranean regions (Boudi, 2012). This is mainly because of the latter’s diet of high alcohol and monounsaturated fatty acids, respectively.
Through the study of the two diseases, it may be concluded that for this biological background report, the probability of our generation contracting these diseases may be largely due to environmental factors. This is because though there are also genetic factors involved in both, the diseases are not entirely specific to the ethnic characteristic of the family lineage.
However, since one may be present in the immediate family, it should be noted that likelihood of developing the disease (i.e. diabetes) may be more for the members of the family than the other members of distant relatives or ethnic groups. Being that both diseases, with emphasis on diabetes, are classified as lifestyle disease, such a discovery must generate self-control and responsibility within the individual and the family to regulate whichever needs to be regulated in order to maintain a healthy life and lifestyle.
Boudi, F.B., 2012. Coronary Artery Atherosclerosis [Web]. USA: Medscape, WebMD LLC. Available at http://emedicine.medscape.com/article/153647-overview [Accessed 14 November 2012]
Geerlings, S.E., Hoepelman, A.I.M., 1999. Immune dysfunction in patients with diabetes mellitus (DM). FEMS Immunology & Medical Microbiology, [e-journal] 26 (3-4), Abstract only. Available through: Wiley Online Library website
Ip, W., Chiang, Y.A., Jin, T., 2012. The involvement of the wnt signaling pathway and TCF7L2 in diabetes mellitus: The current understanding, dispute, and perspective. Cell & Bioscience, [e-journal] 2 (28), Available through: National Center for Biotechnology Information website
Khardori, R., 2012. Type 2 Diabetes Mellitus [Web]. USA: Medscape, WebMD LLC. Available at http://emedicine.medscape.com/article/117853-overview#aw2aab6b2b4 [Accessed 13 November 2012]
Moatti, D., Faure, S., Fumeron, F., El Walid Amara, M., Seknadii, P., McDermott, D.H., Debre, P., Aumont, M.C., de Prost, D., Combadiere, C., 2001. Polymorphism in the fractalkine receptor CX3CR1 as a genetic risk factor for coronary artery disease. Blood, [e-journal] 97 (7), Available through: Blood, Journal of the American Society and Hematology website
Pickup, J.C., 2004. Inflammation and Activated Innate Immunity in the Pathogenesis of Type 2 Diabetes. Diabetes Care, [e-journal] 27 (3), Abstract only. Available through: Diabetes Care, American Diabetes Association website
Wei, G.S., Coady, S.A., Goff, D.C. Jr., Brancati, F.L., Levy, D., Selvin, E., Vasan, R.S., Fox, C.S., 2011. Blood pressure and the risk of developing diabetes in african americans and whites: ARIC, CARDIA, and the framingham heart study. Diabetes Care, [e-journal] 34 (4), Available through: National Center for Biotechnology Information website
Wheeler, E., Barroso, I., 2011. Genome-wide association studies and type 2 diabetes. Briefings in Functional Genomics, [e-journal] 10 (2), Abstract only. Available through: Oxford Journals website