The reality of biological human differences can be nowhere more profoundly delineated outside of the avenue of examining ethnic and gender disparities in chronic illness.
In a state of natural human equality, one might expect illness rates to be congruent across gender and ethnic lines. Looking at the data however, it becomes apparent that this is not the case. In this brief essay, some of the more pertinent examples of how chronic diseases are expressed in different ethnicities and genders will be discussed. The logical conclusion of such information unequivocally provides substantial evidence for, and addresses the implications of, human bio-diversity.
This is not to say that specific genders or ethnicities are biologically determined to develop certain illnesses. There are also social and economic determinants that may exacerbate or make biological predispositions less pronounced. When addressing the question of gender and ethnic disparities regarding chronic diseases, external factors become more pronounced in under or less developed countries where women or certain ethnic minorities have less access to education, nutrition and healthcare – and participate less in public life. (Vlassoff, C. 2007)
These factors obviously have a detrimental effect on how knowledgeable individuals are about disease prevention and treatment – and, in the case of nutrition, explain why certain groups may display higher rates of chronic illness. In industrialized first world nations however, gender and ethnic disparities still persist in the realm of disease. While social norms may play a role in the frequency of certain diseases like eating disorders in women for example, when analyzing things like osteoporosis and hip fracture, biological factors play a prevailing role.
Mostly seen as a disease of postmenopausal women related to bone density and declines of estrogen between the ages of 55 to 74, the disease is much more prevalent in white women than any other demographic. This is because bone density is quite a bit higher in African Americans for example, and in men. (Hochberg 2007) Environmental factors have been purposed to explain why this is the case, but when looking at studies of young children, the biological disparity in bone density becomes clear.
As such, hip fractures are much more prevalent in white women and begin to increase exponentially at age 70. For white men and black women, they increase exponentially at age 75 – and past age 85 for black men. As hip fracture rates double every 5 years, data shows that white men and black women have half the incidences of hip fractures than white women. (Manton K.G., Stallard E. 1997)
Transversely, age-adjusted mortality rates resulting from major cardiovascular diseases for blacks are 1.5 times higher than the rate for whites. When examining circulatory disease, several processes related to circulatory events can be identified as being more highly correlated with race. Atherosclerosis for example, is a degenerative process that increases the risk of many circulatory diseases associated with cholesterol. Follow up studies to the Charleston Heart Study show that mortality is higher at both very low and very high values of cholesterol for white females.
For African American females, the cholesterol-mortality relation was linear. In other words, white females exhibit an increase in the risk of coronary heart disease with an increase of one standard deviation in cholesterol (60 percent for white females compared to 40 percent for black females.) The Charleston study, and others, suggests a higher risk of coronary heart disease for white males than for black males – and show that cholesterol isn’t a significant predictor of risk for cardiovascular diseases for black males.
Adult onset diabetes is not insulin dependent. It is associated with degenerative changes in glucose and fat metabolism. Studies have shown that the age-adjusted incidences of diabetes were 15 percent for black women, 10.9 percent for black men, 7.0 percent for white women and 6.9 percent for white men. Researchers have identified risk factors for diabetes. They include body mass index expression, but age-adjusted diabetes risks have been found to be higher for both lean and overweight blacks. Low education and low activity have also been identified as risk factors for diabetes but do not entirely explain the higher rates among blacks.
Therefore, genetic differences in metabolic adaptation to obesity by race have been identified as a possible factor. (Manton K.G., Stallard E. 1997) This is supported by findings that show the relative risk of diabetes for those with one diabetic parent being 2.3 – and 3.9 for those with two diabetic parents. Explanatory genetic factors involved in the development of diabetes have often been attributed to changes in maternal mitochondrial DNA – which is considered to be a general marker of aging and degenerative disease.
Body iron stores also play an important role in the development of cardiovascular disease as both elevated and depressed levels produce morbidity. The risks for blacks are often attributed to nutritional deficiencies that produce anemia. Elderly black males (36.4 percent) and females (30.3 percent) are over twice as likely to be anemic as white males (14.3 percent) and females (11.6 percent). (Manton K.G., Stallard E. 1997) Additionally, hemoglobin means converged for males and females above age 90 with twice as many males exhibiting anemia as females.
Elevated iron levels may accelerate atherosclerosis in white males because free iron oxidizes LDL cholesterol. In men, serum ferritin (a measure of iron in the body) levels vary moderately with age. For women, ferritin increases following menopause. Another measure of iron in the blood, Hematocrit, has been shown to be related to high blood pressure, possibly associated with high blood viscosity. Using ferritin levels as a predictor of coronary heart disease declined for the elderly because of nutritional deficits, differential survival, and the lower variance of ferritin.
As such, differences in gender risk for hypertension decrease with age dropping from 2.4 to 1 to 1.4 to 1 by age 80. (Manton K.G., Stallard E. 1997) Therefore, excess risk of coronary heart disease in white males can be attributed to higher iron stores than females.Hypertension is also an important cause of heart disease and stroke – and exemplifies the innate genetic variation between different ethnicities. Hypertension reaches its apex at younger ages for blacks than for whites. This has mostly been attributed to the early elevation of blood pressure in blacks, which cause early mortality from stroke, coronary heart disease, and renal disease to be higher than for whites.
The genetic determinants of hypertension are closely associated with an enzyme that affects kidney function, rennin, and a protein affecting vasodilation and dilation of the blood vessels, angiotensinogen. A single gene codes for angiotensinogen and its mutation may predispose a person to hypertension. (Manton K.G., Stallard E. 1997) As such, this mutation was found in 36 percent of whites with normal blood pressure (normotensives) and 47 percent of white hypertensives. The frequency of this mutation among blacks is 80 percent to 90 percent.
Other interesting chronic diseases to examine in order to analyze the effects of genetic variation between ethnicities and genders are the many different types of cancer. Of obvious note are the gender disparities related to these cancers but ethnic and racial disparities exist as well within the genders for cervical, prostate and breast cancer.
Environmental determinants are often blamed for such disparities as certain groups may be less likely to have access to preventative and diagnostic health care services, but studies that show the prevalence of earlier diagnosis for blacks over whites leave the door open for explanatory biological factors – especially when considering age patterns of cancer morbidity and mortality.
In conclusion, to deny biological variation between groups in the treatment of chronic diseases is to put lives at risk. Life is more important than false notions of universal equality. If a doctor were to deny basic human differences when treating patients, there would be dire outcomes – even death. People are not equal.
Hochberg, M. C. (2007). Racial Differences in Bone Strength. Transactions of the American Clinical and Climatological Association, 118, 305–315.
Manton K.G., Stallard E. (1997) Racial and Ethnic Differences in the Health of Older Americans. National Academies Press (US)
Vlassoff, C. (2007). Gender Differences in Determinants and Consequences of Health and Illness. Journal of Health, Population, and Nutrition, 25(1), 47–61.