Dyslipidemia

Definitions

Dyslipidemia describes levels of plasma cholesterol, triglycerides (TGs), or both that are too high or when there is a lower high-density lipoprotein (LDL/ HDL) level in the body. Plasma cholesterol, triglycerides, and high density lipoproteins are lipids or fat that are naturally in the body and present in many foods. Lipids store energy, make up the structure of cell membranes and signaling molecules within the body (Mandal, 2012). Over production or underproduction of these molecules can lead to symptomatic vascular disease such as coronary artery disease, in which plaque builds up inside oxygen- rich blood to the heart muscle (“What Is Coronary Heart Disease?”, 2016), stroke, blood flow to the brain that is interrupted and cause brain cells to die(“Heart Disease and Stroke”), and peripheral arterial disease, circulatory deficits that reduce blood flow to the limbs from arteries that cause leg pain (Mayo Clinic Staff, 2015). Dr. Goldberg of Washington University School of Medicine writes that there is “no natural cutoff between normal and abnormal lipid levels because lipid measurements are continuous” (Goldberg, 2015) While there is a correlation between lipid levels and cardiovascular risk, dyslipidemia can be “applied to lipid levels for which treatment has proven beneficial”.

Causes and Symptoms

Dyslipidemia is primarily caused by genetics where a “single or multiple gene mutations…result in either overproduction or defective clearance of TG and LDL cholesterol, or in underproduction or excessive clearance of HDL” (Goldberg, 2015). Inheritance can be dependent on codominant or complex with multiple genes, dominant, or recessive genes passed on to an offspring. Prevalence of certain dyslipidemias such as Familial hypercholesterolemia is increased in French Canadian, Christian Lebanese, and South African populations while other genetic dyslipidemias such as Familia dysbetalipoproteinemia have a worldwide prevalence. Treatment for genetic dyslipidemias are usually diet, lipid- lowering drugs, weight loss, and sometimes surgery.

Secondary causes are listed as include diabetes mellitus, alcohol overuse, chronic kidney disease, hypothyroidism, cigarette smoking, anabolic steroids, HIV infection, and nephrotic syndrome. The most important cause being, “A sedentary lifestyle with excessive dietary intake of saturated fat, cholesterol, and trans fats” (Goldberg, 2015). Trans fats are in many processed foods and therefore pose a risk for those who eat processed food or cannot afford non-processed foods.

While dyslipidemia has no symptoms, it can lead to heart disease (Leon Bronas, 2009). Skin rashes such as tendinous xanthomas at Achilles, elbow, and knee tendons and metacarpophalangeal joints are also at risk of forming when levels of TGs are high. High levels of LDL can lead to arcus cornea, which is a white ring that forms in the cornea. Extremely high lipid levels can cause paresthesias, dypsnea, and confusion (Goldberg, 2015). These symptoms are indicators of the condition that can lead to further testing of total cholesterol, TGs, HDL cholesterol, and LDL cholesterol. Patients with a family history of abnormal cholesterol levels or peripheral vascular disease could be at risk for dyslipidemia. Screening for children between ages 9 to 11 and adults are screened at age 20 every five years afterwards.

Xanthomas

Image provided by Gary M. White, MD

Arcus Cornea

Image provided by Dr. J. R. Lacey

Dyslipidemia and Politics of Health

A study conducted by Goff et al. titled, “Dyslipidemia Prevalence, Treatment, and Control in the Multi-Ethnic Study of Atherosclerosis”, looked at the disparities between race, socioeconomic status, sex, risk factors, healthcare access variables and the likelihood and control of treatment of dyslipidemia. They also grouped patients with low, intermediate, and high risk of cardiovascular disease (CVD). Average age for participants were 62 years old, education less than high school was 63.9%, The results show that men are less likely to be treated and controlled for lipid-lowering drug therapy than women even though their prevalence of dyslipidemia are generally higher. Chinese Americans were less likely to qualify for drug treatment, Black and Hispanic Americans had similar prevalence rates of dyslipidemia to non-Hispanic whites but were less likely to be treated and controlled (Goff et al, 2006). Groups with intermediate and high risk of developing CVD, influenced by dyslipidemia, had lower control rates than groups with lower risk which means that rates of CVD were not lowered and remained consistent (Goff et al, 2006). Such differences highlighted the relevance of dyslipidemia and its occurrence and treatment within a population. The use of race as a determinant of a condition is similar to the idea of BiDil. While BiDil was directly targeting the effects of drug treatment on one race, the way in which Goff et al. examines prevalence through the category of race is enough to say that racialization is present in this study. It also follows the argument of racial inequalitions in biomedicine in Hatch’s Blood Sugar: Racial Pharmacology and Food Justice in Black America (2016). The results of the study proved that disparities between ethnic groups did not persist when healthcare access variables were adjusted and controlled, proving Hatch and critics of BiDil’s arguments that race or ethnic groups are not reliable or objective categories in medicine. Factors such as access to healthcare and socioeconomic status were found to affect the rates of prevalence of dyslipidemia in this study. These factors indicate that accessibility barriers such as lack of health insurance like Medicaid and Medicare actively contribute to treatment and control of dyslipidemia, and on a larger scale, coronary heart disease. This shows a lack of biocitizenship, where access to certain resources such as health insurance can prevent or significantly lower the chances of developing dyslipidemia. Therefore, policy plays an important role in the health of those at risk or currently diagnosed with dyslipidemia.

Reference

Goff, David C., Alain G. Bertoni, Holly Kramer, Denise Bonds, Roger Blumenthal, Michael Tsai, and Bruce Psaty. “Dyslipidemia Prevalence, Treatment, and Control in the Multi-Ethnic Study of Atherosclerosis (MESA): Gender, Ethnicity, and Coronary Artery Calcium.” Circulation 113, no. 5 (2006): 647-56. Accessed April 3, 2017. doi:10.1161/circulationaha.105.552737.

Goldberg, Anne Carol, MD. “Dyslipidemia – Endocrine and Metabolic Disorders.” Dyslipidemia (Hyperlipidemia). Accessed April 04, 2017. http://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/lipid-disorders/dyslipidemia#v989800).

Hatch, A. (2016). Blood Sugar: Racial Pharmacology and Food Justice in Black America. University of Minnesota Press. Retrieved from http://www.jstor.org/stable/10.5749/j.ctt1b7x5k8

Leon, A. S., & Bronas, U. G. (2009). Dyslipidemia and Risk of Coronary Heart Disease: Role of Lifestyle Approaches for Its Management. American Journal of Lifestyle Medicine, 3(4), 257-273. doi:10.1177/1559827609334518

Mandal, Ananya, MD. “What are Lipids?” News Medical Life Sciences. October 9, 2012. Accessed April 3, 2017. http://www.news-medical.net/life-sciences/What-are-Lipids.aspx.

Mayo Clinic Staff Print. “Peripheral artery disease (PAD).” Mayo Clinic. December 24, 2015. Accessed April 04, 2017. http://www.mayoclinic.org/diseases-conditions/peripheral-artery-disease/home/ovc-20167418.