Jared Markus

Nutrition 445

Case Study 3

Due April 6, 2016

Hypercholesterolemia:

A 36-year old man was found to have hypercholesterolemia. A dietary evaluation indicated that he was consuming about 600 mg/day of cholesterol. His plasma cholesterol concentration on two separate occasions was approximately 330 mg/dL (8.5 mmol/L). Ultracentrifugal analysis revealed that the cholesterol elevation was due to an increase in plasma LDL. He was treated with a cholesterol-free vegetarian diet for 3 months, but his plasma cholesterol level decreased to only 300 mg/dL (7.7 mmol/L). Subsequently he was treated with colestipol hydrochloride, a bile acid-binding resin that is not absorbed. This treatment lowered the fasting plasma cholesterol concentration to 250 mg/dL (6.4 mmol/L).

Questions:

  1. How is dietary cholesterol absorbed?

Dietary cholesterol is absorbed in two steps, first the cholesterol enters the lumen where it is digested and put through hydrolysis. These dietary lipids are then put through solubilization (in the micelles) from phospholipids and bile acid, and allows the cholesterol to move to the surface of the enterocyte. Secondly, the body uses simple and facilitated diffusion to move cholesterol across the mucosal cell membrane and to a transporter for cholesterol within the microvillus membrane where it is esterified once again. The cholesterol ends up becoming apolipoprotein B and is secreted into the lymph. (Turley & Dietschy)

(Altmann)

  1. How is it possible for a patient to continue to have high plasma cholesterol after being on a cholesterol-free diet for 3 months?

It is possible to have high plasma cholesterol after being on a cholesterol-free diet for 3 months due to your body making a certain amount itself as a natural function. If the patient stops eating cholesterol, and yet still have high plasma cholesterol, they more than likely are not living a healthy lifestyle. With this being said, they are either obese, high cholesterol was inherited, low physical activity or getting older. Obesity and as a person ages, they are dealt with the rise of LDL cholesterol and a decrease in HDL cholesterol. The diet will not help if they are not physical active on a regular basis, due to the rise of HDL cholesterol when your body is under a copious amount of physical activity. (Kresser)

If it was inherited, the patient should be aware of this and know not only do they need to watch the amount of cholesterol consumed, but also take proper cautions as to medications and the standard amount of physical activity. Other than lifestyle, the discontinuation of consuming cholesterol will ultimately take a toll on how the body regulates cholesterol and how much it produces. With that being said, the number of lipoprotein receptors, and hence the efficiency of disposal of plasma cholesterol, can be increased by cholesterol-lowering drugs. Regulation of lipoprotein receptors can be exploited pharmacologically in the therapy of hypercholesterolemia and atherosclerosis is man. (Brown)

  1. What connection is there between bile acids and cholesterol?

The connection between bile acids and cholesterol is simply that bile acids allow cholesterol to be regulated and absorbed. “Data are presented which show that bile acids, the major steroids circulating in this cycle, exert direct feedback control of hepatic cholesterol synthesis. This characteristic of bile acids may explain why certain bile acids, when given orally, reduce serum cholesterol levels.” (Barth)

  1. How does a bile acid-binding resin lower the plasma cholesterol concentration?

The bile acid-binding resin lower the plasma cholesterol concentration due to the highly positively charged molecules that bind with the negatively charged bile acids. This disables cholesterol absorption by inhibiting their solubilization. “They also inhibit the reabsorption of bile acids (which is typically 95%) and thus cause a contraction of the bile acid pool which leads to increased bile acid synthesis that competes with cholesterol synthesis in the liver, which also contributes to the lowering of serum cholesterol levels.” (National Institute of Diabetes and Digestive and Kidney Diseases)

  1. What additional treatment would you suggest for a patient with this disease?

The additional treatment suggested for a patient with this disease would be a healthy diet with a mixture of wholegrains, fiber, fruits and vegetables, replacing saturated fats with unsaturated fats, 120 minutes of standard physical activity a week. Other than the basic lifestyle changes, additional treatment would suggest a cholesterol-lowering drug such as atorvastatin, simvastatin, rosuvastatin which inhibits the enzyme within the liver that produces cholesterol or niacin, which would be just as helpful with its ability to reduce triglycerides and raise HDL levels. (Mandal)

Works Cited

Altmann, Scott W. "Scott W. Altmann - Figures & Descriptions - ScienceWatch.com." Scott W. Altmann - Figures & Descriptions - ScienceWatch.com. Thomson Reuters, Mar. 2008. Web. 05 Apr. 2016.

Brown, M. S., P. T. Kovanen, and J. L. Goldstein. "Result Filters." National Center for Biotechnology Information. U.S. National Library of Medicine, 8 May 1981. Web. 05 Apr. 2016.

Kantharia, Ajay. "Lipid Guidelines - Dr. Ajay Kantharia." Lipid Guidelines - Dr. Ajay Kantharia. LinkedIn, 20 Apr. 2011. Web. 05 Apr. 2016.

Kresser, Chris. "The Diet-Heart Myth: Cholesterol and Saturated Fat Are Not the Enemy." Chris Kresser. Chris Kresser, 19 Apr. 2013. Web. 05 Apr. 2016.

Mandal, Ananya. "Hypercholesterolemia Treatment." News-Medical.net. News-Medical.net - An AZoNetwork Site, 18 Feb. 2010. Web. 05 Apr. 2016.

National Institute of Diabetes and Digestive and Kidney Diseases. "Livertox." Bile Acid Resins or Sequestrants. U.S. National Library of Medicine, 3 May 2014. Web. 05 Apr. 2016.

Turley, Stephen D., and John M. Dietschy. "Medscape Log In." Medscape Log In. Le Jacq Communications, Inc., 5 Apr. 2016. Web. 05 Apr. 2016.