Question

A group of 10 overweight patients have increased levels of LDL (low-density lipoprotein) cholesterol. Based on this limited information and using the scientific method: I. Develop a question related to a potential treatment or therapy for this condition followed by a hypothesis (you can look on-line for relevant information). Then . . . II. Design a brief experiment to test your hypothesis; be sure to include a control, and to describe the independent and dependent variables (look these terms up if needed). Describe the predicted results of your experiment.

Answer 1

High cholesterol levels can lead to clogged arteries that come from a process known as atherosclerosis or hardening of the arteries. Having the right level of cholesterol helps lower the risk of problems caused by clogged arteries. That includes heart attacks and strokes. Obesity increases cardiovascular risk through risk factors such as increased fasting plasma triglycerides, high LDL cholesterol, low HDL cholesterol, elevated blood glucose and insulin levels and high blood pressure.

How do high levels of LDL cholesterol contribute to Obesity that increases cardiovascular risk and atherosclerosis?

Hypothesis:
My hypothesis is that high levels of LDL cholesterol contribute to Obesity that increases cardiovascular risk and atherosclerosis. My hypothesis is based on my gathered information that obesity increases cardiovascular risk through risk factors such as increased fasting plasma triglycerides, high LDL cholesterol, low HDL cholesterol, elevated blood glucose and insulin levels and high blood pressure.

Turnover rates of the apolipoprotein of low-density lipoproteins (apoLDL) and cholesterol balance were determined in six obese men and six control men. The two groups were of similar age and matched for apoLDL concentrations. Levels of plasma total cholesterol in obese patients (209 +/- 14 SEM mg/dl) were similar to controls (225 +/- 17 mg/dl). LDL-cholesterol was numerically but not statistically lower in obese subjects (111 +/- 18 mg/dl) compared to controls (145 +/- 13 mg/dl). Synthetic rates of apoLDL, in contrast, were higher in obese patients (1450 mg/day) than in controls (934 mg/day) (p less than 0.002). Three factors could explain the similar concentrations of LDL-cholesterol in obese and control subjects, despite overproduction of apoLDL in the obese. First, LDL was diluted into a larger plasma pool in obese patients; second, fractional catabolic rates of apoLDL were somewhat greater in obese men than in controls; and third, obese patients had higher ratios of protein-to-cholesterol in LDL. The production of apoLDL for all patients was not correlated with total body synthesis of cholesterol. The major finding of this study was that obese patients have increased turnover of apoLDL, not necessarily reflected by high concentrations of LDL-cholesterol. This high turnover rate itself may raise the risk of coronary heart disease in obese patients.

Our independent variable is LDL-cholesterol. The dependent variable is obesity and cardiovascular risk.