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COURSE CODE:BIO1201:

Specification: Name:
1.18: (i) be able to analyse data on the possible significance
for health of blood cholesterol levels and levels of Class/Period:
high-density lipoproteins (HDLs) and low-density lipoproteins
(LDLs) Date:
(ii) know the evidence for a causal relationship between blood
cholesterol levels (total cholesterol and LDL cholesterol) and
cardiovascular disease (CVD)

Key Questions: Notes:

What are cholesterol? ■ Cholesterol is not soluble in water so needs to combine with proteins to form
lipoproteins
■ Many evidence shows a correlation between increased cholesterol levels and
death rate
■ Low fat diet which avoids saturated fats reduces total blood cholesterol
■ HDLs reduce blood cholesterol deposition= high level of HDLs is good

What are LDLs? ■ LDLs are the main cholesterol carrier in the blood
■ Triglycerides from saturated fats in our diet combine with cholesterol and
protein= LDLs
■ LDLs circulate in the bloodstream and bind to receptor sites on cell membranes
and are then taken up by the cells
■ Excess LDLs in diet overload membrane receptors resulting in high blood
cholesterol levels.
■ Saturated fats may also reduce the activity of LDL receptors so LDLs aren’t
removed from the blood, therefore increases blood cholesterol levels
■ Cholesterol may be deposited in artery walls leading to the formation of
atheroma.

What are HDLs? ■ HDLs have a higher percentage of protein compared to LDLs hence their
higher density.
■ HDLs are made when triglycerides from unsaturated fats bind with cholesterol
and protein.
■ HDLs transport cholesterol from body tissues to the liver where they are broken
down. This lowers blood cholesterol levels and helps reduce the formation of
fatty plaques.

References:
COURSE CODE:BIO1201:

Correlation or Causation? ■ Correlation is when two variables are positively correlated where an increase in
one is accompanied by an increase in the other.
■ Large amounts of data are needed to ensure that the correlation is statistically
significant. This ensures that it didn’t happen by chance.
■ Causation is when two variables are causally linked where a change in one is
responsible for a change in the other
■ Therefore, scientists need to set up experiments with control variables. This
means they can see if altering one variable has the predicted effect.
■ To do this a null hypothesis is set up where they assume that there will be no
difference between an experimental group and the control group.
■ This is then testes using statistical analysis

Is lowered cholesterol leading to There are many substantial reasons to believe that high cholesterol and heart disease
lowered risk of CVD a causal are closely linked. For one thing, there is a plausible-sounding explanation as to why
relationship? they should be. This explanation states that LDLs are the “bad” type of cholesterol,
which can stick to the inner walls of the blood vessels and potentially clog them,
leading to heart conditions such as stroke, atherosclerosis, angina and coronary heart
disease (CHD). Whereas HDLs (high density lipoproteins), are the “good” type of
cholesterol, and these have the opposite effect.

There are some reasons to suggest that this hypothesis is correct. Firstly, there is
evidence of a correlation between high cholesterol/LDL levels and heart disease. The
Framingham Study, a prospective cohort study beginning with over 5,000 participants,
published a paper in 1977 which concluded that higher HDL levels and lower LDL
levels were associated with a reduced risk of coronary heart disease.

In addition to this, some medical treatments which reduce cholesterol/LDL levels also
reduce your risk of heart disease. Statins, for example are effective in both lowering
cholesterol levels, and reducing the rates of CHD, cardiovascular disease (CVD) and
stroke.

This evidence seems to point towards there being a causal connection between
cholesterol in heart disease. However, a closer examination of the issue may decrease
the validity of this conclusion.

A follow-up from the initial Framingham study suggested that there was only an
increase in mortality, by heart disease or other causes, in people with higher
cholesterol levels under the age of 50. This is significant if we want to offer medication
or lifestyle advice about preventing heart disease to those over 50 years old.

References:
COURSE CODE:BIO1201:

A recent systematic review even suggests that patients over the age of 60 actually lived
longer if they had higher LDL levels, directly contradicting the hypothesis that you are
more likely to die of heart disease the higher your cholesterol levels are.

Moreover, despite statins showing a correlation between lowered cholesterol levels and
a reduced risk of heart disease, some other medications do not show this connection.
Niacin, for example, is a cholesterol lowering drug which is known to decrease LDL
levels, but has been shown to cause no significant reduction in risk of heart attack,
stroke or mortality by heart disease.

In the case of risk factors like cholesterol, a ‘cause’ does not mean that the presence of
this risk factor will always and invariably lead to a certain disease. This depends on a
number of other factors, like age, other diseases, lifestyle, and possibly plain luck.

Instead we are looking at a complex array of inter-related mechanisms, all of which


may or may not lead to someone becoming ill. And when it is unclear about exactly
how these mechanisms work or how they relate to each other, making predictions
about health outcomes will inevitably be difficult.

Summary

References:

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