It is well-established that individuals with heart disease are more likely to suffer from depression, and vice versa. Now in a new study, researchers at the University of Cambridge in the U.K. have identified an important factor linking these two conditions: inflammation.
Although inflammation is the body’s natural response to fighting off infection, chronic inflammation is very harmful. Long-term inflammation can be caused by psychological stress as well as lifestyle factors such as smoking, excessive alcohol intake, physical inactivity and obesity.
The association between heart disease and depression is well documented. Heart attack patients are at a significantly greater risk of depression. Yet scientists have been unable to determine whether this is due to the two conditions sharing common genetic factors or shared environmental factors.
“It is possible that heart disease and depression share common underlying biological mechanisms, which manifest as two different conditions in two different organs — the cardiovascular system and the brain,” says Dr. Golam Khandaker, a Wellcome Trust Intermediate Clinical Fellow at the University of Cambridge. “Our work suggests that inflammation could be a shared mechanism for these conditions.”
For the study, Khandaker with Dr. Stephen Burgess and a team of Cambridge researchers investigated this link by studying the data of nearly 370,000 middle-aged individuals from the UK Biobank.
First, they looked at whether family history of coronary heart disease was tied to a risk of major depression. They discovered that individuals who reported at least one parent having died of heart disease were 20 percent more likely to develop depression at some point in their life.
Next, the researchers calculated a genetic risk score for coronary heart disease — a measure of the contribution made by the various genes known to increase the risk of heart disease. Heart disease is a “polygenic” disease; caused not by a single genetic variant, but rather by a large number of genes, each increasing a person’s risk of developing heart disease by a small amount.
Unlike for family history, however, the researchers did not find a strong link between the genetic predisposition for heart disease and the likelihood of experiencing depression.
Together, these findings suggest that the association between heart disease and depression cannot be explained by a common genetic predisposition to the two diseases. Rather, it suggests that something about an individual’s environment, such as the risk factors they are exposed to, not only increases their risk of heart disease, but also raises their risk of depression.
This finding was further supported by the next stage of the study. The team used a randomizing technique to investigate 15 biomarkers, or biological “red flags,” associated with increased risk of coronary heart disease.
Of these common biomarkers, they found that triglycerides (a type of fat found in the blood) and the inflammation-related proteins IL-6 and CRP were also risk factors for depression. Both IL-6 and CRP are inflammatory markers that are produced in response to damaging stimuli, such as infection, stress or smoking.
Research by Khandaker and others has previously shown that individuals with heightened levels of IL-6 and CRP in the blood are more prone to developing depression, and that levels of these biomarkers are high in some patients during an acute depressive episode. Elevated markers of inflammation are also seen in people with treatment resistant depression.
“This study adds important new insight into the emergence and risk of depression, a significantly under researched area,” said Dr. Sophie Dix. “Taking a holistic view of a person’s health — such as looking at heart disease and depression together — enables us to understand how factors like traumatic experiences and the environment impact on both our physical and mental health.”
“We need to stop thinking about mental and physical health in isolation and continue this example of bringing sciences together to create real change.”
The findings are published in the journal Molecular Psychiatry.
Source: University of Cambridge