Within the human body there are few diseases that aren’t influenced by some kind of environmental factors (stress, obesity, smoking, lack of sleep). Put another way, even diseases that have a genetic link (cancer, heart disease, diabetes) are not fully explained by genetics – environmental factors also play a role. Teasing apart the ‘who does what to whom’ puzzle of these diseases is one of the major challenges in biomedicine. Researchers at the University of California Los Angeles (USA) focused their study on the environmental influence. Instead of one gene, they looked at thousands of human genes and in particular how they were ‘expressed’ as proteins (DNA providing the blueprint for amino acids and then proteins).

The work was conducted at the cellular level, using cells derived from heart transplant tissue. The cells were kept in vitro (Petri dishes) and subjected to stress, in particular fats known to cause inflammation and atherosclerosis.

“The genes responded differently to inflammation depending on their genetic makeup,” said first author Casey Romanoski, a UCLA graduate student in human genetics. “About 35 percent of the most affected genes were influenced by the interaction between their genetic variants and the fats.”

“You can’t effectively study genes divorced from their environment,” she added. “The missing link lies in the intersection of genes with their environment.”

[Source: EurekAlert]

If you think you’ve heard some of this before, you probably have – only from a different angle. There are many studies based on studies of people with heart disease and their personal habits that lead to conclusions such as “Obesity linked to heart disease.” These are largely statistical studies. Many other studies, more laboratory oriented statistical studies, find links between specific genes and incidences of a disease with conclusions such as “Gene found linked to heart disease.” The UCLA study is at the cellular level, with biochemistry being the principle interest, and results looking like “Body fats contribute breakdown of protein construction.”

The links between, say obesity and heart disease are more or less intuitive, but also very generalized. The UCLA study begins the task of pinning down not only the genes involved, but also the specific molecular pathways that lead from the wrong kind of body fats interacting with genes to produce the wrong kind of proteins. There is still much more detailed work yet to be done.