A new study suggests one reason heart-related deaths go up in winter is because the cold causes brown fat to accelerate the build-up of plaque in blood vessels.
Researchers from Sweden and China, who made this breakthrough discovery while studying mice, write about their findings in the July 2nd online issue of Cell Metabolism.
We have known for a while that deaths from cardiovascular diseases go up in winter, and we have put this down to the fact that we tend to be more sedentary in winter. When we do perform something physically demanding, like shoveling coal, we over-exert ourselves. But while these reasons seem plausible, the underlying mechanisms have never been explained.
Now Yihao Cao, of the Karolinska Institutet and Linköping University in Sweden, and colleagues propose a completely unexpected alternative reason. One they arrived at after studying a strain of mice genetically engineered to develop atherosclerosis, a process where fatty deposits called plaques build up on the inside walls of arteries, raising the risk of heart attack, stroke and other serious cardiovascular events.
Like humans, mice have two types of body fat: white fat and brown fat. White fat stores calories, such as in the flab that accumulates around waists and hips, while brown fat burns calories to generate heat.
Cold temperatures trigger brown fat to generate heat. This was thought to be “healthy” for the body because it also helps reduce white flabby fat.
But what corresponding author Cao and colleagues found was that exposure to cold accelerated the formation of fatty deposits or atherosclerotic plaques in the mice, which can lead to heart attack and brain hemorrhaging.
It seems that the lower temperatures activated the breakdown of fatty acids in the mice’s brown fat, causing levels of small low-density lipoprotein (LDL) remnants in the blood to rise, thus encouraging more of it to deposit as plaque.
And, not only did the lower temperature accelerate plaque build-up, but also it made the plaque less stable. Unstable plaque is more likely to rupture and leak stored fat into the blood, causing blockages in vessels in the heart and brain.
At first, the researchers thought the mice would get thinner and healthier when the cold temperatures activated the brown fat.
“Instead, we found that they ended up having more fat stored in the blood vessels. This came as a surprise and was the opposite of what we thought would happen,” says Cao, a professor in the Department of Microbiology, Tumor and Cell Biology at Karolinska.
If the same is true of humans, then perhaps we should be advising people with cardiovascular diseases to avoid getting cold and to don warm clothes when they step outside in the winter months, he adds.
Cao and the team now hope to take their findings further and study this effect in humans. If they indeed do find that the same happens in humans as in the mice, then this would be “an extremely important discovery,” says Cao.
There are drugs that can block the activation of brown fat, something the team is also keen to look into in light of their findings.
At first it was thought that humans only had white fat. Then it was discovered that babies have brown fat, then that adult humans have it, too.
Researchers have since been looking at how to exploit the fact that brown fat burns calories instead of storing them as a possible way to fight obesity.
In 2012, US scientists who discovered a biochemical trigger that switches on brown fat cells, suggested this might offer a drug target for fighting obesity.
This present study by Cao and his team now suggests this may not be a good idea, in that activating brown fat as a way to lose weight could worsen any cardiovascular risk or disease that might be present.
Grants from several bodies including the Swedish Research Council, the Swedish Cancer Society, the Torsten Söderberg Foundation, the European Research Council, and EU Framework funding helped finance the study.
Written by Catharine Paddock PhD