While hamburgers can’t cause heart attacks, we have long known that lifestyle choices – including diet, exercise, and sleep patterns – all play a role in cardiovascular health. What we don’t really know is how these factors actually affect our various bodily functions.
Filip K. Swirski, Director of the Cardiovascular Research Institute at the Icahn School of Medicine on Mount Sinai, outlined what is already known about the interaction between lifestyle, brain and cardiovascular health and what areas scientists are still working on. The former Harvard Medical School professor spoke on Thursday at a virtual event in the Topics in Bioengineering series presented by the Harvard John A. Paulson School of Engineering and Applied Sciences.
Swirski acknowledged that genetics “unquestionably” plays a role in cardiovascular health, but in recent years four risk factors – stress, sleep disruption or fragmentation, diet, and sedentary lifestyle – have been clearly identified as contributing to atherosclerosis, generally induration the arteries, which can lead to a variety of complications, including death.
Current and ongoing research is trying to uncover the mechanism by which these factors “alter tissue at the cellular and molecular levels,” he said, focusing on “inter-organ communication.” The aim is to “discover ways to develop therapeutic approaches and also to change health policy”, just as research on smoking shaped public policy.
In a brief summary of the latest insights into sleep – “on average we don’t get enough” – and the widely recognized role of diet and lifestyle, Swirski then delved deeply into the role of stress. Citing unpublished research, he used slides to illustrate how neutrophils – a type of white blood cell – “swarm” in the ears of stressed mice. This is not surprising, he said, referring to a study 10 years ago that won the Curt Richter Prize and showed the redistribution of such immune cells through stress.
However, current research traces these studies back to the cellular level, examining the movements of various blood components associated with the immune system, both during induced acute stress and in subsequent recovery. For example, in response to stress, neutrophil levels seem to rise in the lungs, liver, and spleen – but decrease in the bone marrow. “It may be that the source of neutrophils is the bone marrow,” he said. “And that they mobilize very quickly” to the other organs.
However, two other components – B and T cells – increase bone marrow under acute stress. While Swirski emphasized that this work was still ongoing, he hypothesized. “We believe that in response to acute stress there is mass migration of B and T cells into the bone marrow,” he said. “They hide in the bone marrow, perhaps as a safe haven, and after the storm is over they return to the blood.”
Further research attempts to understand the mechanisms behind these changes. Since these large-scale shifts are induced by stress, he pointed out that “centers of stress in the brain are the likely culprits”. Ongoing studies in mice suggest that the two primary centers of stress appear to have different functions. For example, the hypothalamic-pituitary-adrenal axis controls two of these blood components, lymphocytes and monocytes, but the sympathetic nervous system controls another, norepinephrine release.
Such a split is “unexpected,” said Swirski, raising both more questions and opportunities to explore. “We think these processes evolved for reasons that benefit the host, but they can also backfire,” he said.
When asked about the adaptive nature of these responses after his lecture, Swirski discussed the evolutionary meaning of stress. Stress not only evokes the noticeable “fight, flight or freeze reaction” that can save us when threatened, on a molecular level these immune-related reactions could also have helped our body to fight off antigens – like the germs on the teeth of a predator after one Bite.
However, these adaptive responses come at a price. Recovery – the time it takes to get back to pre-stress levels – is not only slow, but ongoing research shows that with repeated stress, the level reacts faster and faster and jumps into emergency mode. “Remember, there are two systems in our body – the immune system and the nervous system – that learn,” said Swirski. “They need input and are very intertwined.”
This has an impact on the current pandemic. “The health of our immune system has a socio-economic component,” he said, pointing out, among other things, the harmful effects of the “stress of not being able to feed the family”. “Stressed mice are much more likely to die from COVID than non-stressed mice,” he said.
“This permeates all health and disease,” Swirski concluded. “Some parts of stress are beneficial. We need stress, but it’s that balance of positive and negative stress. It’s a complicated subject. “
The daily newspaper
Sign up for daily email for the latest Harvard news.