According to new research from the Shenzhen Institutes of Advanced Technology (SIAT) of the Chinese Academy of Sciences, chronic stress may be a catalyst for bone loss. The study found that a central neural circuit from the forebrain to the hypothalamus can mediate chronic stress-induced bone loss.
The clinical study set out to find how the brain receives and processes external signals which are sent to the peripheral bones. The study adds to mounting evidence that bone mineral density in patients with anxiety or depression is lower than in people without a mental health problem.
With many people experiencing isolation because of COVID-19, this study offers an interesting perspective of the side effects of the pandemic. Isolation is something that many people have been forced to deal with in recent months, and new information is starting to come to light as to how it is affecting society. One way that researchers found insolation affects health is that it can significantly increase anxiety levels, which can then lead to bone loss due to the peripheral sympathetic nervous system.
Using biochemical analysis, researchers were able to find that prolonged isolation increases the concentration of norepinephrine and decreases osteogenic markers in serum. These changes have previously been associated with elevated anxiety and reduced bone formation in patients.
To identify the neural mechanism that researchers believe initiated the chronic stress-induced bone loss, a mouse model was subjected to unpredictable chronic mild stress.
After four to eight weeks of chronic stress, the mice displayed significant anxiety behaviors, and their bone mineral density showed a significant decrease. The control group had no stress and no drop in bone density.
Confirming the correlation between stress-induced anxiety and bone density, this animal study provides a starting point for a follow-up neural mechanism analysis. Researchers were able to identify a population of inhibitory neurons in the brain nucleus that was shown to be activated when animals showed anxiety. These neurons took the “anxiety” information and transmitted it into the ventromedial hypothalamus (VMH).
“Activating the BNST-VMH neural circuit can simultaneously induce anxiety-like behaviors and generate bone loss in the mice, whereas inhibition of this circuit can prevent stress-induced anxiety and bone loss at the same time,” said Prof. YANG Fan from SIAT, the co-first author of the study.
Researchers also found that glutamatergic neurons in nucleus tractus solitarius (NTS) and the sympathetic system were used to regulate stress-induced bone loss. This information can help to provide a new perspective for the study of brain homeostasis and endocrine function of the body when under chronic stress. This may help physicians understand low bone density occurrence in patients under chronic stress and offer preventative treatments.