It is known that significant and prolonged stress promotes the development of cancer. This relationship, however, is not universally recognized or well understood. But a Chinese team, working in connection with many other teams from different countries, The Journal of Clinical Investigation results of work linking chronic stress and cancer via adrenaline.
The authors worked on an experimental model of mice with high-risk breast cancer. These mice were stationed for a week in a tight cabinet, causing continuous stress. Then the mice were divided into two batches, one kept in the tight compartment, the other placed in a cabinet large enough and comfortable to remove the stress. Mice exposed to stress not only changed their behavior, evidencing their level of anxiety and depression, but also developed larger mammary tumors in size and growing faster than their non-stressed counterparts.
Biological and histological analyzes showed that the tumors developed in stressed mice contained a much larger number of cancer stem cells, which affect not only the growth rate of tumors but also their remote swarming (metastases).
If stress promotes oncogenesis, it is via cortisol that inhibits the immune system. However, this work shows that cortisol levels are lower in mice exposed for one month to stress than in mice in the control group. If stress promotes cancer, it is not due to immunosuppression induced by high level of cortisol. The authors of the study show that mice exposed to chronic stress, but receiving an adrenergic receptor blocker (ADRB2), have smaller tumors and less cancerous stem cells than mice exposed to the same stress but do not receive this drug. According to these researchers, it is the adrenaline that would create the link between stress and cancer because, once linked to ADRB2 receptors, this hormone would increase levels of lactate dehydrogenase, which in turn activates oncogenes and the production of cancer stem cells , releasing large amounts of lactate that feeds cancer cells to ensure their proliferation.
Based on these findings, the authors used data from 83 women with breast cancer. And they found a strong correlation between the size of the tumor and its degree of aggressiveness, on the one hand, and the level of lactate dehydrogenase, on the other.
Returning to their animal model, the authors show that vitamin C makes it possible to reduce the impact of these elevated lactate dehydrogenase levels on oncogenesis, not hesitating to suggest that this vitamin could be a weapon against cancer induced or favored by chronic stress.