Common antidepressants could help the immune system fight cancer (SSRIs)

A widely used antidepressant drug could help the immune system fight cancer, according to a new research study.

Selective serotonin reuptake inhibitors, or SSRIs, significantly enhanced the ability of T cells to fight cancer and suppressed tumor growth across a range of cancer types in both mouse and human tumor models found.

Yang and her team first began investigating serotonin's role in fighting cancer after noticing that immune cells isolated from tumors had higher levels of serotonin-regulating molecules.

The researchers tested SSRIs in mouse and human tumor models representing melanoma, breast, prostate, colon and bladder cancer. They found that SSRI treatment reduced average tumor size by over 50% and made the cancer-fighting T cells, known as killer T cells, more effective at killing cancer cells.

"SSRIs made the killer T cells happier in the otherwise oppressive tumor environment by increasing their access to serotonin signals, reinvigorating them to fight and kill cancer cells," said Yang.

The team also investigated whether combining SSRIs with existing cancer therapies could improve treatment outcomes. They tested a combination of an SSRI and anti-PD-1 antibody—a common immune checkpoint blockade, or ICB, therapy—in mouse models of melanoma and colon cancer. ICB therapies work by blocking immune checkpoint molecules that normally suppress immune cell activity, allowing T cells to attack tumors more effectively.

The results were striking: the combination significantly reduced tumor size in all treated mice and even achieved complete remission in some cases.

"Immune checkpoint blockades are effective in fewer than 25% of patients," said James Elsten-Brown, a graduate student in the Yang lab and co-author of the study. "If a safe, widely available drug like an SSRI could make these therapies more effective, it would be hugely impactful."

90% of the bodies serotonin is produced by the Enterochromaffin Like Cells (ECL Cells) in the lining of the gut.

SSRI’s do not work to increase the serotonin in the synaptic cleft if there is an overall deficiency of serotonin in the body.

The ECL Cells respond to gastrin, released by the stomach’s G-Cells into the bloodstream when the stomachs expands from eating.

ECL Cells produce Histamines, Serotonin, and Somatotropin.

I met with my oncologist this past week and provided him medical research journal articles. I think I found the root cause of my lung cancer. It was in the ECL Cells and lack of Histamine regulation.

He is a top oncologist at a major university hospital and was unaware of the biochemical processes I explained to him. He and my primary care Dr are reading my research now. The key is an enzyme that degrades Histamines.

The gut biom is far more complex than most realize. I attended a conference symposium on “Psychiatry and the Gut” a few years ago at an APA Conference where Michael Gershon of Columbia University, author of “The Second Brain” presented on this topic. I have been following the gut biom research ever since.

Gershon has been called the “father of neurogastroenterology” because, in addition to his work on neuronal control of gastrointestinal behavior and the development of the enteric nervous system,

The research is lacking on the influence of the vagus nerve on the gut and the enteric nervous system.

Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.