Stress: Your Brain’s Role in Immunity and Cancer

Our bodies aren’t isolated systems— the brain, immune defenses, hormones, and nervous system form a dynamic network called psychoneuroimmunology, or PNI. This interplay explains why emotions and stress can influence health outcomes like cancer. Let’s break it down step by step.

Primary and Secondary Immune Organs: The Foundation
Primary immune organs include the bone marrow and the thymus gland, tucked in the upper chest in front of the heart. Here, immune cells mature before traveling to secondary lymphoid organs like the spleen and lymph glands. Fibers from the central nervous system directly supply both primary and secondary organs, enabling instant brain-to-immune communication.

Endocrine glands, which produce hormones, are also wired to the central nervous system. This allows the brain to directly signal the thyroid, adrenal glands, testes, ovaries, and more.

Bidirectional Communication: Immune Signals Reach the Brain
Hormones from endocrine glands and substances from immune cells directly impact brain activity by binding to receptors on brain cells, shaping behavior. We’ve all felt “sickness behavior”—fever, loss of appetite, fatigue, and sleepiness—triggered by cytokines, chemicals secreted by immune cells. These adaptations conserve energy to fight illness, but inappropriate cytokine release can cause chronic fatigue or dysfunction.

Remarkably, lymph cells and white blood cells produce nearly all brain and nervous system hormones, including endorphins, the body’s natural painkillers and mood boosters. These immune cells even have receptors for brain-originated hormones, creating a two-way street.

The HPA Axis: Stress Response Central
At PNI’s core lies the hypothalamic-pituitary-adrenal (HPA) axis, activated by psychological or physical threats. Emotional centers in the limbic system—including parts of the cerebral cortex and deeper structures—evaluate stimuli. If threatening, the hypothalamus prompts the pituitary to release adrenocorticotropic hormone (ACTH), which triggers cortisol release from the adrenal cortex.

The hypothalamus also signals the sympathetic “fight-or-flight” nervous system to the adrenal medulla, releasing adrenaline to rev up cardiovascular and nervous responses. Psychological stressors like uncertainty, conflict, lack of control, or information gaps most strongly activate the HPA axis. Conversely, a sense of control or “consummatory behavior”—actions that resolve tension, from Latin consummare (“to complete”)—quickly suppresses it. This includes fulfilling emotional needs like love, abolishing the stress response.

Cancer: Beyond DNA Damage to Mind-Body Factors
Emotions interact with hormones, immunity, and nerves via PNI, playing roles in cancer. The mechanistic view pins cancer on DNA damage from toxins like tobacco in lung cells. Yet it doesn’t explain why some smokers get cancer and others don’t, despite identical exposure.

Cancer unfolds in stages: initiation (normal cell turns abnormal), promotion, and progression. Initiation requires multiple DNA lesions—up to ten in lung cells from tobacco smoke—but most are transient, repaired by DNA mechanisms or eliminated via apoptosis, programmed cell death essential for healthy tissue turnover.

Dysregulated apoptosis contributes to tumors, autoimmune issues, immunodeficiencies, and neurodegeneration. HPA-driven steroid hormones regulate apoptosis, but chronic stress from emotional repression creates abnormal hormone levels, disrupting it. Natural killer (NK) cells also aid cell death; depression—marked by repressed anger—combined with smoking lowers NK activity.

DNA damage alone isn’t enough for cancer; failed repair or impaired apoptosis is key, both hindered by stress and emotion suppression.

Promotion and Progression: The Internal Environment Matters
Surviving malignant cells form tumors during promotion and progression, influenced by the body’s milieu. Hormones play dual roles: many tumors are hormone-dependent, with receptors on cancer cells for growth-promoting substances. Breast cancer exemplifies this—often estrogen-driven, treated with blockers like tamoxifen. Less known: some breast cancers respond to androgens, progestins, prolactin, insulin, vitamin D, and more, all tied to or regulated by the HPA axis.

In organs like ovaries or testes, hormonal ties amplify risks. This underscores how chronic stress and emotional patterns can foster a cancer-permissive environment.

Source : When the Body Says No: The Cost of Hidden Stress by Gabor Maté

Goodreads :https://www.goodreads.com/book/show/450534.When_the_Body_Says_No

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