What is behind Overthinking & Racing Thoughts
Serotonin — the neurotransmitter of mood and satiety, and the precursor the body converts to melatonin for sleep. Evidence A — Human trial evidence.
The hypothalamic–pituitary–adrenal axis and its hormone cortisol — the body's central stress-and-recovery command. Evidence A — Human trial evidence.
The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down. Evidence B — Preclinical.
Insulin-like growth factor-1 — the dermal-papilla growth factor that drives follicle proliferation and prolongs anagen (the active growth phase). Evidence A — Human trial evidence.
How well the brain's inward-facing default network stands down when a task begins — measured as anticorrelation with the task-positive networks.
Thought that drifts away from the task at hand.
Evidence on these pathways
HPA Axis / Cortisol → Cognition. “Whereas treatments used in previous studies generally affect more than one memory phase and therefore cannot detect possible differential effects of glucocorticoids on the distinct phases of acquisition, consolidation and retrieval, here we show that treatment of healthy humans with cortisone at acute-stress levels specifically impaired retrieval of declarative long-term memory for a word list.” — Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nature Neuroscience, 2000, vol 3, pp 313-314. doi:10.1038/73873
HPA Axis / Cortisol → Digestive Function. “Reports have consistently established that central administration of CRF acts in the brain to inhibit gastric emptying while stimulating colonic motor function through modulation of the vagal and sacral parasympathetic outflow in rodents.” — Corticotropin-Releasing Factor and the Brain-Gut Motor Response to Stress. Canadian Journal of Gastroenterology, 1999, vol 13, pp 18A-25A. doi:10.1155/1999/375916
HPA Axis / Cortisol → Prolactin. “Stress is also an important physiologic cause of hyperprolactinemia, and its clinical significance is still being explored.” — Stress-Induced Hyperprolactinemia: Pathophysiology and Clinical Approach. Obstetrics and Gynecology International, 2018, volume 2018, article ID 9253083. doi:10.1155/2018/9253083
HPA Axis / Cortisol → Muscle Recovery. “Glucocorticoids elicit the atrophy of muscle by increasing the rate of protein degradation by the ubiquitin-proteasome system and autophagy lysosome system.” — The Regulation of Muscle Mass by Endogenous Glucocorticoids. Frontiers in Physiology, 2015, 6, article 12. doi:10.3389/fphys.2015.00012
Formulas that act on these pathways
Acts on 4 of these pathways: Serotonin, HPA Axis / Cortisol, NF-κB, Default Mode Suppression.
Acts on 3 of these pathways: Serotonin, HPA Axis / Cortisol, NF-κB.
Acts on 3 of these pathways: Serotonin, HPA Axis / Cortisol, NF-κB.
Acts on 3 of these pathways: Serotonin, HPA Axis / Cortisol, NF-κB.
Acts on 3 of these pathways: Serotonin, HPA Axis / Cortisol, NF-κB.
Acts on 3 of these pathways: Serotonin, HPA Axis / Cortisol, NF-κB.
What this page does not claim
This page names the pathways involved and the published evidence on each. It does not claim that any formula treats, cures or prevents Overthinking & Racing Thoughts. A pathway opens here only on graded, published evidence, under a standard fixed before the evidence was gathered, and every figure above carries its grade.
These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.