TUDCA and Depression: What ER Stress in the Brain Has to Do With Mood
Three rodent models show antidepressant-like effects. Human studies find altered bile acids in depression but give nobody TUDCA. Why that gap matters.
Three rodent models show antidepressant-like effects. Human studies find altered bile acids in depression but give nobody TUDCA. Why that gap matters.
Pooled rodent data show a real motor benefit at two weeks. The one study that watched for six weeks found it did not last. No human trial exists.
Three preclinical studies find TUDCA cuts trypsin activation and lung inflammation in pancreatitis. Every one gave it before the injury, not after.
Five studies find TUDCA protects hair cells from cisplatin, gentamicin and a genetic deafness mutation. All are in rodents, at doses no capsule delivers.
TUDCA preserved vision in diabetic mice, but only when started early. The human data measure bile acids in blood and give nobody TUDCA. What that means.
TUDCA improves blood glucose in mouse models of type 1 diabetes, and the mechanism is more interesting than it first appears. Here is what the beta-cell research found, including the part that is not about making more insulin.
Progressive MS is one of the very few conditions where TUDCA has been through a double-blind, placebo-controlled human trial. Here is what that trial was designed to answer, what it found, and the large question it deliberately left open.
TUDCA has been given to human patients in registered amyloidosis trials, paired with prescription doxycycline. This is the clearest case of TUDCA’s chaperone activity being tested in people, and also the clearest case of why it is not a supplement protocol.
Twenty days of TUDCA increased muscle mass and restored fibre size in 18-month-old mice. Combined with the human insulin-sensitivity trial, it is the most interesting muscle evidence TUDCA has. Here is how far it goes.
A bile acid cut infarct size roughly in half in a rat stroke model. That was 2002. Two decades later there is still no human stroke trial. Here is what the research showed and why the gap matters.
Endoplasmic reticulum stress drives cardiac hypertrophy and fibrosis, and TUDCA reduced both in a mouse pressure-overload model. What that animal evidence does and does not say about human heart health.
TUDCA reached a human Alzheimer’s trial as half of a combination drug. The clinical endpoints missed. The biomarker results were more interesting. An honest read of where this research stands.