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Anxiety And Depression Linked To Stress Causing Gut Bacteria


Senior Member

Researchers exposed mice to early life stress by way of maternal separation. From age 3-days old to age 21-days old, the infant mice were separated from their mothers for three hours daily and then returned. The mice with complex gut bacteria that were separated from their mothers displayed more anxious and depressed behavioral characteristics, and also tested with abnormally high levels of the hormone corticosterone, a hormone that rises in the body in an attempt to calm anxieties.

The mice also showed increased disturbed gut function as shown by a disruption in acetylcholine, a neurotransmitter that has recently been thought to be the primary cause of depression.

According to Premysel Bercik, primary author of the study, neonatal stress increases stress and disturbed gut function. This changes the gut bacteria, which then interrupts the proper functioning of the brain...

sarah darwins

Senior Member
Cornwall, UK
Here's the abstract from Nature Communications (full paper is paywalled):


Early-life stress is a determinant of vulnerability to a variety of disorders that include dysfunction of the brain and gut. Here we exploit a model of early-life stress, maternal separation (MS) in mice, to investigate the role of the intestinal microbiota in the development of impaired gut function and altered behaviour later in life. Using germ-free and specific pathogen-free mice, we demonstrate that MS alters the hypothalamic–pituitary–adrenal axis and colonic cholinergic neural regulation in a microbiota-independent fashion. However, microbiota is required for the induction of anxiety-like behaviour and behavioural despair. Colonization of adult germ-free MS and control mice with the same microbiota produces distinct microbial profiles, which are associated with altered behaviour in MS, but not in control mice. These results indicate that MS-induced changes in host physiology lead to intestinal dysbiosis, which is a critical determinant of the abnormal behaviour that characterizes this model of early-life stress.

Link: http://www.nature.com/ncomms/2015/150728/ncomms8735/full/ncomms8735.html#author-information

There's some interesting stuff in here, and an interesting interview with the lead author, Premysel Bercik, here: http://www.gutmicrobiotaforhealth.com/dr-premysl-bercik-clinically-relevant-gut-brain-axis-8178 [looks like an interesting site for anyone wanting to know more about microbiome research], though I do wish Bercik and others would get on with a bit more human research. From the interview:

What’s your current understanding of 'normal' gut-brain communication?

We still don’t know how this gut-brain axis works and most of the data which is available is coming from animal models. It’s difficult to apply this directly to humans.

[Some clinical data will be available soon, but] what we know so far [is] that it’s bidirectional communication. We know that in the presence of bacteria, the behavior is different compared to germ-free mice. We know if we perturb the microbiota, we change the behavior and also [the] brain chemistry of these mice.

Now if I go back to clinical scenarios, there are at least some case reports of patients who receive antibiotics and they suddenly change their behavior. It was termed 'antibiotic-induced psychosis'. Interestingly, when you discontinue the antibiotics, the patients normalize. We also know that patients who have chronic GI disorders, mainly those related to gut inflammation, have psychiatric co-morbidities that I already mentioned: anxiety, depression. It also applies to patients with IBD [inflammatory bowel disease].

So what is normal, what is abnormal? I think it’s a dynamic relationship. And probably it’s the balance.

"It’s difficult to apply this directly to humans." Yeah, no kidding. They're mice.