For years allopathic medicine has tried to discredit the validity of “leaky gut syndrome” with many medical practitioners outright claiming that the condition doesn’t exist.
However cutting edge scientific research shows that “leaky gut syndrome” or increased intestinal permeability, which is the correct terminology for “leaky gut” may well play a role in the pathophysiology of a number of serious health problems including major depression, chronic fatigue syndrome/ME, auto-immune diseases, gum disease and even cardiovascular disease.
Scientific research into the pathophysiology of depression in recent years has been largely focused on exploring the inflammatory and oxidative stress connection to the development of major depressive disorders and several studies have unearthed some very interesting findings.
At this current point in time, the “monoamine hypothesis” of depression is looking very outdated and severely lacking in the overall understanding of the biomechanics of depressive disorders, with current scientific research indicating that major depression may actually be the result of abnormalities in inflammatory, immune and oxidative stress pathways.
We are also seeing more and more research being done on the so-called “gut-brain-axis” and the vital importance of the gut microbiome in keeping us healthy and mentally well.
I truly feel that gastrointestinal and gut flora issues(dysbiosis, IBS, GERD, candida overgrowth, leaky gut etc) are an under-investigated factor for individuals with major depression, anxiety and stress disorders, many of whom exhibit a high degree of gastrointestinal complaints that often continue to remain unaddressed.
Major Depression & “Leaky Gut Syndrome”
One study from 2008 examined whether an increased gastrointestinal permeability(leaky gut) with an increased translocation of LPS from gram-negative bacteria may play a role in the pathophysiology of major depressive disorder.
“There is now evidence that major depression (MDD) is accompanied by an activation of the inflammatory response system (IRS) and that pro-inflammatory cytokines and lipopolysacharide (LPS) may induce depressive symptoms.”
The present study examines the serum concentrations of IgM and IgA against LPS of the gram-negative enterobacteria, Hafnia Alvei, Pseudomonas Aeruginosa, Morganella Morganii, Pseudomonas Putida, Citrobacter Koseri, and Klebsielle Pneumoniae in MDD patients and normal controls.
We found that the prevalences and median values for serum IgM and IgA against LPS of enterobacteria are significantly greater in patients with MDD than in normal volunteers. These differences are significant to the extent that a significant diagnostic performance is obtained, i.e. the area under the ROC curve is 90.1%.
The symptom profiles of increased IgM and IgA levels are fatigue, autonomic and gastrointestinal symptoms and a subjective feeling of infection.
“The results show that intestinal mucosal dysfunction characterized by an increased translocation of gram-negative bacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression.
It is suggested that the increased LPS translocation may mount an immune response and thus IRS activation in some patients with MDD and may induce specific “sickness behavior” symptoms. It is suggested that patients with MDD should be checked for leaky gut by means of the IgM and IgA panel used in the present study and accordingly, should be treated for leaky gut.” 
Another study from 2012 once again confirmed that “leaky gut” and increased bacterial translocation with immune responses to the LPS of commensal bacteria may play a role in the pathophysiology of depression, particularly chronic depression.
Bacterial translocation may a) occur secondary to systemic inflammation in depression and intensify and perpetuate the primary inflammatory response once the commensals are translocated; or b) be a primary trigger factor associated with the onset of depression in some vulnerable individuals.
The findings suggest that “translocated” gut commensal bacteria activate immune cells to elicit IgA and IgM responses and that this phenomenon may play a role in the pathophysiology of (chronic) depression by causing progressive amplifications of immune pathways. 
1. The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression.
2. Increased IgA and IgM responses against gut commensals in chronic depression: further evidence for increased bacterial translocation or leaky gut.
The information in this article has not been evaluated by the FDA and should not be used to diagnose, cure or treat any disease, implied or otherwise.