Medicine Finally Admits Leaky Gut Is A "real" Disease

[haidut]

I was not even aware that official medical guidelines consider leaky gut a "quack" diagnosis...

http://www.thedailybeast.com/articles/2 ... eases.html

 

[pboy]

at first thought it does seem ridiculous that leaky gut is the cause of all diseases...but when I think about it more...everything besides what you breath or soak in through skin...everything that eventually gets into or builds your body has to start in the gut...so it probably is hugely important

 

[Amazoniac]

Stress Induces Endotoxemia and Low-Grade Inflammation by Increasing Barrier Permeability

"Stressful stimuli activate the sympathetic nervous system (SNS) and hypothalamic–pituitary–adrenal (HPA)-axis. Activation of both systems increases the availability of water, minerals, and energy-rich substances in order to meet with the body’s metabolic demand (41, 42). The SNS responds instantly to physical and psychological stress by reallocating energy into different organs by neuronal regulation of heart rate, blood flow, release of catecholamines (adrenalin and noradrenalin) from the adrenal medulla (43), and stimulation of the renin–angiotensin–aldosterone system (44), involved in retention of water and sodium from the kidneys. In addition to the kidneys, water and sodium reabsorption can also be achieved at the level of the intestine. The intestinal wall is innervated by adrenergic sympathetic nerve fibers that upon stimulation increase water and sodium absorption (45, 46), which is paralleled by increases in intestinal permeability."

"Besides inflammatory cytokines, prostaglandins synthesized via the cyclooxygenase system play a central role in inflammation and HPA-axis activation. Zimomra et al. (65) demonstrated that in rats the initial activation of the HPA-axis by LPS is mediated by prostaglandins, like PGE2, while inflammatory cytokines maintain corticosterone levels at later time-points. In this study, it was suggested that prostaglandins stimulated corticosterone release in a direct manner, since the peak in circulating corticosterone levels was observed long before the peak in circulating ACTH. This idea was confirmed by a study in rodents, showing that PGE2 directly stimulated the release of glucocorticoids from the adrenal gland (66). In human adrenal cells expressing TLR2 and TLR4, LPS stimulation resulted in the release of cortisol. This effect was mediated by PGE2, since inhibition of cyclooxygenase-2 attenuated cortisol release (67)."

"Chronic psychological stress is known to dysregulate the immune system. These alterations are accompanied by low-grade inflammation, delayed wound healing, and increased susceptibility to infectious diseases (79). Chronic stress leads to hypercortisolemia (77), long-term permeability of barriers, endotoxemia, and low-grade inflammation (our hypothesis and theory). Normally, the release of glucocorticoids puts a limit on the maximum activity of the immune system; however, chronic HPA-axis stimulation can result in glucocorticoid resistance at the level of the immune system, making it insensitive to its inhibitory and modulatory actions (2). This process is observed in several conditions (including conditions related to psychosocial stress), whereby immune cells from patients are less responsive to the inhibitory actions of glucocorticoids on cytokine release and cell proliferation after stimulation in vitro (80–83). In addition, chronic stress induces a shift in the production of type 1 cytokines toward type 2 cytokine production. It can be deducted that by this mechanism, the part of the immune system involved in the clearance of extracellular bacteria and bacterial toxins (the type 2 response) is prevented from being suppressed and protection against ongoing microbial infiltration (endotoxemia) is guaranteed, while the type 1 response, involved in clearance of intracellular pathogens (like viruses) is inhibited (71, 84)."

"exposure to social stress changed the composition of the gut-microbiota in mice (95, 96) and prenatal stress altered the microbiome in rhesus monkeys by reducing the overall numbers of the Gram-positive Bifidobacteria and Lactobacilli (97), indicating that chronic stress affected the composition of the gut microbiome. Stress influences gut motility, secretions, and mucin production, thereby altering the habitat of resident bacteria, promoting changes in the composition of the gut microbiome (98), and allowing the growth of pathogenic bacteria (99)."

"Patients suffering from NAFLD exhibited significantly higher serum endotoxin levels in contrast to healthy controls (14). Farhardi et al. (136) indicated that elevated plasma endotoxin levels in these patients were related to an impaired intestinal barrier function, because, only in the patient group, the intake of a permeability stressor (aspirin) increased the 0–24 h urinary excretion of sucralose (a marker of whole-gut permeability). Furthermore, augmented plasma LBP levels in concert with increased plasma levels of TNF-α were observed in obese NAFLD patients compared to healthy controls (137)."​