Scientific Articles

Related Articles to support SecondBrain

Supporting Documents

Brain Stimulation Can Alter Immune Response by Targeting Vagus Nerve – Click Here

The Vagus Nerve at the Interface of the Microbiota-Gut-Brain Axis – Click Here

Bacteria in the gut may alter aging process – Click Here

Natural killer cells, T cells, and neutrophils are recruited upon SDF-1 secretion – Click HereAnti-inflammatory reflex action of splanchnic sympathetic nerves is distributed across abdominal organs – Click Here

Role of the Microbiota in Immunity and inflammation – Click Here

Linking the Human Gut Microbiome to Inflammatory Cytokine Production Capacity – Click here

Bioelectric neuromodulation for gastrointestinal disorders: effectiveness and mechanisms – Click Here

The Microbiome-Gut-Brain Axis in Health and Disease – Click Here

Clinical implications of the microbiome in urinary tract diseases – Click Here

A review of 10 years of human microbiome research activities at the US National Institutes of Health, Fiscal Years 2007-2016 – Click Here

The Urinary Tract Microbiome in Health and Disease – Click Here

Related Supporting Scientific Articles

Bioelectric neuromodulation for gastrointestinal disorders: effectiveness and mechanisms – Click Here

Bioelectric regulation of innate immune system function in regenerating and intact Xenopus laevis. – Click Here

Bioelectric neuromodulation for gastrointestinal disorders: effectiveness and mechanisms – Click Here

Sonic hedgehog regulates the proliferation, differentiation, and migration of enteric neural crest cells in gut – Click Here

Wound healing treatment by high frequency ultrasound, microcurrent, and combined therapy modifies the immune response in rats – Click Here

Optimal electrode position for abdominal functional electrical stimulation – Click Here

Bioelectric neuromodulation for gastrointestinal disorders: effectiveness and mechanisms – Click here

Mechanisms and potential applications of intestinal electrical stimulation. – Click here

Think Twice:  How the Gut’s “Second Brain” Influences Mood and Well Being 

The Vagus Nerve at the Interface of the Microbiota-Gut-Brain Axis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5808284/

Electro-acupuncture attenuates inflammatory responses and intraabdominal pressure in septic patients

A randomized controlled trial

Abstract

Background:

A pathological increase in intraabdominal pressure (IAP) and inflammatory responses have negative effects on splanchnic, respiratory, cardiovascular, renal, and neurological function in septic patients with intestinal dysfunction. Electro-acupuncture (EA) has been evidenced to have a bidirectional neuron-endocrine-immune system regulating effect in patients with intestinal dysfunction. The purpose of current study was to evaluate the effects of EA at “Zusanli” (ST36) and “Shangjuxu” (ST37) on inflammatory responses and IAP in septic patients with intestinal dysfunction manifested syndrome of obstruction of the bowels Qi.

Methods:

Eighty-two septic patients with intestinal dysfunction manifested syndrome of obstruction of the bowels Qi were randomly assigned to control group (n = 41) and EA group (n = 41). Patients in control group were given conventional therapies including fluid resuscitation, antiinfection, vasoactive agents, mechanical ventilation (MV), supply of enteral nutrition, and glutamine as soon as possible. In addition to conventional therapies, patients in EA group underwent 20-minutes of EA at ST36-ST37 twice a day for 5 days. At baseline, posttreatment 1, 3, and 7 days, serum levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and IAP levels, were measured, respectively. And days on MV, length of stay in intensive care unit (ICU) and 28 days mortality were recorded.

Results:

The serum levels of TNF-α and IL-1β and IAP levels at posttreatment 1, 3, and 7 days were lower significantly in the EA group compared with the control group (mean [SD]; 61.03 [20.39] vs 79.28 [20.69]; P < .005, mean [SD]; 35.34 [18.75] vs 66.53 [30.43]; P < .005 and mean [SD]; 20.32 [11.30] vs 32.99 [20.62]; P = .001, respectively, TNF-α. Mean [SD]; 14.11 [5.21] vs 16.72 [5.59]; P = .032, mean [SD]; 9.02 [3.62] vs 12.10 [4.13]; P = .001 and mean [SD]; 5.11 [1.79] vs 8.19 [2.99]; P < .005, respectively, IL-1β. Mean [SD]; 14.83 [5.58] vs 17.55 [3.37]; P = .009, mean [SD]; 11.20 [2.57] vs 14.85 [3.01]; P < .005 and mean [SD]; 8.62 [2.55] vs 11.25 [2.72]; P < .005, respectively, IAP). There were no significant differences in the duration of MV, length of stay in ICU, and 28d mortality between the groups.

Conclusion:

EA at ST36-ST37 attenuated inflammatory responses through reduction in serum levels of TNF-α and IL-1β and IAP in septic patients with intestinal dysfunction manifested syndrome of obstruction of the bowels Qi.

Gut Microbiota: A New Strategy to Study the Mechanism of Electroacupuncture and Moxibustion in Treating Ulcerative Colitis

Acupuncture Regulating Gut Microbiota in Abdominal Obese Rats Induced by High-Fat Diet

Bioelectric neuromodulation for gastrointestinal disorders: effectiveness and mechanisms

Electroacupuncture accelerates gastric emptying in association with changes in vagal activity

Electroacupuncture targeting the gut–brain axis to modulate neurocognitive determinants of eating behavior—toward a proof of concept in the obese minipig model

 

The Vagus Nerve May Carry Serotonin Along the Gut-Brain Axis

The effect of acupuncture on tumor growth and gut microbiota in mice inoculated with osteosarcoma cells

 
 

Neuromodulatory processes of the brain-gut axis

 
 

Electroceuticals: The Wave of the Future Is Now

 

The Serotonin Signaling System: From Basic Understanding 

Electrical stimulation alleviates depressive-like behaviors of rats: investigation of brain targets and potential mechanisms

Vagus Nerve as Modulator of the Brain–Gut Axis in Psychiatric and Inflammatory Disorders

 
The gut-brain-axis and the heart

Abstract

Background: The normal physiology and pathophysiology of gut-brain, heart-axis needs further evaluation. There is evidence that brain-gut axis can influencene uropsychiatric and cardiometabolic dysfunction resulting in to obesity, insulin resistance, metabolic syndrome and cardiovascular diseases (CVDs) which is of great public health interest.
Methods: Internet search via Medline and Pub-Med and discussion with colleagues.
Results: In experimental as well as clinical studies, it has been observed, that chronic gut inflammation, predispose systemic inflammation resulting into neuropsychiatric dysfunction causing chronic anxiety disorders and memory dysfunction as well as cardiovascular dysfunction which are important risk factors of cardiometabolic diseases (CMDs). The basis of the gut-brain axis comprises; neuroanatomy and the pathophysiology represented by the vagal and spinal afferent neurons, the neuroendocrine-hypothalamic-pituitary-adrenal (HPA) axis, via the gut hormones, immune routes via the multiple cytokines, microbially-derived neurotransmitters, and finally the gate keepers of the intestinal and brain barriers. A failure in the interactions and mutual adaptations predispose a number of inflammatory, autoimmune, neurodegenerative, metabolic, mood, behavioral, cognitive, autism-spectrum, stress and pain-related disorders. Nutritional approaches; antioxidant status, microbiome manipulations, enteric and brain barrier reinforcement and sensing and trafficking modulation might improve pathophysiology of gut-brain-heart axis leading to improvement in the physical and mental health outcomes. Gut flora metabolites from foods such as choline obtained from red meat and lecithin from egg have been reported to predispose CVDs by increasing trimethyl amine N-oxide (TAMO). Recent evidence shows that TMAO, enhances both; atherosclerosis in animal models and cardiovascular risks in clinical studies. There is a need to study the impact of targeted inhibition of the first step in TMAO generation, commensal microbial TMA production, on diet-induced atherosclerosis. A structural analog of choline, 3,3-dimethyl-1-butanol (DMB), is shown to non-lethally inhibit TMA formation from cultured microbes, to inhibit distinct microbial TMA lyases, and to both inhibit TMA production from physiologic polymicrobial cultures (e.g., intestinal contents, human feces) and reduce TMAO levels in mice fed a high-choline or L-carnitine diet. Other preventive measures early in life or corrective measures such as use of psychobiotics, fecal microbiota transplantation, and flavonoids are may be protective. A high w-6/w-3 ratio in the diet in conjunction with antioxidant flavonoids as well as probiotics in the diet in a milieu of higher BDNF levels in the gut and the brain could be important in healthy gut-brain-heart-axis for health promotion.
Conclusion: Recent evidence indicates the existence of gut-brain-axis which can interact with gut microbiota dependent on food ingestion. The gut-brain-axis can predispose systemic inflammation, more so in tissues with underlying deficiency of w-3 fatty acids and antioxidants. The pathophysiological mechanisms of gut-brain-heart connection, appear to be bidirectional, resulting into neuropsychiatric diseases as well as CMDs. It is proposed that the cause of CMDs may be; existence of a gut-brain-heart-axis similar to gut-brain-axis which could be important in prevention of these diseases.

Gut Microbiota in Cardiovascular Health and Disease – Dr. Wilson Tang et al. Cleveland Clinic Heart Failure Team 

Abstract

Significant interest in recent years has focused on gut microbiota-host interaction because accumulating evidence has revealed that intestinal microbiota play an important role in human health and disease, including cardiovascular diseases. Changes in the composition of gut microbiota associated with disease, referred to as dysbiosis, have been linked to pathologies such as atherosclerosis, hypertension, heart failure, chronic kidney disease, obesity and type 2 diabetes mellitus. In addition to alterations in gut microbiota composition, the metabolic potential of gut microbiota has been identified as a contributing factor in the development of diseases. Recent studies revealed that gut microbiota can elicit a variety of effects on the host. Indeed, the gut microbiome functions like an endocrine organ, generating bioactive metabolites, that can impact host physiology. Microbiota interact with the host through a number of pathways, including the trimethylamine (TMA)/ trimethylamine N-oxide (TMAO) pathway, short-chain fatty acids pathway, and primary and secondary bile acids pathways. In addition to these “metabolism dependent” pathways, metabolism independent processes are suggested to also potentially contribute to CVD pathogenesis. For example, heart failure associated splanchnic circulation congestion, bowel wall edema and impaired intestinal barrier function are thought to result in bacterial translocation, the presence of bacterial products in the systemic circulation and heightened inflammatory state. These are believed to also contribute to further progression of heart failure and atherosclerosis. The purpose of the current review is to highlight the complex interplay between microbiota, their metabolites and the development and progression of cardiovascular diseases. We will also discuss the roles of gut microbiota in normal physiology and the potential of modulating intestinal microbial inhabitants as novel therapeutic targets.