Chronic intestinal inflammation and its health consequences

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Chronic intestinal inflammation and its health consequences

We have already talked in another article about the most common causes (and others not so much) of inflammation in the intestine. We have to know now that, a chronic intestinal inflammation or consistently, it predisposes you to a host of chronic diseases, ranging from Inflammatory Bowel Disease (IBD) and colon cancer to autism and Alzheimer’s disease.

12 Health Effects Caused by Chronic Intestinal Inflammation

stop the chronic intestinal inflammation dry is essential for both the prevention and treatment of chronic diseases. These are 12 consequences of having a chronically inflamed intestine.

Allergies caused by chronic intestinal inflammation

Intestinal inflammation may be at the root of seasonal allergies. An imbalance between beneficial and harmful gut microbes increases the release of pro-inflammatory cytokines in the gut. These cytokines stimulate the activity of mast cells, basophils, and eosinophils, which induce allergic inflammation. Intestinal inflammation associated with dysbiosis is related to atopic dermatitis and food allergies.

A healthy gut, on the other hand, inhibits allergic sensitization through the release of anti-inflammatory short-term fatty acids (SCFAs) and regulatory T cells that balance the immune system.

Autoimmune diseases

Chronic intestinal inflammation is a preceding factor in the development of autoimmune diseases. People with type 1 diabetes show higher circulating levels of Lipopolysaccharide (LPS) compared to people without diabetes.

Zonulin, a protein released in the gut when the gut barrier is compromised, is higher in people with autoimmune diseases compared to healthy controls, denoting the role of leaky gut in autoimmune diseases. Gluten sensitivity and chronic stress are two triggers of intestinal inflammation that often precede autoimmunity.


Inflammatory alterations in the oral and intestinal microbiota, including overgrowth of cariogenic bacteria Porphyromonas gingivalis and decreased commensal bacteria are associated with the progression of arthritis.

Dysbiosis and leaky gut induce a systemic inflammatory response, triggering the release of cytokines that cause musculoskeletal degeneration. In contrast, commensal anti-inflammatory bacteria and SCFAs have been found to relieve arthritis and protect against bone loss.

heart disease

Cardiovascular disease (CVD) is the leading cause of death worldwide, and medication and surgery are the mainstays of conventional medical treatment. However, mounting evidence of the link between gut and heart health suggests that gut-targeted therapies may be the treatment of the future for CVD.

Multiple inflammatory processes within the gut affect the course of CVD. (74) Dysbiosis contributes to CVD through the release of LPS and peptidoglycan (PG), components of the inflammatory cell wall of gram-negative and gram-positive bacteria that promote atherosclerotic plaque formation and hypertension. Dysbiosis also affects the metabolism of bile acids, altering the excretion of blood lipids such as cholesterol and triglycerides.

Gastrointestinal disorders

Inflammatory Bowel Disease (IBD)

Intestinal inflammation is a key feature of IBD, including ulcerative colitis and Crohn’s disease. A number of deleterious intestinal changes, including dysbiosis and increased intestinal permeability, contribute to the progression of IBD.

Irritable Bowel Syndrome (IBS)

Until recently, the role of intestinal inflammation in IBS was unclear. However, since then, research has clarified the role of mast cells, immune cells that release irritating compounds such as histamine, and persistent low-grade inflammation in the pathogenesis of IBS.

In people with diarrhea-predominant IBS or mixed IBS, autoimmunity may also play a role in intestinal inflammation. In these forms of IBS, a previous episode of food poisoning can lead to the production of autoantibodies that damage the gastrointestinal tract.

colorectal cancer

Colorectal cancer is the fourth most common cancer in the United States in both men and women, and the third leading cause of cancer-related deaths in the United States. Research suggests that pre-existing gastrointestinal inflammation precedes the development of colorectal cancer. Several inflammatory triggers of colorectal cancer have been identified, including intestinal pathogens, low levels of butyrate-producing bacteria, and the processed and refined Western diet.


Diverticulitis, an irritation of the lining of the intestines, is triggered by intestinal inflammation. It is characterized by dysbiosis in the colon and elevated fecal calprotectin, a protein released by white blood cells when there is active inflammation in the GI tract.

Depression and anxiety

New research indicates that activation of the immune system plays a central role in the development of depression and anxiety. The human gut houses approximately 70 percent of the immune system, so it’s no surprise that gut inflammation significantly affects mental health.

The gut-brain axis, a bidirectional signaling network between the enteric nervous system of the gut and the central nervous system, mediates the relationship between gut inflammation and mental health. The inflammatory stimuli in the gut they send signals along this axis to the brain, inducing neuroinflammation and altering neurotransmitter production. The consequence of these biochemical changes is altered brain activity, including depression and anxiety.

neurodegenerative disease

The gut-brain axis also plays a fundamental role in neurodegenerative diseases. Intestinal inflammation is recognized as a “silent driver” of Parkinson’s disease, with inflammation preceding the onset of symptoms by up to two decades. An inflammatory response derived from the gut has also been found to precipitate the deposition of amyloid-beta plaques, which contribute to neuronal degeneration and cognitive dysfunction in Alzheimer’s disease.

neurodevelopmental disorders

Neurodevelopmental disorders are exploding in prevalence around the world; the prevalence of autism has risen to one in 59 children while, as of 2016, 11 percent of children and adolescents have been diagnosed with attention deficit hyperactivity disorder (ADHD) or attention deficit disorder.

Pediatric acute-onset neuropsychiatric syndrome (PANS) and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) are emerging neurodevelopmental disorders characterized by the sudden onset of tics and obsessive-compulsive disorder.

Research indicates that dysbiosis and intestinal inflammation are contributing factors to each of these disorders. Children with ADHD show decreased gut microbial alpha diversity, a measure of the number of bacterial species in the gut; greater diversity is generally associated with better health outcomes.

Children on the autism spectrum and those with PANS/PANDAS also show dysbiosis. These inflammatory changes alter the crosstalk between the gut and the brain, ultimately inducing neurobehavioral deficits.


Several lines of evidence indicate that the chronic intestinal inflammation promotes osteoporosis by altering the balance between cells that build bone and those that resorb bone, leading to a net loss of bone mass. Intestinal inflammation also decreases the absorption of critical bone-building nutrients, such as vitamin D, calcium, and magnesium.

skin conditions

Like the gut-brain axis, the gut-skin axis is a network of signaling molecules that connects the gut and its microbes to the skin. Inflammatory changes in the gut, including dysbiosis and increased intestinal permeability, are linked to a spectrum of skin conditions including acne, psoriasis, rosacea, and eczema.

Metabolic syndrome, type 2 diabetes and obesity

Metabolic syndrome, type 2 diabetes (T2D), obesity, and intestinal inflammation form a vicious cycle: blood sugar dysregulation and excess body fat promote intestinal inflammation, while intestinal inflammation exacerbates metabolic dysfunction .

Gut dysbiosis and circulating LPS induce insulin and leptin resistance, key features of the metabolic syndrome, T2D, and obesity. Acellular carbohydrates and exposure to obesogenic environmental toxins, including BPA and phthalates, alter the gut microbiota. These microbial changes incite intestinal inflammation and influence the progression of metabolic dysfunction.

Non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD), a buildup of excess fat in the liver in people who consume little or no alcohol, is closely linked to metabolic syndrome, T2D, and obesity.

A compromised gut microbiota appears to drive inflammation in NAFLD, while beneficial gut-targeted therapies, such as probiotics, alleviate inflammation and liver dysfunction.

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