Gluten and Brain Function: The Connection to Behavioral Changes

Gluten and Brain Function: The Connection to Behavioral Changes

The connection between gluten and brain function represents a complex interplay between various metabolic, immunologic, and endocrine processes. This interplay leads to a direct connection between gluten and behavioral changes.

There are several mechanisms that connect gluten and brain function, which can interfere with normal brain function:

Gluteomorphins or gliadorphins
Digestion of gluten results in the formation of small protein fragments known as gluteomorphins or gliadorphins. These fragments behave as morphine-like narcotics. Because individuals with gluten intolerance often have a more porous small intestine, these fragments are absorbed more rapidly and cause extreme fatigue and disruption of normal brain function. Traditionally, gluteomorphins or gliadomorphins are linked to the development of chronic fatigue, autism, and dyslexia.

Another mechanism of affecting gluten and brain function is based on the ability of gluten to trigger specific inflammatory and autoimmune processes. In susceptible individuals, when their immune cells are exposed to gluten, this results in the production of various pro-inflammatory (unhealthy) molecules known as cytokines. Cytokines affect the normal work of nerve cells and can change the blood flow in specific areas of the brain. Both processes disrupt the normal function of the brain and cause bipolar disorder and attention deficit.

Antibodies against gliadin and transglutaminase
An antibody is a protein that your immune system uses to neutralize foreign materials such as bacteria and viruses. Recently, it has been noted that antibodies against gliadin (protein present in wheat) and tissue transglutaminase (tTG), are frequently found in patients with gluten intolerance and celiac disease. These can cross-react with specific molecules in the brain and activate a cascade of biochemical events in human nerve cells causing deviations in normal brain chemistry.

As gluten is not digestible by humans, our enzymes can only break gluten apart into large fragments. Left on their own, these large gluten fragments wouldn’t cause any problems. They’d be acted upon by tTG and excreted along with the other unusable parts of the food we eat. But in genetically susceptible individuals, in combination with certain environmental factors, the interaction of these gluten fragments with anti-tTG antibodies launches an immunological chain reaction.

Yeast overgrowth
Gluten intolerance and celiac disease disrupt the composition of normal gut microflora which frequently results in the intestinal overgrowth of Candida albicans (yeast). Candida overgrowth is associated with a massive histamine release, causing allergic reactions and increased permeability of the blood brain barrier. The blood brain barrier prevents harmful materials from the blood to enter the brain.

Furthermore, the byproducts of metabolizing yeast (for example, ammonia) penetrate into the blood circulation and have a detrimental effect on the brain function causing fatigue, depression, and mood swings.

Endocrine link
The endocrine system is the collection of glands that produce hormones that regulate metabolism, growth and development, tissue function, sexual function, reproduction, sleep, and mood, among other things. It is made up of the pituitary gland, thyroid gland, parathyroid glands, adrenal glands, pancreas, ovaries (in females) and testicles (in males). The link between gluten and the endocrine system is based on the ability of gluten to change (either inhibit or stimulate) the production of certain hormones, including thyroid hormones, testosterone, prolactin, and estrogens, which in turn can modify brain activity causing undesirable mental effects.

the endocrine system

The Endocrine System

Neurological Disorders
Gluten intolerance is also associated with purely neurological entities the most popular being cerebellar ataxia and peripheral neuropathy as the second most common.

Ataxia is a neurological condition involving significant lack of muscular coordination. Cerebellar ataxia is caused by disrupted neurological activity in the cerebellum. When your doctor asks you to close your eyes and touch your nose with the tip of your index finger, she’s testing cerebellar coordination. Likewise, when a police officer asks a person to step out of the car and walk a straight line, heel-to-toe, she’s testing cerebellar coordination—which can be disrupted by excessive alcohol intake.

Cerebellar ataxia and gluten

Not every case of ataxia is caused by gluten. The association with gluten is a diagnosis of exclusion, when other alternative explanations have been considered and eliminated.

Peripheral neuropathy is a disorder of the long nerves in your body. For example, the sciatic nerve in your leg or the median nerve in your forearm. The most common symptoms are pain and numbness.

A 2008 review published in The Cerebellum suggests that gluten ataxia is a common cause of idiopathic sporadic ataxia—irregularly occurring ataxia of unknown origin. Anti-gluten antibodies are frequently found in higher proportions in such cases than in the general population. Also, peripheral neuropathy has been found in up to 49% of patients with celiac disease.

Importantly, studies have shown that a gluten-free diet has consistently improved symptoms of idiopathic sporadic ataxia.

One systematic study reported on 43 patients with gluten ataxia. Twenty-six patients in the treatment group began a gluten-free diet and after one year achieved significant improvement in neurological testing and overall clinical impressions. The study concluded that a gluten-free diet appeared to be an effective treatment for gluten ataxia. Additionally, it is widely accepted that patients with ataxia of unknown cause should be screened for gluten intolerance and celiac disease.

A diagnosis of gluten intolerance is typically based on a combination of laboratory test results including blood, salivary, or fecal antibodies against gliadin or its fragments, antibodies against tTG (transglutaminase), and the presence of genetic markers (HLA DQ2, DQ8) associated with celiac disease.

However, even in the absence of the laboratory markers, gluten intolerance may still be a problem. Therefore, the ultimate diagnosis is based on not eating gluten for 3-months followed by eating gluten again (gluten challenge). Reproduction of the underlying symptoms by the gluten challenge is obvious proof of gluten intolerance. If your symptoms come back, then it is best for you to be on a gluten-free diet. You don’t need test results to know you don’t feel well—your body will tell you.

While gastrointestinal problems are the common symptom associated with gluten, gluten can affect many systems of the body, including brain and behavioral changes. If you are experiencing unexplained behavioral changes, the connection between gluten and brain function should be explored.

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