Many people suffer from Celiac disease (CD) which is an inflammatory autoimmune disorder. The disease causes people who eat foods containing gluten to form antibodies to gluten which attack the lining of the intestine. This causes inflammation in the intestines and damages the villi, the hair-like structures on the lining of the small intestine. Nutrients from food are normally absorbed by the villi. If the villi are damaged, the person cannot absorb nutrients properly and ends up malnourished, no matter how much he or she eats.
Some researchers have hypothesized that celiac disease causes a systemic impact on the human body with wide spread inflammation. Support for this theory comes from clinical observations of extra-intestinal manifestations such as dermatologic, hepatic, osteologic, endocrine and neurological signs. Some studies have reported amnesia, ataxia, acalculia, epilepsy, chronic neuropathies, confusion and personality changes. There is notable impact when a gluten free diet is consumed.
The researchers in this study attempted to analyze the concept of brain fog and its association with celiac disease. Brain fog can include difficulty concentrating, problems with attentiveness, lapses in short-term memory, word-finding difficulties, temporary loss in mental acuity and creativity, and confusion or disorientation. The pilot study examined the relationships between cognitive function and mucosal healing in patients who had been recently diagnosed with CD, and who adhered to a gluten free diet (GFD) over the first year of treatment. The study demonstrated the presence of cognitive impairment that improved with therapy and was correlated with histological evidence of mucosal recovery and/or healing.
The level of cognitive impairment was described as similar to that in people with a blood alcohol level of 0.05 g/100 mL, which is the upper legal limit for driving in Australia. In people with undiagnosed CD, such cognitive deficits might result in impaired performance in driving and at work.
The researchers attribute three reasons why cognition may be impaired in patients with untreated CD.
1. Nutrient deficiencies involving, for example, iron, vitamin D and folate have been associated with cognitive impairment.As part of the malabsorption that might occur in patients with CD, such micronutrient deficiencies do occur. In this study however, changes in iron levels were not associated with cognitive performance, and the persisting low levels of vitamin D in six participants argues against a link to the cognitive improvement found over the duration of the study.
2. Cognitive impairment in patients with untreated CD may be due to the high levels of circulating cytokines associated with systemic inflammation. Elevated concentrations of circulating cytokines have been associated with changes in behavior, mood and cognition.] The brain possesses receptors for circulating cytokines, whilst cytokine activation of neurons and subsequent central signalling may also be important.
3. Cognitive improvement may be related to reduced exposure to gluten per se. Animal studies have shown dietary gluten may reduce brain tryptophan concentrations. Since tryptophan is the precursor of the neurotransmitter, serotonin, it has been speculated that gluten may impair cognitive function by lowering brain serotonin levels. Alternatively, opioid peptides derived from partially digested gluten, so-called ‘exorphins’, can have several effects on higher brain function in rodents.
The overall findings of this study demonstrated that improvements in cognition in CD are significantly correlated with the extent of intestinal healing. The researchers highlight the fact that significant correlations between disease activity measures and cognitive function were obtained with a sample of just 11 participants, underscoring the magnitude of the effect sizes.
I. T. Lichtwark, E. D. Newnham, S. R. Robinson, S. J. Shepherd, P. Hosking, P. R. Gibson and G. W. Yelland. Cognitive impairment in coeliac disease improves on a gluten-free diet and correlates with histological and serological indices of disease severity. Issue Alimentary Pharmacology & Therapeutics Volume 40, Issue 2, pages 160–170, July 2014