The autoimmune aspect of hair loss

A fascinating study was just published in Medicinski arhiv (Medical Archives, Journal of the Academy of Medical Sciences of Bosnia and Herzegovina) that illuminates the type of autoimmune dysfunction involved in alopecia areata, a common cause of hair loss. The authors state:

Alopecia areata (AA) is a heterogeneous disease characterized by nonscarring hair loss on the scalp or other parts of the body. A wide range of clinical presentations can occur-from a single patch of hair loss (alopecia unilocularis, AUl), multiple patches (alopecia multilocularis, AM) to complete loss of hair on the scalp (alopecia totalis, AT) or the entire body (alopecia universalis, AU). The cause of AA is unknown although most evidence supports the hypothesis that AA is a T-cell mediated autoimmune disease of the hair follicle and that cytokines play an important role.”

The authors set out to evaluate serum concentrations of interferon-gamma (IFN-g, a major proinflammatory cytokine) in 60 patients with AA in comparison to 20 healthy subjects. They also investigated for an association between IFN-g and the clinical type of AA and duration of the disease. What did their data show?

“The serum concentration of IFN-g in patients with AA was significantly higher than that in the control group. Significantly elevated serum IFN-g were noticed in patients with AU type, especially those suffering from AT, compared with both patients with AUI and patients with AM clinical type. There was no significant difference in serum IFN-g concentration between patients with AUI and AM group, as well as between patients with AT and AU. No correlations were found between duration of disease and the serum levels of IFN-g.”

This clearly shows the autoimmune basis of hair loss in general and the role of IFN-g in particular. Autoimmune conditions require a functional approach that uses up-to-date methods to objectively define the underlying causal factors such as IFN-g for treatments that are targeted, physiological and rational. The authors conclude:

Our findings confirm previously published data that the Th1 type cytokine IFN-g is elevated in the serum of AA patients.

Gluten-free diet can improve depression and behavioral problems in adolescents

BMC PsychiatryAs the authors of this study published in the journal BMC Psychiatry observe:

“Coeliac disease in adolescents has been associated with an increased prevalence of depressive and disruptive behavioural disorders, particularly in the phase before diet treatment.”

We are equally concerned with the ‘non-celiac’ aspects of gluten sensitivity. Gluten related inflammation in the brain can manifest as a host of cognitive, emotional and neurodegenerative disorders in the absence of intestinal manifestations. This is often referred to as “silent celiac disease”:

“Coeliac disease is an under-diagnosed autoimmune type of gastrointestinal disorder resulting from gluten ingestion in genetically susceptible individuals. Non-specific symptoms such as fatigue and dyspepsia are common, but the disease may also be clinically silent.”

They further note that:

“”Depressive symptoms and disorders are common among adult patients with coeliac disease, and depressive and disruptive behavioural disorders are highly common also among adolescents, particularly in the phase before diet treatment. Recently 73% of patients with untreated coeliac disease – but only 7% of patients adhering to a gluten-free diet – were reported to have cerebral blood flow abnormalities similar to those among patients with depressive disorders.”

Their data revealed abnormalities in tryptophan assimilation (tryptophan is the amino acid precursor to serotonin) and prolactin levels in adolescents with celiac disease and depression prior to treatment. Consequently…

A significant decrease in psychiatric symptoms was found at 3 months on a gluten-free diet compared to patients’ baseline condition, coinciding with significantly decreased coeliac disease activity…”

They also make a fascinating observation that links gluten sensitivity, inflammation, and the serotonergic aspect of depression unrelated to malabsorption:

“…increased production of interferon-γ (IFN-γ), known to be the predominant cytokine produced by gluten-specific T-cells in active coeliac disease, can suppress serotonin function both directly and indirectly by enhancing tryptophan and serotonin turnover…even without malabsorption.”

To diagnose gluten sensitivity in the absence of celiac disease the gluten gene sensitivity test is the most reliable method for a number of reasons.