New research supports an emerging theory that a PH imbalance in our body causes unexpected panic attacks. Panic disorder is a syndrome characterized by spontaneous and recurrent episodes of incapacitating anxiety.
The condition typically emerges during adolescence or early adulthood and is often emotionally and physically debilitating.
Physical symptoms can include heart palpitations, sweating and/or chills, trouble breathing and dizziness, nausea and even chest pain.
Although significant progress in both diagnosis and treatment has been made with panic disorder, professionals are uncertain as to what triggers the panic symptoms.
However, there is new evidence that a pH imbalance disruption in the body, known as acidosis, can unexpectedly cause the panic attack.
In a new study, researchers at the University of Cincinnati (UC) have found that a particular receptor in the body — acid-sensing T cell death associated gene-8 (TDAG8) — may be associated with the physiological response in panic disorder.
The research, a collaboration between Jeffrey Strawn, M.D., and Renu Sah, Ph.D., appears online in advance of publication in the journal Brain, Behavior, and Immunity.
The TDAG8 receptor, a pH sensor, was first identified in immune cells of the body where it regulates inflammatory responses. Studies of animal models in Sah’s lab identified TDAG8 in immune cells of the brain, called microglia.
“Although we had reported the potential relevance of TDAG8 in panic physiology in the lab, we were uncertain whether the receptor would play a role in panic disorder. It was important for us to validate this in patients with this disorder,” says Sah.
To do this, the UC research team embarked on a basic science-clinical collaboration, seeking to understand the receptor’s expression in adolescents and young adults.
“We evaluated the role of this receptor in patients with panic disorder (including adolescents who were close to the onset of panic disorder).
We saw a relationship between this receptor and panic disorder symptoms, in addition to differences between patients with panic disorder and healthy individuals,” says Strawn.
The study evaluated blood samples of 15 individuals between the ages 15 to 44 with a diagnosis of panic disorder and 17 healthy control participants. Anxiety symptom severity was also assessed in the study.
The pilot study is the first to evaluate the relationship between the TDAG8 genetic expression among individuals with panic disorder as compared to people without the disorder.
“We found an association with TDAG8 and symptom severity, and we observed that there was a relationship between this receptor and treatment response in patients who had been treated with antidepressants.”
Strawn says the findings show a direct link between increased genetic expression and severity of panic disorder. Moreover, treatment for the disorder was associated with a lower genetic expression and raises the possibility that pharmacological therapy facilitates a “remission” of symptoms because of suppressed actions of TDAG8.
“It will be important for additional studies to further explain the functional relevance of TDAG8 and associated inflammatory processes as well as other acid sensors in patients with panic disorder to explore the role of TDAG8 with predicting treatment response,” he says.
Sah notes that further research could demonstrate whether altered TDAG8 is a result of a genetic variation or other factors.
She also says that in future studies, perhaps drugs targeting TDAG8 or associated inflammatory responses may be developed for panic disorder.
Source: University of Cincinnati