Traditional risk factors associated with idiopathic intracranial hypertension (IIH) include obesity, weight gain, and female sex. The incidence of IIH is increasing and yet the underlying trigger and the fueling pathological mechanisms are still poorly understood.
Review of ophthalmology, neurology, general surgery, obesity, endocrinology, nutrition, and neurosurgery literature was made.
The facts that implicate sex and obesity in IIH and headache are examined. The role of fat distribution in IIH is questioned, and the concept of adipose tissue functioning as an endocrine organ driving IIH is discussed. The impact of androgen metabolism in IIH is reviewed as is the emerging role of glucagon-like-peptide-1 analogues in modulating intracranial pressure. This introduces the concept of developing targeted disease-modifying therapeutic strategies for IIH.
This review will discuss the possible role of the adipose/gut/brain metabolism axis in IIH and speculate how this may impact the pathogenesis of IIH and therapeutic opportunities.
This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Department of Metabolic Neurology (CH, SPM, HB, AJS), Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom; Birmingham Neuro-Ophthalmology Unit (SPM, AJS), Ophthalmology Department, University Hospitals Birmingham NHS Foundation Trust, Birmingham, United Kingdom; Centre for Endocrinology, Diabetes and Metabolism (HB, MWOR, AJS), Birmingham Health Partners, United Kingdom; and Department of Neurology (AJS), University Hospitals Birmingham NHS Foundation Trust, Birmingham, United Kingdom.
Address correspondence to Alexandra J. Sinclair, MRCP, PhD, Department of Metabolic Neurology, Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom; E-mail: email@example.com
A. J. Sinclair is funded by an NIHR Clinician Scientist Fellowship (NIHR-CS-011-028) and by the Medical Research Council, United Kingdom.
The authors report no conflicts of interest.
Joint first authors are C. Hornby and S. P. Mollan.