Effect of Vestibular Stimulation on Fat Consumption and Energy Expenditure as Assessed Using Indirect Calorimetry

There is a growing realization that obesity can, in many ways, be viewed as a neurological disease triggered by lifestyle factors. There is clear evidence that the central melanocortin system, which is centered in the arcuate nucleus of the hypothalamus, regulates a "set-point" for how much fat the body should have. It does so by altering appetite and metabolic rate so that deviations too far in either direction are strongly resisted. This set-point is determined by genetic, epigenetic and lifestyle factors. Thus, excessive exposure to dietary monosaccharides, such as glucose, and saturated fats, especially in childhood and adolescence, can damage the neurons of the arcuate nucleus and push the set-point up. This then can condemn sufferers to a lifetime of obesity, despite individual efforts to combat it using diet and/or exercise.

Establishing a method of tuning down the set-point for body fat thus has to be a goal if the current obesity pandemic is to be successfully combatted. A significant amount of animal work suggests that stimulating the vestibular system in the inner ear, by means of chronic centrifugation, actually does just that and causes a reduction in body fat. This is likely because chronic vestibular activation is taken by the brain to represent a state of increased physical activity, and in order to optimize homeostasis it would be appropriate for the body to have a leaner physique, by reducing unnecessary energy expenditure from carrying excess fat.

It is possible to stimulate the vestibular nerve in humans by applying a small electrical current to the skin behind the ears. This is an established technology that is believed to be safe, but only previously used for research purposes. The investigators found in a pilot study that recurrent stimulation of this kind for two or three hours a week over four months led to a statistically significant reduction in truncal fat in the active group as opposed to the control group who underwent sham stimulation.

Given the current, and increasing levels of global obesity, it is important to determine whether non-invasive electrical vestibular nerve stimulation (VeNS), otherwise known as galvanic vestibular stimulation (GVS), is a viable treatment option, since if it were this would be of significant scientific importance.

The investigators wish to use the technique of indirect calorimetry to explore this. This involves wearing a tight face mask to collect all inspired oxygen and expired carbon dioxide and using formulae to calculate total energy expenditure and the component of metabolism that is derived from fat as compared to carbohydrate.

Inclusion criteria

• Signed informed consent
• Body mass index (BMI) > 25 kg/m2
• 18-65 years of age inclusive on starting the study.
• Successfully completed the screening questionnaire.

Exclusion criteria

• History of vestibular dysfunction.
• History of bariatric surgery, fundoplication, gastric resection or major upper-abdominal surgery (acceptable surgeries include cholecystectomy, hysterectomy).
• History of skin breakdown, eczema or other dermatological condition (e.g. psoriasis) affecting the skin behind the ears, or of the head and neck.
• History of weight loss device implantation (e.g. VBloc Maestro or Abiliti).
• Positive response in Physical Activity Readiness Questionnaire.
• Currently taking medication for asthma or other breathing conditions.
• Untreated thyroid disorder (stable treatment for 3 months is acceptable).
• Other endocrinological causes of weight gain (e.g. Cushing's disease, Cushing's syndrome or acromegaly)
• Previous diagnosis of HIV infection or AIDS (HIV is known to cause a vestibular neuropathy which would prevent VeNS from working).
• History of cirrhosis, or liver, kidney or heart failure.
• Chronic pancreatitis.
• Treatment with prescription weight-loss drug therapy in the year before starting the study.
• Tobacco or marijuana smoking in the 6 months prior to study.
• Known genetic cause of obesity (e.g., Prader-Willi Syndrome).
• Diabetes mellitus (Types 1 & 2).
• Diagnosis of epilepsy or use of anti-epileptic medication within six months of starting the study (e.g. for the treatment of peripheral neuropathy)
• Chronic (more than a month of daily use) treatment with opioid analgesic drugs within the last year.
• Regular use (more than twice a month) of anti-histamine medication.
• Use of oral or intravenous corticosteroid medication within two years of starting the study.
• Use of the beta-blockers atenolol, metoprolol or propranolol within 3 months of starting the study.
• Current use of tricyclic antidepressant medication for whatever reason.
• Current alterations in treatment regimens of anti-depressant medication for whatever reason (other than tricyclic antidepressants) (Note: stable treatment regimen for prior six months acceptable).
• An active diagnosis of cancer.
• A previous myocardial infarction.
• A history of stroke or severe head injury (as defined by a head injury that required intensive care). (In case this damaged the neurological pathways involved in vestibular stimulation).
• Presence of permanently implanted battery powered medical device or stimulator (e.g., pacemaker, implanted defibrillator, deep brain stimulator, vagal nerve stimulator etc.).
• Psychiatric disorders (including untreated severe depression, schizophrenia, substance abuse, bulimia nervosa etc.)
• Current participant in a clinical trial for weight loss.