Easier Vagal Nerve Stimulation Via the Ear
Vagal nerve stimulation is typically delivered via a stimulator in the chest wall.
Vagal nerve stimulation (VNS) is an FDA-approved treatment for seizures and treatment-resistant depression. It typically requires an operation to insert a stimulator in a patient’s chest wall that delivers electrical impulses to their left vagus nerve via electrodes placed on the patient’s neck. New research by Bashar W. Badran and colleagues may have identified a less invasive and less expensive way to stimulate the vagal nerve—via electrodes placed on the ear.
The researchers tested different parameters for vagal nerve stimulation via the ear on 15 healthy volunteers and found that this type of VNS was feasible, tolerable, and reasonably safe. Among the different parameters tested, a stimulation pulse width of 500 microseconds at 25Hz had the greatest effect on heart rate, slowing it by about 4.25 beats per minute compared to a sham treatment.
Next Badran and colleagues plan to study the effects of this type of VNS on brain activity using functional magnetic resonance imaging (fMRI).
Lithium Treatment Reduces Inflammation, Mania-Like Behavior in Rats
Patients with bipolar disorder often show increases in signs of inflammation, including levels of the proteins IL-2, IL-4, Il-6, IL-10 and tumor necrosis factor in their blood. Lithium is the most effective treatment for bipolar disorder, but it is not yet clear how it works. A recent study by researcher Joao de Quevado and colleagues determined that lithium can reduce the same inflammatory markers in rats.
Rats were treated with amphetamine to induce mania-like behavior, which was accompanied by increases in some of the same inflammatory markers in the blood and brain that are increased in people with bipolar disorder. Lithium treatment reduced both the manic behavior and levels of these inflammatory proteins in the rats.
The researchers concluded that lithium may treat mania by reducing inflammation.
Low Vitamin D Linked to Small Hippocampus & Schizophrenia
Low levels of vitamin D have been linked to schizophrenia in several studies. In one, infants with low vitamin D were more likely to develop schizophrenia in adulthood, but supplementation reduced this risk. A 2015 article by Venkataram Shivakumar and colleagues in the journal Psychiatry Research: Neuroimaging found that among patients with schizophrenia who were not currently taking (or in some cases, had never taken) antipsychotic medication, low levels of vitamin D were linked to smaller gray matter volume in the right hippocampus, an area involved in schizophrenia.
Vitamin D has neuroprotective effects and is important to normal brain development and function. Vitamin D is essential to the production of brain-derived neurotrophic factor (BDNF), a protein that is important for learning and memory, and vitamin D also reduces oxidative stress. BDNF deficiency and oxidative stress have both been linked to schizophrenia, and they both can cause abnormalities in the hippocampus.
Crack Cocaine Use and Early Life Stressors Shorten Telomeres
Telomeres are repeated DNA sequences that sit at the end of chromosomes and protect them during cell replication. Shorter telomeres are associated with aging and an increase in multiple medical and psychiatric disorders, while some healthy behaviors including exercising, eating healthy, meditating, and avoiding smoking can help maintain telomere length. Lithium treatment also increases telomere length.
Recent research by Mateus Levandowski and colleagues found that people who were dependent on crack cocaine had shorter telomeres than elderly women without psychiatric illnesses, particularly if the crack cocaine users had also experienced stress early in life, such as maltreatment or neglect.
Since short telomeres are associated with a variety of medical and psychiatric problems and premature aging, the combined effects of drug use and early life stressors are likely to have an adverse impact on people who have experienced both.
Thiamine (Vitamin B1) May Increase Effectiveness of Antidepressants
A new study suggests that the nutritional supplement vitamin B1, also known as thiamine, can improve symptoms of depression when taken with an antidepressant. Edith Holsboer-Trachsler and colleagues presented the research from their randomized, double-blind, placebo-controlled study at a recent scientific meeting. In a 12-week study, about 50 adults (averaging 35 years of age) with major depression were prescribed a selective-serotonin reuptake inhibitor (SSRI) antidepressant. In addition, half received thiamine supplements while the other half were given placebos. Starting at six weeks, those receiving thiamine with their antidepressant showed more improvement in their depressive symptoms than those receiving the antidepressant alone.
Thiamine is an essential nutrient for humans. It is found in foods such as yeast, pork, cereal grains, and certain vegetables. Thiamine deficiency has been linked to irritability and symptoms of depression, while thiamine supplementation can improve mood and reduce feelings of stress. No side effects were reported in the study.
Holsboer-Trachsler and colleagues hope that thiamine supplementation may help patients adhere to their antidepressant regimens by decreasing the time it takes until their moods begin to lift.
