A recent study found that tart cherry juice helped soccer players recover after muscle-damaging exercise better than a placebo.
The 16 athletes in the study were randomly assigned to receive either a Montmorency tart cherry concentrate mixed with water twice a day for four days prior to and three days following exercise, or a drink with the same number of calories but less than 5% fruit content on the same schedule.
The semiprofessional male soccer players (aged 21 to 29) showed better performance on sprints, jumps, and agility tests; less inflammation; and less muscle soreness when taking tart cherry juice compared to the placebo drink.
Editor’s Note: Tart cherry juice is rich in polyphenols, chemicals found in plants with anti-oxidant effects. The juice also has melatonin-like effects, improving sleep in people with insomnia.
A recent study found that mice that ate more cinnamon got better and faster at learning. In the study, published in the Journal of Neuroimmune Pharmacology in 2016, separated mice into good learners and poor learners based on how easily they navigated a maze to find food. After the poor learners were fed cinnamon for a month, they could find the food more than twice as quickly as before.
The benefits of cinnamon come from sodium benzoate, a chemical produced as the body breaks down the cinnamon. Sodium benzoate enters the brain and allows the hippocampus to create new neurons.
Feeding cinnamon to the poor learning mice normalized their levels of receptors for the neurotransmitter GABA, closing the gap with good learners. Sodium benzoate also improved the structural integrity of some brain cells. Cinnamon also can help sensitize insulin receptors.
Doctors hope these findings may eventually contribute to treatment research on Alzheimer’s and Parkinson’s diseases.
Cinnamon should be consumed in moderate quantities because the Chinese variety most commonly found in North American supermarkets has high levels of coumarin, a compound that can be toxic to the liver when consumed in large quantities. Ceylon (Sri Lankan) cinnamon has lower levels of coumarin.
The atypical antipsychotic drug molindone was used to treat schizophrenia for decades before it was pulled from the market in 2010 for business reasons. Now Supernus Pharmaceuticals is studying whether a reformulation of the drug may be used to treat attention deficit hyperactivity disorder (ADHD) that is accompanied by impulsive aggression.
Supernus tested an extended-release form of the drug in 118 children aged 6–12 with ADHD and impulsive aggression. They received either placebo or between 12mg and 54mg per day of molindone for 39 days. Those children who received between 12mg and 36mg per day of molindone showed fewer symptoms of impulsive aggression that those who received placebo. Side effects included headache, sedation, and increased appetite. Clinical trials of molindone will continue.
The pharmaceutical company Supernus identifies older drugs that may be repurposed to treat other disorders. The company believes it may have found a new use for the discontinued antidepressant viloxazine, as a treatment for attention deficit hyperactivity disorder (ADHD).
Viloxazine is a selective norepinephrine reuptake inhibitor, or SNRI, that was approved in Europe but not in the US and was eventually removed from the market due to competition from other drugs. Its structure and mechanism of action resemble those of the ADHD treatment atomoxetine, so Supernus has begun trials of viloxazine for ADHD in adults.
At the 2015 meeting of the American Academy of Child and Adolescent Psychiatry, the researchers reported that compared to placebo, viloxazine was about twice as likely to reduce ADHD symptoms. Side effects included nausea, decreased appetite, headache, and insomnia. Supernus hopes to create an extended release form of the drug for both adults and children.
MTHFR is an enzyme needed for the body to break down vitamin B9, also known as folate or folic acid. It also helps convert the toxic amino acid homocysteine into the antidepressant amino acid s-adenysl-methionine. However, a significant segment of the population (some estimate 40%) have a genetic mutation in the MTHFR gene that interferes with the body’s ability to break down B vitamins and is linked to higher levels of homocysteine. MTHFR mutations are also linked to depression.
A 2016 study by Arnold W. Mech and Andrew Farah in the Journal of Clinical Psychiatry found that treating people with major depression and a MTHFR deficiency using a combination of micronutrients and already-broken-down B vitamins improved their depression and reduced their homocysteine levels compared to placebo.
The study included 330 adult patients with major depression and one of two genetic variants in the MTHFR gene—C677T or A1298C. Of those who received the metabolized vitamins, 82.4% showed reduced homocysteine levels. Those who received placebo showed a small average increase in homocysteine. The vitamin group also saw a large drop in depression symptoms on average after 8 weeks, with 42% achieving full remission. There were no side effects.
These findings suggest that homocysteine levels play a role in depression and that metabolized B vitamins can be an effective treatment for depression, particularly in those with a MTHFR deficiency. A metabolized form of folate that is commercially available is called L-methylfolate.
The drug ketamine has been used intravenously for years to rapidly treat depression, because it can take effect within hours. Unfortunately, its antidepressant effects fade in 3–5 days, and it has some unpleasant side effects. In larger doses ketamine is used as an anesthetic and sometimes as a club drug, for its ability to induce hallucinations and dissociation. It can be addictive as well.
A 2016 animal study by Todd Gould and colleagues published in the journal Nature identified a byproduct of ketamine that may be able to provide the drug’s benefits without its side effects.
When the body breaks down ketamine, it produces several chemicals that are known as ketamine metabolites. The researchers found that one of these, called hydroxynorketamine, reversed a depression-like state in mice, without producing the side effects that would be expected of ketamine.
Gould and colleagues also determined that blocking the transformation of ketamine into hydroxynorketamine prevented ketamine’s antidepressant effects.
Ketamine’s unpleasant anesthetic and dissociative effects result from the blockade of a particular receptor for the neurotransmitter glutamate (the NMDA glutamate receptor). Researchers originally thought that the NMDA blockade was linked to ketamine’s antidepressant effects, but this appears not to be the case. Instead, hydroxynorketamine seems to activate a different type of glutamate receptor, the AMPA receptor.
Gould and colleagues plan to test hydroxynorketamine in humans soon. Because it has already been present in the human body following ketamine administration, they expect it to be safe.
We have written many times before about intravenous ketamine as a fast-acting antidepressant treatment that can produce results within hours. Unfortunately, these quick results tend to fade within a few days. Current research is focused on possible ways of extending ketamine’s antidepressant effects.
A 2016 article by Jaskaran B. Singh and colleagues in the American Journal of Psychiatry reported that giving depressed patients infusions of ketamine (0.5mg/kg of body weight) twice or three times per week improved their depression compared to placebo over a period of up to 2 weeks.
Side effects included headache, anxiety, dissociation, nausea, and dizziness. The dissociation was temporary and improved with repeated dosing.
Depression and poor cardiovascular health often go hand in hand. Now it seems a treatment for high cholesterol may also help treat depression. A 2016 study by E. Salagre and colleagues in the Journal of Affective Disorders analyzed evidence from 3 earlier studies of drugs called statins, which inhibit an enzyme needed for the production of cholesterol, for people with depression.
The three studies included a total of 165 participants taking an antidepressant (citalopram or fluoxetine) for moderate or severe depression. Of these participants, 82 were prescribed an additional statin (lovastatin, atorvastatin, or simvastatin), while the remaining were given a placebo. After 6 to 12 weeks, those who had received a statin reported greater improvement in their depression than those who had received a placebo in addition to the antidepressant. No serious side effects were reported.
These data are also consistent with other studies showing that women on statins had fewer depressions over subsequent years than those not taking statins.
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).
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.