A 2016 study by researcher David Arterburn and colleagues in the Journal of Clinical Medicine suggests that taking an antidepressant for two years is associated with an increase in body weight. Luckily, bupropion (trade name Wellbutrin) is an exception that may be a good choice for obese or overweight patients.
The researchers analyzed links between which antidepressants patients in a large health system in Washington State were prescribed and their body weight two years later.
The researchers used fluoxetine (Prozac) as a reference. Most antidepressants did not differ significantly from fluoxetine in terms of the weight gain experienced by people taking the drug.
There were a few exceptions. Compared to non-smoking fluoxetine users, who gained an average of 4.6 pounds in two years, non-smoking bupropion users actually lost weight—an average of 2.4 pounds. (Smokers taking bupropion still gained an average of 6.9 pounds.)
Sertraline (Zoloft) was another exception. Sertraline users gained more than users of other antidepressants—an average of 10.5 pounds over two years.
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.
For decades, researchers have known that a pregnant mother’s diet, hormone levels, and psychological state can affect her offspring’s development, altering organ structure, cellular response, and gene expression. It is now becoming clear that a father’s age and lifestyle at the time of conception can also shape health outcomes for his offspring.
Older fathers have offspring with more psychiatric disorders, possibly because of increased incidence of mutations in sperm.
A 2016 article by Joanna Kitlinska and colleagues in the American Journal of Stem Cells reviewed findings from human and animal studies about the links between fathers’ behaviors and their offspring’s development.
Father’s behavior can shape gene expression through a phenomenon described as epigenetics. Epigenetics refers to environmental influences on the way genes are transcribed. While a father’s behavior is not registered in his DNA sequences, it can influence the structure of his DNA or the way in which it is packaged.
Kitlinska suggests that these types of findings should eventually be organized into recommendations for prospective parents. More research is also needed into how maternal and paternal influences interact with each other.
Some findings from the article:
- A newborn can have fetal alcohol spectrum disorder even if the mother doesn’t drink. “Up to 75% of children with [the disorder] have biological fathers who are alcoholics,” says Kitlinska.
- Father’s alcohol use is linked to low birth weight, reduced brain size, and impaired cognition.
- Dad’s obesity is linked to enlarged fat cells, diabetes, obesity, and brain cancer in offspring.
- A limited diet in a father’s early life may reduce his children and grandchildren’s risk of death from cardiovascular causes.
- Dad’s advanced age is correlated with higher rates of schizophrenia, autism, and birth defects in his children.
- Psychosocial stress on dads can affect their children’s behavioral traits.
Smoking, alcohol use, obesity, and diabetes aren’t just harmful to the body. They may actually lead to dementia.
Behavioral risk factors for cardiovascular disease like those listed above have been linked to reduced volume in the brain as a whole and several brain regions, including the hippocampus, precuneous, and posterior cingulate cortex. A 2015 study by researcher Kevin King and colleagues found that these reduced brain volumes are early indicators of cognitive decline.
King and colleagues analyzed data on 1,629 participants in the long-term Dallas Heart Study. Their cardiovascular risk factors were assessed when they began the study, and their brain volume and cognitive function were measured seven years later.
Alcohol use and diabetes were associated with lower total brain volumes, while smoking and obesity were linked to low volumes in the posterior cingulate cortex.
Low hippocampal volume was linked to past alcohol use and smoking, while lower precuneous volume was linked to alcohol use, obesity, and blood glucose levels.King and colleagues suggested that subtle differences in brain volumes in midlife are the first sign of developing dementia in participants who were still younger than 50 years of age.
The couch potato lifestyle common in the US may have consequences later, in the form of deficits in memory, executive functioning (including planning and execution) and processing speed.
At the 2015 Alzheimer’s Association International Conference, researcher Kristine Yaffe and colleagues reported that low levels of physical activity and high rates of television viewing in young adulthood may reduce cognitive capabilities in midlife.
The Centers for Disease Control report that less than 50% of adults aged 18–64 get the recommended minimum of physical activity each week. The guidelines recommend at least 150 minutes of moderate intensity aerobic activity (such as walking briskly) and two or more days of muscle-strengthening activities that work all major muscle groups.
Yaffe says that physical activity can protect against cognitive decline or dementia later on.
Participants in the long-term study who reported burning fewer than 300 calories per 50-minute session three times per week during two-thirds of their followup visits had worse cognition at year 25 than those participants who were more active. Those who watched more than four hours of television per day also had reduced cognition in midlife.
Yaffe stresses that exercising regularly is not just important in keeping weight down and protecting the heart, but also in protecting the brain. Regular physical activity may even prevent illnesses such as Alzheimer’s disease.
Depression and Bipolar Disorder in Adolescence Linked to Early-Onset Cardiovascular Disease and Hardening of the Arteries
The link between mood disorders and cardiovascular illnesses has been clear for some time. Now there is evidence that this link begins early in life. In 2015, the American Heart Association issued a statement that adolescents with major depressive disorder and bipolar disorder are at increased risk for both accelerated atherosclerosis (narrowing and hardening of the arteries) and early-onset cardiovascular disease.
In the statement, the American Heart Association recommended that major depressive disorder and bipolar disorder be classified as “tier II” conditions (which also include HIV and chronic inflammatory disease) that confer a moderate risk of disease.
Until recently, it had been assumed that the increased risk of cardiovascular disease among people with depression or bipolar disorder was a result of behaviors linked to these illnesses, such as higher rates of smoking, obesity, or diabetes, which increases heart disease. Some psychiatric medication can also bring about risk factors for cardiovascular problems. It turns out that these types of factors could not fully explain the increased risk of atherosclerosis and cardiovascular disease among people who had depression or bipolar disorder in their teens.
It is not clear why depression and bipolar disorder make cardiovascular illness more likely, though it may be due to blood vessel damage resulting from inflammation or oxidative stress.
The American Heart Association recommends that pediatricians and cardiologists pay particular attention to this link by identifying and treating mental illness as early as possible and by making sure that their colleagues understand the role of mental illnesses in cardiovascular risk.
Professional football players face repeated mild traumatic brain injuries throughout their careers, and may face a variety of brain impairments, from depression to dementia, as a result.
A recent study by researcher Jennifer Coughlin and colleagues clarified how these impairments may be caused by repeated brain impacts. The researchers used positron emission tomography (PET) scans to observe the volume of translocator protein, a marker of brain injury and repair, in the brains of seven active or recently retired National Football League (NFL) players. Compared to healthy, athletic volunteers who were age-matched to the NFL players, the NFL players showed greater volume of translocator protein in several brain regions, including the left and right thalamus, the left and right temporal poles, and the brainstem.
It is not yet clear whether the increased volume of translocator protein is a sign of the brain’s attempts to repair itself, or whether it shows deterioration toward chronic traumatic encephalopathy. Translocator protein is also considered a marker of microglial activation, which occurs with inflammation.
High levels of translocator protein have also been seen in patients with depression and schizophrenia.
Liraglutide is taken as a daily injection and is meant to be used alongside a calorie-reduced diet and increased physical activity. Liraglutide works by mimicking a peptide (GLP-1) that regulates appetite and calorie intake.
Recommended dosage is 3 mg/day, but should begin at 0.6 mg/day for the first week and gradually increase by 0.6mg each week to reduce the likelihood of gastrointestinal side effects.
In three clinical trials, participants who were overweight or obese, some of whom had weight-related conditions such as high blood pressure, type 2 diabetes, or high cholesterol, either received training about following a reduced-calorie diet and increasing physical activity or had already lost up to 5% of their body weight by engaging in these practices.
Among those participants who did not have diabetes or a weight-related condition, 62% lost up to 5% of their body weight after a year of taking liraglutide, compared to 34% of those who were given a placebo injection.
Of the participants who had type 2 diabetes, 49% lost up to 5% of their body weight after a year of liraglutide, compared to 16% of those who received placebo.
Of those who had a weight-related condition other than diabetes, 42% lost up to 5% of their body weight compared to 21.7% who took placebo.
DNA has several ways of repairing itself. Serious damage, including breaks to both strands of the double helix and problems with replication, prompt a process known as DNA damage repair, or DDR. Researcher Stephen J. Elledge of Harvard Medical School won the 2015 Albert Lasker Basic Medical Research Award for his findings about DDR. He summarized these findings in a September article in the journal JAMA.
DDR occurs because of DNA’s remarkable self-awareness. Through the DDR process, DNA can detect when it has been damaged and prompt the right kind of repair. When damage occurs, DDR allows for the activation of enzymes that can remodel DNA to maintain the integrity of the genome.
When DDR pathways are activated, they can alter more than 1000 different proteins. DDR can affect immune function, blood and bone marrow, viral response, cancer, aging, and brain development.
Mutations in components of the DDR pathway can lead to problems with brain development, including Seckel syndrome (characterized by dwarfism, brain and facial abnormalities, and mental retardation) and ataxia telangiectasia (loss of control of bodily movements along with weakened immune system).
DDR is particularly relevant to cancer, since properly functioning DDR promotes a stable genome. Classic cancer treatments such as radiation and chemotherapy also rely on DDR to prompt cell death.
DDR also plays a role in aging. When we get older or have certain illnesses, telomeres, bits of material at the end of DNA strands that protect the DNA during replication, get shorter. This prompts DDR to engage in tumor prevention measures, either killing off the cells or changing them into what’s called senescent cells. Senescent cells prevent tumors, but their accumulation is associated with chronic inflammation, aging, and age-related diseases.
Editor’s Note: You can protect your telomeres and possibly hold off the age-related effects of DDR. Healthy diet, exercise, meditation, goal setting, and making positive contributions to society all help maintain telomere length. Lithium treatment also directly increases telomere length.
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).