High Levels of Leptin Associated With Lower Depression

Leptin is a hormone released by adipocytes (fat cells) that signals excess, or fullness, after a meal. Studies in chubby people have found that there is a coupling between weight gain and an ineptitude to produce adequate amounts of leptin. A group study looks at a new role excessive levels of the hormone may also demote symptoms of depression.

Leptin Levels Influence a Variety of Body Processes

Elizabeth Lawson MD of Massachusetts Blended Hospital and Harvard Medical Credo and colleagues studied the relationship between leptin levels and symptoms of foreboding and depression in 64 women of odd weights. Fifteen of the women had anorexia nervosa, an eating brouhaha characterized by abnormally low force and body fat.
Twelve were of ordinary weight but had hypothalamic amenorrhea, or the cessation of menstruation. Leptin is also known to flatter a role in regulation of reproductive go. Twenty of the remaining women were of orthodox weight and 17 were overweight or pot-bellied, but all in good health.
 The on participants were asked questions to assess symptoms of downheartedness and anxiety with higher scores indicating more symptoms. Blood leptin levels were regulated and BMI was assessed. The researchers establish that higher leptin levels were linked to decreased symptoms of anxiety and depression, a relationship that was neutral of BMI.
The finding, also seen in subhuman studies, indicates that leptin may mediate symptoms of impression and that this really is not a function of weight stature, Dr. Lawson said. Leptin injections are already being tested in gross models as an obesity treatment and supplementary research in humans “commitment be important in understanding whether this hormone has a potency role in the treatment of sadness,” concluded the authors.
It is provocative to note that a aforesaid study conducted at the University of Florida initiate that exercise can suffer with a positive effect on leptin levels, allowing the hormone to incite properly in the body. Worry has long been associated with a contract in depression symptoms, the buy generic Valium online, a find that could be relative in future studies as satisfactory.

Newer Antidepressants Not Always Better

New antidepressants might be no more effective than the best existing drugs, according to two new systematic reviews that compared 12 commonly used medications.
“Patients are usually encouraged to take the newest medication,” said lead author Andrea Cipriani, M.D., of the University of Verona, in Italy. “But it’s better to have an old depression treatment that has been proved with many patients and many years in the market.”
The reviews suggest that sertraline — sold under the brand name Zoloft since 1991— could be the best initial choice of antidepressant in people with acute major depression. The generic formulation produced the best balance of effectiveness, tolerability and purchase price, the authors say.
Patients also did well on one of the newest antidepressants, escitalopram (Lexapro), but it is not yet available in lower-cost generic form. The authors note that comprehensive economic studies are necessary to evaluate overall cost-effectiveness of various treatments.
Cipriani said that the review recommendations are for new episodes of depression. “If a patient is taking another drug and doing well, we are not saying he has to change.”
The reviews appear in the most recent issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic.
Depression is the fourth-leading cause of disease burden worldwide and antidepressant drugs are now the mainstay of treatment for moderate to severe cases.
The aim of the two reviews was to compare the benefits and side effects of sertraline and escitalopram, respectively, with those of other antidepressants during the first six to 12 weeks of treatment.
Cipriani noted that all of the included studies compared one depression drug against another — not to a placebo — so the results reveal not the absolute effect, but rather the relative advantages and disadvantages of various medications.
In addition, these reviews rely on summary data from each study, rather than individual patient data. Future studies that go into greater detail can help identify the best depression medications for various subgroups of patients such as men vs. women, teens vs. adults and so on.
For sertraline, the reviewers included 59 randomized controlled trials totaling about 10,000 participants. Sertraline proved more effective than fluoxetine (Prozac), but less effective than mirtazapine (Remeron). In terms of side effects, bupropion (Wellbutrin) was easier to tolerate than sertraline, while the latter outscored amitriptyline (Elavil), imipramine (Tofranil), paroxetine (Paxil) and mirtazapine (Remeron).
For escitalopram, the reviewers included 22 randomized controlled trials totaling about 4,000 participants. Few statistically significant differences appeared in this review, although escitalopram was more effective than citalopram (Celexa) and fluoxetine (Prozac) and had fewer side effects than duloxetine (Cymbalta). The drug manufacturer sponsored most of the studies in this review, so there may be biases in favor of escitalopram.
Rather than seeking genuine advances in treatment, the review authors say, some pharmaceutical companies seem to be introducing close chemical cousins of generic medications. By gaining patent protection for the “new” drug, a company can market it as a higher-priced brand name product.
Sponsorship bias is a recurring concern in trials of virtually all new medications. In the Cochrane reviews themselves, one of the co-authors has received research funds and speaking fees from the companies Asahi Kasei, Astellas, Dai-Nippon Sumitomo, Eisai, Eli Lilly, GlaxoSmithKline, Janssen, Kyowa Hakko, Meiji, Nikken Kagaku, Organon, Otsuka, Pfizer and Yoshitomi. The Japanese Ministry of Education, Science and Technology, and the Japanese Ministry of Health, Labour and Welfare have also funded some of his research.
However, the co-authors of these Cochrane reviews also published a recent study in The Lancet that was free of any potential funding bias. The study also used a more complex statistical method to analyze data from 117 randomized controlled trials involving 25,928 participants.

Mechanism For Postpartum Depression Found In Mice

Researchers have pinpointed a mechanism in the brains of mice that could explain why some human mothers become depressed following childbirth. The discovery could lead to improved treatment for postpartum depression.Supported in part by the National Institute of Mental Health (NIMH), part of the National Institutes of Health, the study used genetically engineered mice lacking a protein critical for adapting to the sex hormone fluctuations of pregnancy and the postpartum period.
“For the first time, we may have a highly useful model of postpartum depression,” said NIMH Director Thomas R. Insel, M.D. “The new research also points to a specific potential new target in the brain for medications to treat this disorder that affects 15 percent of women after they give birth.”
“After giving birth, female mice deficient in the suspect protein showed depression-like behaviors and neglected their newborn pups,” explained Istvan Mody, Ph.D., of the University of California at Los Angeles (UCLA), who led the research. “Giving a drug that restored the protein’s function improved maternal behavior and reduced pup mortality.”
Researchers had suspected that postpartum depression stemmed from the marked fluctuations in the reproductive hormones estrogen and progesterone that accompany pregnancy and childbirth. Yet manipulating the hormones experimentally triggers depression only in women with a history of the disorder. The roots of their vulnerability remain a mystery.
Evidence suggested that the hormones exert their effects on mood through the brain’s major inhibitory chemical messenger system, called GABA, which dampens neural activity, helping to regulate when a neuron fires.
Mody and Maguire discovered that a GABA receptor component, called the delta subunit, fluctuated conspicuously during pregnancy and postpartum in the brains of female mice, hinting that it might have pivotal behavioral effects. To find out, they used mice lacking the gene for this subunit and studied them in situations that can elicit responses similar to human depression and anxiety.
Much like human mothers suffering from postpartum depression, the genetically altered mouse mothers were more lethargic and less pleasure-seeking than normal mice. They also shunned their pups and failed to make proper nests for them.
This abnormal maternal behavior was reversed and pup survival increased after the researchers gave the animals a drug called THIP that acts on the receptor in a way that specifically restores its function in spite of the reduced number of subunits.
“Improper functioning of the delta subunit could impair the GABA system’s ability to adapt to hormone fluctuations during the highly vulnerable post partum period,” explained Maguire. “Targeting this subunit might be a promising strategy in developing new treatments for postpartum depression.”