Depressed pregnant women have twice the risk of preterm delivery than pregnant women with no symptoms of depression, according to a new study by the Kaiser Permanente Division of Research.  The study is published online in the Oxford University Press’s journal Human Reproduction on behalf of the European Society of Human Reproduction and Embryology.

The study found that pregnant women with symptoms of depression have an increased risk of preterm delivery, and that the risk grows with the severity of the depressive symptoms.  These findings also provide preliminary evidence that social and reproductive risk factors, obesity, and stressful events may exacerbate the depression-preterm delivery link, according to the researchers.

Because the majority of the women in the study did not use anti-depressants, the study provides a clear look at the link between depression and preterm delivery.

The study -which is among the first to examine depression and pre-term delivery in a representative and diverse population in the United States -looked at 791 pregnant Kaiser Permanente members in San Francisco city and county from October 1996 through October 1998.

Researchers interviewed the women around their 10th week of pregnancy and found that 41 percent of the women reported significant or severe depressive symptoms.  The women with less severe depressive symptoms had a 60 percent higher risk of preterm delivery -defined as delivery at less than 37 completed weeks of gestation -compared with women without significant depressive symptoms, and the women with severe depressive symptoms had more than twice the risk.

“Preterm delivery is the leading cause of infant mortality, and yet we don’t know what causes it.  What we do know is that a healthy pregnancy requires a healthy placenta, and that placental function is influenced by hormones, which are in turn influenced by the brain,” said lead author Dr. De-Kun Li, a reproductive and perinatal epidemiologist at Kaiser Permanente’s Division of Research in Oakland.

“This study adds to emerging evidence that depression during early pregnancy may interfere with the neuroendocrine pathways and subsequently placental function.  The placenta and neuroendocrine functions play an important role in maintaining the health of a pregnancy and determining the onset of labor,” Li explained.

“Post-partum depression has been extensively studied and discussed by the public, but depression during pregnancy is significantly under-recognized and under-diagnosed.  Clinicians should pay close attention to depression during pregnancy to catch it early,” Li said.  “If prenatal depression is indeed as prevalent as reported in this and other studies and doubles the risk of preterm delivery, then bringing depression to the forefront of prenatal care could lead to a significant reduction of preterm deliveries.”

In addition to being the leading cause of infant mortality and morbidity, preterm delivery is also the leading medical expenditure for infants, with estimated annual cost of about $26 billion in the United States alone.  Presently, other than a prior history of preterm delivery and some pregnancy complications, very little is known for its risk factors and origins.

“The key strengths of this study are that it ascertained the depressive symptoms early in pregnancy, long before the preterm delivery occurred, therefore avoiding recall bias.  In addition, the study was not clouded by antidepressant use because only 1.5 percent of the study population was prescribed antidepressants and we could exclude them in the analyses,” Li said.  “Considering the increased use of antidepressants among pregnant women, this study’s findings may provide a rare opportunity to evaluate the effect of depression on risk of preterm delivery without the entanglements of antidepressants.”

Now, a study conducted by a team of scientists at the University of California, Santa Barbara has found that a mechanism exists within the human brain that enables people to determine with uncanny accuracy the fighting ability of men around them by honing in on their upper body strength. What’s more, that assessment can be made even when everything but the men’s faces are obscured from view. A paper highlighting the researchers’ findings appears in the current issue of the Proceedings of the Royal Society.

“Assessing fighting ability was important for our ancestors, and the characteristic that the mind implicitly equates with fighting ability is upper body strength,” said Aaron Sell, a postdoctoral fellow at UCSB’s Center for Evolutionary Psychology and the paper’s lead author. “That’s the component of strength that’s most relevant to premodern combat. The visual assessment of fighting ability is almost perfectly correlated with the perception of strength, and both closely track actual upper body strength. What is a bit spooky is that upper body strength can even be read on a person’s face.

Sell conducted the study with Leda Cosmides, a professor of psychology and co-director of the Center for Evolutionary Psychology; John Tooby, a professor of anthropology and also co-director of the Center for Evolutionary Psychology; Michael Gurven, an associate professor of anthropology; and graduate students Daniel Sznycer and Christopher von Rueden.

The study consisted of four sections, each of which asked the test subjects to assess the physical strength of individuals based on photographs of their faces, their bodies, or both. Subjects were asked to rank the physical strength or fighting ability of the people in the photographs on a scale of one to seven. When the photographs depicted men whose strength had been measured precisely on weight-lifting machines, the researchers found an almost perfect correlation between perceptions of fighting ability and perceptions of strength. “When you see that kind of correlation it’s telling you you’re measuring the same underlying variable,” said Tooby.

They also found that perceptions of strength and fighting ability reflected the target’s actual strength, as measured on weight-lifting machines at the gym. In other sections of the study, the researchers showed that this result extended far beyond the gym. Both men and women accurately judge men’s strength, whether those men are drawn from a general campus population, a hunter-horticulturalist group in Bolivia, or a group of herder-horticulturalists living in the Argentinian Andes.

Leg strength was measured along with upper body strength in both the United States and Bolivian populations, but the results showed that perceptions of men’s strength and fighting ability reflect upper body strength, not that of legs. “That makes sense,” said Cosmides. “If, for example, you’re trying to lift something really heavy, or run a long distance, your lower body –– your legs –– will also be significant. But for fighting at close quarters, it’s the upper body that really matters.”

Added Tooby: “Whether people are assessing toughness or strength, it’s upper body strength they implicitly register. And that’s the critical information our ancestors needed in deciding –– or feeling –– whether to surrender a disputed resource or escalate aggressively.”

The researchers suggest that the ability to judge physical strength and fighting ability serves different, but equally important, purposes for men and women. In men, the mechanism is a barometer for measuring potential threats and determining how aggressive or submissive they should be when facing a possible enemy. For women, the mechanism helps identify males who can adequately protect them and their children. Men have a lot more experience with rough and tumble play and direct experience with fighting, yet women are just as good at assessing these variables. The authors also point out that neither men nor women fare as well in assessing women’s strength. This is entirely expected because, ancestrally, inflicting violence was mostly the province of men.

“The next step is to isolate what it is in the face that indicates upper body strength,” said Sell. He suggests that the correlation may lie in the heavier brow ridge and thicker jaw that result from increased levels of testosterone. “Many studies have been done on the effects of testosterone on the face. There’s a good chance testosterone is involved in regulating the body for battle, and men with high testosterone –– those with a heavy brow ridge and thicker jaw –– developed bodies that were more prepared for combat.”

“One reason we evolved the ability to perceive physical strength in the face may be that it’s where we focus our attention when we look at someone,” said Cosmides.

“Even if we are able to see someone’s body, we always look at the face. It’s so rich in social information –– what a person is thinking or feeling –– and adding the assessment of physical strength is a huge benefit. A person who is angry and strong offers a much greater threat than the person who is angry but weak.”

Targeted memory erasure is no longer limited to the realm of science fiction.  A new study describes a method through which a selected set of memories can be rapidly and specifically erased from the mouse brain in a controlled and inducible manner.  The research, published by Cell Press in the October 23 issue of the journal Neuron, may eventually lead to development of strategies amenable to the human brain that would permit selective erasure of traumatic memories or unwanted fear while leaving other memories intact.

Memory is generally separated into four different stages: acquisition, consolidation, storage, and retrieval.  Previous research has identified specific molecules and events that appear to play a role in the various phases of the memory process.  One such “memory molecule,” calcium/calmodulin-dependent protein kinase II (CaMKII), is an enzyme that has been linked to multiple aspects of learning and memory.

A research team led by Dr. Joe Z. Tsien, from the Brain and Behavior Discovery Institute at the Medical College of Georgia, developed a method for rapidly manipulating CaMKII activity in the brains of transgenic mice.  “We recently developed a chemical genetic strategy that combines the molecular specificity of genetics with the high time-resolution of pharmacological inhibition.  Using this technique, we examined the manipulation of transgenic ?CaMKII activity on the retrieval of short-term and long-term fear memories and novel object recognition memory,” explains Dr. Tsien, who is also renowned for his 1999 creation of Doogie, the smart transgenic mouse with enhanced learning and memory abilities.

Dr. Tsien and colleagues found that transient overexpression of ?CaMKII at the time of recall impaired retrieval of newly formed 1 hr novel object recognition memory and fear memories, as well as 1-month-old fear memories.  The researchers went on to show that recall deficits linked to excessive ?CaMKII activity were not caused by a blockade of the recall process but instead seemed to be due to rapid erasure of the stored memories.  Further, the erased memories were limited to those being retrieved while others remained intact.

The results demonstrate a successful genetic method for rapidly and specifically erasing specific memories, such as new and old fear memories, in a controlled and inducible manner without doing harm to the brain cells.  “Given the fact that so many war veterans often suffer from reoccurring traumatic memory replays after returning home, our report of selective erasure of fear memories in an inducible and rapid way suggests the existence of molecular paradigm(s) under which traumatic memories can be erased or degraded while preserving other memories in the brain,” says Dr. Tsien.  However, he goes on to caution, “No one should expect to have a pill do the same in humans any time soon, we are barely at the foot of a very tall mountain.”

A new animal model has provided insight into the cellular and molecular mechanisms associated with behavioral therapy for depression.  The study, published by Cell Press in the October 9th issue of Neuron, may provide a good model system for testing cellular and molecular interactions between antidepressive medications and behavioral treatments for depression.

Organisms ranging from simple invertebrates to mammals have evolved mechanisms for instinctive and learned fear that are critical for survival.  However, in humans, pathological forms of learned fear can contribute to anxiety disorders, posttraumatic stress, and depression.  “The fact that learned fear can be associated with psychopathologies in humans suggests that this form of learning is not always appropriate and that effective inhibitory constraints are likely to exist,” explains Eric Kandel from Columbia University.

Previous research investigating how learned fear is processed in the brain has made use of a conditioned inhibition learning paradigm wherein an animal is conditioned to associate a target signal with protection from an impending aversive event, resulting in a reduction of conditioned fear.  This process, where an animal learns to take advantage of sources of security in the environment, is thought to represent a form of “learned safety.”

Daniela Pollak in the Kandel lab was interested in attempting to characterize some of the behavioral consequences of learned safety as well as exploring the phenomenon at the molecular level.  She observed that learned safety reduced depression-like behavior in mice in a manner that was comparable to that seen with pharmacological antidepressants.  Consistent with the behavioral antidepressant effects, learned safety also shared neurobiological hallmarks associated with other antidepressant therapies.  Specifically, learned safety promotes the survival of newborn nerve cells and expression of critical growth factors in the hippocampus.

The researchers went on to search for differentially regulated genes in the amygdala of safetyand fear-conditioned mice.  The amygdala is a brain region associated with emotional symptoms that are a hallmark of depression.  Learned safety led to decreased expression of genes involved in dopamine and substance P signaling, but not serotonin signaling.  This is significant because serotonin receptors are a major target of popular antidepressant medications.

“We propose a model in which the stress-reducing and antidepressant effects of learned safety are mediated through the interaction of (at least) two different neurotransmitter systems.  Our findings suggest that learned safety is an animal model of a behavioral antidepressant that shares some of the neuronal modifications typical of pharmacological antidepressant, but is mediated by different molecular pathways,” offers Kandel.

New research findings suggest that structural abnormalities in the brains of cocaine addicts are related in part to drug use and in part to a predisposition toward addiction.  The research, published by Cell Press in the October 9th issue of the journal Neuron, maps the topography of the addicted brain and provides new insight into the effect of cocaine on neural systems mediating cognition and motivation.

“Human studies have shown differences in how addicts make judgments and decisions, but it is not well understood how these differences relate to alterations in the structure of the brains of addicts.  Claims have been made that cocaine, potentially in connection with alcohol or other drugs, may be toxic to brain cells.  We sought evidence supporting a hypothesis that brain thickness is reduced in some brain regions in addicts, is related to altered decision-making and cognition, and might to some limited degree, be connected to their exposure to cocaine,” explains senior study author Dr. Hans Breiter from Massachusetts General Hospital.

Dr. Breiter and colleagues found that brain regions involved with regulation of attention and reward, specifically the dorsolateral prefrontal cortex (DLPFC) and insular cortices, were significantly thinner in cocaine addicts when compared with matched controls.  Behavioral tests revealed that the thinner cortex was associated with restrictions in preference-based judgment and decision-making, and with less accurate effortful attention.  A general reduction in the level of preference and in the range of decisions reflecting these preferences can be considered an example of a fundamental feature of addiction—the loss of interest in many things outside of drug use.

Some cortical thickness differences were associated with years of drug use, but the researchers also observed differences in the symmetry of DLPFC thickness between control subjects and cocaine addicts that suggested predisposition to drug abuse.  “In human and animal studies, differences in the structure of the right and left sides of the brain are important for many behaviors, and when these normal differences in brain structure are altered, there may be a genetic basis for the change.  We found an altered right/left relationship in a part of the frontal cortex that was also associated with altered judgment and decision-making in addicts.  We further found that the overall brain thickness in the cocaine addicts was more uniform across the brain, which is quite different from what is observed in non-drug users.  These differences did not correlate with any drug use measure.  Together, this set of findings point to predisposing factors being a potential contributing factor to the addiction,” explains Dr. Breiter.

In total, these observations provide evidence that cortical thickness abnormalities associated with cocaine addiction may be a reflection of both drug use and a preexisting inclination to drug abuse.  “A fundamental component of addiction may involve adaptations and/or developmental predispositions involving brain regions necessary for judgment and decision-making regarding complex rewards and attention towards goal-objects.  Addiction thus may represent a complex phenotype with multiple effects necessary for compulsive drug use, and the resulting restriction in the range of behaviors they show,” concludes Dr. Breiter.

New research provides support for the use of St. John’s wort extracts in treating major depression.  A Cochrane Systematic Review backs up previous research that showed the plant extract is effective in treating mild to moderate depressive disorders.

“Overall, we found that the St. John’s wort extracts tested in the trials were superior to placebos and as effective as standard antidepressants, with fewer side effects,” says lead researcher, Klaus Linde of the Centre for Complementary Medicine in Munich, Germany.

Extracts of the plant Hypericum perforatum, commonly known as St. John’s wort, have long been used in folk medicine to treat depression and sleep disorders.  The plant produces a number of different substances that may have anti-depressive properties, but the whole extract is considered to be more effective.

Cochrane Researchers reviewed 29 trials which together included 5,489 patients with symptoms of major depression.  All trials employed the commonly used Hamilton Rating Scale for Depression to assess the severity of depression.  In trials comparing St. John’s wort to other remedies, not only were the plant extracts considered to be equally effective, but fewer patients dropped out of trials due to adverse effects.  The overall picture is complicated, however, by the fact that the results were more favourable in trials conducted in German speaking countries, where St. John’s extracts have a long tradition and are often prescribed by doctors.

Despite the favourable findings for St. John’s wort, researchers are anxious not to make generalisations about the plant’s use as an anti-depressant and recommend consulting a doctor in the first instance, especially as the extracts can sometimes affect the actions of other beneficial drugs.

“Using a St. Johns wort extract might be justified, but products on the market vary considerably, so these results only apply to the preparations tested,” says Linde.