Not sure if you are feeling enough mental pain to be classified as depressed? A blood test can detect depression.
The initial assessment of a blood test to help diagnose major depressive disorder indicates it may become a useful clinical tool. In a paper published in the journal Molecular Psychiatry, a team including Massachusetts General Hospital (MGH) researchers reports that a test analyzing levels of nine biomarkers accurately distinguished patients diagnosed with depression from control participants without significant false-positive results.
"Traditionally, diagnosis of major depression and other mental disorders has been made based on patients' reported symptoms, but the accuracy of that process varies a great deal, often depending on the experience and resources of the clinician conducting the assessment," says George Papakostas, MD, of the MGH Department of Psychiatry, lead and corresponding author of the report. "Adding an objective biological test could improve diagnostic accuracy and may also help us track individual patients' response to treatment."
Use of a test to detect response to treatment isn't just of clinical value. It also has uses in the development of new ways to treat depression. If drug candidates, diet and life style changes can have their impact measured by shifts blood depression biomarkers then new methods of intervention can be tested more quickly and reliably.
The initial pilot phase of the study enrolled 36 adults who had been diagnosed with major depression at the MGH, Vanderbilt University or Cambridge Health Alliance in Cambridge, Mass., along with 43 control participants from St. Elizabeth's Hospital in Brighton, Mass. MDDScores for 33 of the 36 patients indicated the presence of depression, while only 8 of the 43 controls had a positive test result. The average score for patients was 85, while the average for controls was 33. A second replication phase enrolled an additional 34 patients from the MGH and Vanderbilt, 31 of whom had a positive MDDScore result. Combining both groups indicated that the test could accurately diagnose major depression with a sensitivity of about 90 percent and a specificity of 80 percent.
Can other mental states eventually be measured with blood tests? Imagine that blood biomarkers for highly productive mental states can be found. One could then start to try to control one's biochemistry to keep oneself in a more productive mental zone.
In a study published in the November issue of the Journal of Adolescent Health, nearly 40 percent of young adults who said they had tried suicide said that they made their first attempt before entering high school.
One lesson here: Parents especially shouldn't be complacent about the mental health of their kids before high school. If Johnnie or Jill seems depressed in 7th grade take note. Is there a good way to measure risk of suicide to identify higher risk cases?
The researchers also found that suicide attempts during childhood and adolescence were linked to higher scores of depression at the time of the attempts, validating for the first time that young adults can reliably recall when they first attempted suicide.
Near the end of their teen years nearly 9% had attempted suicide.
As part of an ongoing survey, Mazza and his collaborators asked 883 young adults aged 18 or 19 about their history of suicide attempts. Seventy-eight respondents, nearly 9 percent, said that they had tried suicide at some point.
5th grade sounds like it is the end of low worry childhood and 6th grade the beginning of unhappy adulthood.
Suicide attempt rates showed a sharp increase around sixth grade, about age 12, with rates peaking around eighth or ninth grade. For the 39 respondents reporting multiple suicide attempts, their first attempt was significantly earlier – as young as 9 – than those making a single attempt.
How many of the depressed 12 and 14 year olds remain depressed in adulthood? That a life of depression can start at a pre-teen age is a depressing thought.
Analogous to heart pacemakers, an electrical pacemaker can drive currents into a few key locations in the brain to lift otherwise untreatable depression. Imagine a more refined device with many more implants that would allow dialing up various moods and mental states.
Nearly ten percent of all cases of depression are so severe that the patients do not respond to any established treatment method. Targeted stimulation of areas in the brain using a type of "brain pacemaker" has recently raised hopes: According to initial studies, half of patients with the most severe depression treated in this manner see a significant improvement in mood. Physicians from the University of Bonn, together with colleagues from the US, have suggested a new target structure for deep brain stimulation (as it is technically called). They hope to achieve an even better success rate with fewer side effects. The work has been published in the renowned Neuroscience and Biobehavioral Reviews (doi: 10.1016/j.neurobiorev.2010.12.009).
In deep brain stimulation, physicians implant electrodes in the brain. Using an electrical pacemaker implanted under the patient's clavicle, physicians can influence the function of certain areas of the brain in a lasting manner. The method was originally developed for treating patients with Parkinson's disease, in order to alleviate the typical movement problems.
Stimulating any one of 3 connected areas works for relief of depression.
Deep brain stimulation has been tested to date in three different areas of the brain: the nucleus accumbens, the internal capsule, and a structure known as cg25. Surprisingly, the effects are nearly identical - regardless of which of these centers the physicians stimulate. Together with colleagues from Baltimore and Washington, the Bonn researchers have since been able to explain why this is the case: Using a novel tomography method, they were able to make the "cable system" of the three brain centers visible. "In doing this, we determined that at least two of these three areas - probably even all three - are attached to one and the same cable harness," explains the Bonn brain surgeon, Professor Dr. Volker Coenen.
How about an implant that turns off boring droning on? A remote control would be useful for this. Get one of these installed in any bore in the office and any time they start going on just hit a button. Would work on dates and in relationships too.
Then there are criminals. How about brain implants that would stop them from committing crimes? The electric restraint gadget wouldn't even need to work in the brain for some types of crimes. Condition of parole: Anyone threatened with harm could use their cell phone (or perhaps a button on their watch or ring) to turn the beast off and make a monster into a lamb.
A meta-study finds the short version of a serotonin transporter gene. Serotonin is a neurotransmitter.
ANN ARBOR, Mich. — University of Michigan Health System researchers have found new evidence that our genes help determine our susceptibility to depression.
Their findings, published online today in the Archives of General Psychiatry, challenge a 2009 study that called the genetic link into question and add new support to earlier research hailed as a medical breakthrough.
The 2009 meta-analysis called into question a 2003 study that found those who suffered physical sexual abuse or other stress were more likely to get depressed if they also had the short version of this serotonin neurotransmitter gene. But using a larger number of study participants from more studies a U Mich team finds a connection between the gene and depression.
Today Srijan Sen, M.D., Ph.D, an assistant professor of psychiatry at the University of Michigan Medical School, and his colleagues are presenting a new, broader analysis of the follow-up studies to date. The U-M team examined 54 studies dating from 2001 to 2010 and encompassing nearly 41,000 participants – making it the largest analysis of the serotonin gene's relationship to depression.
"When we included all the relevant studies, we found that an individual's genetic make-up does make a difference in how he or she responds to stress," says Sen.
The U-M analysis supports previous findings that individuals who had a short allele on a particular area the serotonin gene had a harder time bouncing back from trauma than those with long alleles.
Once we all get ourselves genetically tested (assuming the US Food and Drug Administration and like agencies in other countries don't ban direct-to-consumer genetic testing) we will be able to find out whether stresses predispose ourselves to depression. Imagine a court ruling on child custody guided by the need to minimize the stress a kid might experience by avoiding a custody grant to an especially stressful parent.
Curiously, the gene version that predisposes to depression is at higher frequency in China even though the rate of depression is thought to be much lower. Read that Wired article for how cultural factors might play a role in keeping depression down in China.
Well, if you are depressed this might seem like a depressing report since you can't (yet) change your genes. But look on the bright side (literally): very bright lights reduce depression in elderly patients. A light box would be worth a try.
A theory holds that auto-immune diseases and some other disorders related to the immune system are caused by a lack of exposure to microorganisms that our immune systems are designed to handle (this idea is known as the Hygiene Hypothesis). The absence of real enemies makes the immune system incorrectly attack friendlies and to otherwise malfunction. Are imbalanced immune systems due to clean environments making people depressed?
In an effort to pinpoint potential triggers leading to inflammatory responses that eventually contribute to depression, researchers are taking a close look at the immune system of people living in today's cleaner modern society.
Rates of depression in younger people have steadily grown to outnumber rates of depression in the older populations and researchers think it may be because of a loss of healthy bacteria.
In an article published in the December issue of Archives of General Psychiatry, Emory neuroscientist Charles Raison, MD, and colleagues say there is mounting evidence that disruptions in ancient relationships with microorganisms in soil, food and the gut may contribute to the increasing rates of depression.
According to the authors, the modern world has become so clean, we are deprived of the bacteria our immune systems came to rely on over long ages to keep inflammation at bay.
To view a video with Dr. Raison: http://bit.ly/wearetooclean
I find this argument at least plausible because the immune cells have function in the brain beyond just wiping out pathogens.
STANFORD, Calif. - Molecules assumed to be in the exclusive employ of the immune system have been caught moonlighting in the brain - with a job description apparently quite distinct from their role in immunity.
Carla Shatz, PhD, professor of neurobiology and of biology, and her colleagues at the Stanford University School of Medicine have shown that members of a large family of proteins critical to immune function (collectively known as HLA molecules in humans and MHC molecules in mice) also play a role in the brain. "We think that this family of molecules has an important role in learning and memory," Shatz said. Surprisingly, the absence of one or another of them in the brain can trigger improved motor learning, although perhaps at the expense of other learning ability.
The study will be published online on March 30 in the journal Proceedings of the National Academy of Sciences.
A healthy immune system is needed for a healthy brain.
Update: Another recent study found that an immune system protein altered in utero neuronal development in mice. The researchers suspect infections during pregnancy could cause autism or schizophrenia.
Gene therapy to deliver the gene for a protein p11 in to mouse brains lifted their depressive state. The thinking is this technique could be replicated with humans. Want to reprogram your brain genes to make you happier? You okay with permanently altering your pesonality using gene therapy.
NEW YORK (Oct. 20, 2010) -- In a report published in the Oct. 20 issue of Science Translational Medicine, researchers at NewYork-Presbyterian Hospital/Weill Cornell Medical Center say animal and human data suggest gene therapy to the brain may be able to treat patients with major depression who do not respond to traditional drug treatment.
The researchers hope to rapidly translate their findings into a human clinical trial using the same kind of gene therapy modality the investigators have pioneered to treat Parkinson's disease. A 45-patient randomized blinded phase II multicenter clinical trial using the gene therapy to treat Parkinson's has recently ended and results are being readied for publication.
"Given our findings, we potentially have a novel therapy to target what we now believe is one root cause of human depression," says the study's senior investigator, Dr. Michael Kaplitt, associate professor and vice chairman for research of neurological surgery at Weill Cornell Medical College and a neurosurgeon at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
Suppose this will really work in humans. Okay, so a gene therapy could permanently alter your mental state. Is this the last gene therapy discovered that alters personality or brain performance? Most certainly not. We will witness the development of more ways to alter the brain's performance via gene therapies and other long-lasting methods of altering the brain.
This has suspense thriller science fiction potential. Use gene therapy tourn a guy into an amoral killer before sending him on a killing mission. Then when he comes back and his handlers reprogram him again to lack killer ambitions.
Imagine rich or powerful people getting gene therapy without their even knowing it in order to make them do the bidding of a rival group (e.g. a mugging could include an injection of a gene therapy or a the gene therapy could be delivered by a lover). Their personality would be altered and they'd start making decisions in ways that play to the Machiavellian plans of the group that surreptitiously delivered gene therapy into their brains.
SALT LAKE CITY—The Intermountain West is renowned for the beauty of its towering mountains and high deserts, but according to new research from an investigator with the University of Utah Brain Institute the region's lofty altitudes significantly influence a deadly problem: the high prevalence of suicides in this part of the country.
In the Sept. 15, 2010, online edition of the American Journal of Psychiatry, Perry F. Renshaw, M.D., Ph.D., MBA, professor of psychiatry at the U School of Medicine and an investigator with Utah Science Technology and Research (USTAR) initiative, and colleagues report that the risk for suicide increases by nearly one-third at an altitude of 2,000 meters, or approximately 6,500 feet above sea level.
In the United States the Western states have the highest suicide rates. What's with Alaska? Vitamin D deficiency? Or just the bitter cold?
In 2006, the latest year for which national data was available, Montana, Idaho, Wyoming, Utah, Colorado, Nevada, New Mexico, Arizona, and Oregon accounted for nine of the 10 highest suicide rates in the country. Alaska also was in the top 10 in suicide rates.
The researchers analyzed data at the level of individual counties to reach their conclusion.
After analyzing data from a U.S. Centers for Disease Control and Prevention (CDC) database with information on 3,108 counties in the lower 48 states and District of Columbia, Renshaw and his colleagues from the University of Utah Brain Institute, Veteran Affairs Salt Lake City Health System, and Case Western Reserve University concluded that altitude is an independent risk factor for suicide, and that "this association may have arisen from the effects of metabolic stress associated with mild hypoxia (inadequate oxygen intake)" in people with mood disorders. In other words, people with problems such as depression might be at greater risk for suicide if they live at higher altitudes.
What I want to know: Does high altitude living also correlate with earlier onset of dementia or Alzheimer's Disease? Mild hypoxia has got to be bad for you.
What I also want to know: Does the link between altitude and suicide risk become greater with age as lung capacity declines? More hypoxia in old age and hence more suicide?
The pattern holds for South Korea as well.
To verify the study conclusions, Namkug Kim, Ph.D., the study's first author and a former post-doctoral fellow under Renshaw, conducted a similar data study in South Korea and found that the suicide rate in areas at 2,000 meters increased by 125 percent in that country.
The pattern might break down for Tibetans and other populations that are genetically adapted to high altitude living.
Yale researchers have discovered how a novel anti-depressant can take effect in hours, rather than the weeks or months usually required for most drugs currently on the market. The findings, described in the August 20 issue of the journal Science, should speed development of a safe and easy-to-administer form of the anti-depressant ketamine, which has already proven remarkably effective in treating severely depressed patients.
The Yale scientists found that, in rats, ketamine not only quickly improves depression-like behaviors but actually restores connections between brain cells damaged by chronic stress.
"It's like a magic drug—one dose can work rapidly and last for seven to 10 days," said Ronald Duman, professor of psychiatry and pharmacology at Yale and senior author of the study.
This reminds me of another recent study where ketamine caused amazingly rapid relief from bipolar disorder.
A single intravenous dose of the anesthetic agent ketamine appears to reduce symptoms of depression within 40 minutes among those with bipolar disorder who have not responded to other treatments, according to a report in the August issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
"Bipolar disorder is one of the most severe psychiatric disorders and ranks in the top 10 causes of medical disability worldwide," the authors write as background information in the article. About 4 percent of Americans will develop bipolar disorder in their lifetimes, and depressive symptoms dominate for most of the course of the illness. Several treatments for bipolar depression are currently approved, but some patients do not respond to these therapies despite adequate trials. In addition, existing treatments are associated with a lag of onset; most patients do not respond within the first week of therapy, resulting in considerable illness and increased suicide risk.
“We found that in a sample of young adults during a 15-year period, those who started out reporting high levels of depression gained weight at a faster rate than others in the study, but starting out overweight did not lead to changes in depression,” said UAB Assistant Professor of Sociology Belinda Needham, Ph.D.. The study appears in the June issue of the American Journal of Public Health.
“Our study is important because if you are interested in controlling obesity, and ultimately eliminating the risk of obesity-related diseases, then it makes sense to treat people’s depression,” said Needham, who teaches in the UAB Department of Sociology and Social Work. “It’s another reason to take depression seriously and not to think about it just in terms of mental health, but to also think about the physical consequences of mental health problems.”
One can easily imagine a number of mechanisms for how this would work. For example, depressed people are more lethargic, often sleep longer hours, and therefore burn fewer calories. Also, depressed people might seek out the pleasure of eating food as a temporary relief from the pain of living.
The fact that humans get depressed in the first place is interesting. One evolutionary purpose might be to help people store up food and burn less food during winter months. In other words, depression could be a milder version of hibernation. Dampen down activity once the crops are in and just eat and gain weight until spring. This might explain seasonal affective depression which comes on when the days are shorter.
Most anti-depressants show beneficial effects only after a few weeks. By contrast, scopolamine joins ketamine as a rapid depression lifter.
Philadelphia, PA, 1 March 2010 - Conventional antidepressant treatments generally require three to four weeks to become effective, thus the discovery of treatments with a more rapid onset is a major goal of biological psychiatry. The first drug found to produce rapid improvement in mood was the NMDA glutamate receptor antagonist, ketamine.
In a new issue of Biological Psychiatry, published by Elsevier, researchers from the National Institutes of Health report that another medication, scopolamine, also appears to produce replicable rapid improvement in mood. Scopolamine temporarily blocks the muscarinic cholinergic receptor, thought to be overactive in people suffering from depression.
For people with severe depression just getting it lifted in a few days could provide hope that a life of depression need not be a permanent state of affairs.
Drs. Wayne Drevets and Maura Furey recruited outpatients with major depressive disorder who were randomly assigned to receive placebo and then scopolamine treatment, or vice versa, in a double-blinded design so that neither the researchers nor the patients knew which treatment they were receiving.
"Scopolamine was found to reduce symptoms of depression within three days of the first administration. In fact, participants reported that they experienced relief from their symptoms by the morning after the first administration of drug," explained Dr. Furey. "Moreover, one-half of participants experienced full symptom remission by the end of the treatment period. Finally, participants remained well during a subsequent placebo period, indicating that the antidepressant effects persist for at least two weeks in the absence of further treatment."
An analysis of randomized trials indicates that compared with placebo, the magnitude of benefit of antidepressant medications varies with the severity of depressive symptoms, and may provide little benefit for patients with mild or moderate depression, but appear to provide substantial benefit for patients with very severe depression, according to an article in the January 6 issue of JAMA.
Antidepressant medications (ADM) are the current standard of treatment for major depressive disorder (MDD), but there is little evidence that they have a specific pharmacological effect relative to placebo for patients with less severe depression, according to background information in the article.
On the bright side the mildly depressed aren't as urgently in need of help. Best that a drug does the most good for those severely depressed.
The authors found that the efficacy of ADM treatment for depression varied considerably, depending on symptom severity. “True drug effects (an advantage of ADM over placebo) were nonexistent to negligible among depressed patients with mild, moderate, and even severe baseline symptoms, whereas they were large for patients with very severe symptoms.”
MADISON — A new study at the University of Wisconsin-Madison suggests that depressed patients are unable to sustain activity in brain areas related to positive emotion.
The study challenges previous notions that individuals with depression show less brain activity in areas associated with positive emotion. Instead, the new data suggest similar initial levels of activity, but an inability to sustain them over time. The new work was reported online this week (Dec. 21) in the Proceedings of the National Academy of Sciences.
"Anhedonia, the inability to experience pleasure in things normally rewarding, is a cardinal symptom of depression," explains UW-Madison graduate student Aaron Heller, who led the project. "Scientists have generally thought that anhedonia is associated with a general reduction of activity in brain areas thought to be important for positive emotion and reward. In fact, we found that depressed patients showed normal levels of activity early on in the experiment. However, towards the end of the experiment, those levels of activity dropped off precipitously.
"Those depressed subjects who were better able to sustain activity in brain regions related to positive emotion and reward also reported higher levels of positive emotion in their everyday experience," Heller continues.
If depressed people were to receive more rewards would a higher frequency of rewards keep the positive emotion areas lit up? Or do these areas lack energy or chemicals needed to maintain higher activity levels? Do these brain areas fatigue? Or do other brain areas send them signals that dampen down the positive emotions?
COLUMBUS, Ohio – While depression is often linked to negative thoughts and emotions, a new study suggests the real problem may be a failure to appreciate positive experiences.
Researchers at Ohio State University found that depressed and non-depressed people were about equal in their ability to learn negative information that was presented to them.
But depressed people weren’t nearly as successful at learning positive information as were their non-depressed counterparts.
If you are interested in the details of this study then click thru. But what to do about it? This makes me flash on Life Of Brian and an important message: Always Look On The Bright Side of Life
I picture Jack Nicholson saying "you can't handle the truth" and Tom Cruise says "I got the genetic profile that says I can". Of course, maybe he doesn't. Post-traumatic stress disorder (PTSD) has a big genetic component for vulnerability to it after a great shock.
Earthquakes have aftershocks — not just the geological kind but the mental kind as well. Just like veterans of war, earthquake survivors can experience post-traumatic stress disorder, depression and anxiety.
In 1988, a massive earthquake in Armenia killed 17,000 people and destroyed nearly half the town of Gumri. Now, in the first multigenerational study of its kind, UCLA researchers studying survivors of that catastrophe have discovered that vulnerability to PTSD, anxiety and depression runs in families.
Armen Goenjian, a research psychiatrist in the UCLA Department of Psychiatry and Biobehavioral Sciences, and colleagues studied 200 participants from 12 multigenerational families exposed to the earthquake. Participants suffered from varying degrees of the disorders. The researchers found that 41 percent of the variation of PTSD symptoms was due to genetic factors and that 61 percent of the variation of depressive symptoms and 66 percent of anxiety symptoms were attributable to genetics. Further, they found that a large proportion of the genetic liabilities for the disorders were shared.
The research appears in the December issue of the journal Psychiatric Genetics.
These genetic factors that contribute to PTSD will eventually be identified. I see this as a problematic turn of events for police departments, fire departments, militaries, and other organizations that put people in dangerous situations. People whose genetic profiles show they will get messed up permanently from getting into firefights are better off not getting into combat. Of course, combat poses other threats like getting one's leg or arm blown off that are going leave you seriously messed up or dead regardless of your genetic inheritance. But the total average cost of going into combat will be higher for people who have a genetic predisposition to get PTSD.
On the bright side, a discovery of which genes contribute to PTSD risk will help in the development of drugs that will prevent PTSD. That'll work better for combat troops than for people who get into natural disasters since the combat troops can start taking the protective drugs before they go into battle. Whereas many types of disasters like tornadoes and volcanic eruptions can come on too quickly for people to start using drugs in advance to prevent mental changes that'll permanently scar them.
Puppets, your environment yanks your chain down in winter if you have a mutation in your eye pigment that lets light intensity play puppeteer with your emotions. A mutation of a photopigment of the eye might contribute to the development of the form of depression called seasonal affective disorder (SAD).
A new study indicates that SAD may be linked to a genetic mutation in the eye that makes a SAD patient less sensitive to light.
"These individuals may require brighter light levels to maintain normal functioning during the winter months," said Ignacio Provencio, a University of Virginia biology professor who studies the genetics of the body's biological clock, or circadian rhythms.
Provencio and his colleagues have discovered that melanopsin, a photopigment gene in the eye, may play a role in causing SAD in people with a recently discovered mutation.
"We believe that the mutation could contribute to increasing the amount of light needed for normal functioning during winter for people with SAD," Provencio said. "Lack of adequate light may be a trigger for SAD, but not the only explanation for the disorder."
This mutation might not by itself cause winter depression. But it seems to boost the chances of SAD.
The study was conducted with several other institutions, including the National Institute of Mental Health. It involved 220 participants, 130 of whom had been diagnosed with SAD and 90 participants with no history of mental illness.
Using a genetics test, the study authors found that seven of the 220 participants carried two copies of the mutation that may be a factor in causing SAD, and, strikingly, all seven belonged to the SAD group.
"While a person diagnosed with SAD does not necessarily carry the melanopsin mutation, what we found strongly indicates that people who carry the mutation could very well be diagnosed with SAD," Provencio said. "We think that if an individual has two copies of this gene, he or she has a reasonable chance of having the disorder."
The researchers found that a person with two copies of the gene is five times more likely to have symptoms of SAD than a person without the mutation.
These results only strengthen the argument for using a bright light box to treat SAD. Do you get depressed in winter? Think about getting a light box to wake up to in the morning.
Methyl groups placed on the DNA backbone of our genomes regulate gene expression. People who commit suicide have more methylation on a gene that produces a receptor for a neurotransmitter. Maybe a reduction in the amount of that neurotransmitter receptor causes depression and suicide.
There are an increasing variety of epigenetic mechanisms that have been described, including the regulation of gene function via the methylation or demethylation of DNA. The study by Drs. Michael Poulter and Hymie Anisman and colleagues in the October 15th issue of Biological Psychiatry illustrates one exciting new example in this area of research, an epigenetic study of depression/suicide. The researchers compared the brain tissues of those who had major depressive disorder and committed suicide to those from a control group who died suddenly, from heart attacks and other causes.
They found the genome in people who have committed suicide as a result of major depression was being chemically modified by a process that is normally involved in regulating cell development. As Poulter explains, "We have about 40,000 genes in every cell and the only reason a skin cell becomes a skin cell as opposed to a heart cell is because only a fraction of the genes are being expressed, and the other genes not being expressed are shut down by this genetic process of DNA methylation." The rate of methylation in the suicide brains was found to be nearly ten times that of the control group, and the gene being shut down was a neurotransmitter receptor that plays a major role in regulating behavior. John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, comments, "This is exciting new evidence that genetic and environmental factors may interact to produce specific and long-lasting modifications in brain circuits. Further, these modifications may shape the course of one's life in extremely important ways, including increasing the risk for major depressive disorder and perhaps suicide."
So if people in the future build a time machine, go back to 1991, and demethylate Kurt Cobain's DNA then suddenly we'll have more Nirvana albums. If you notice a change in the number of Nirvana albums you can attribute the change to time travelers.
Two years ago, Zarate and colleagues reported that ketamine, which targets the brain chemical glutamate, can lift depressions in just hours, instead of the weeks it takes conventional antidepressants, which work through the brain chemical serotonin. Evidence suggests that glutamate likely acts closer to the source of the depression than serotonin, and is not dependant on slower mechanisms, such as the synthesis of new neurons.
Earlier imaging studies with conventional antidepressants had hinted that increased activity of the mood-regulating hub, called the anterior cingulate cortex (ACC), signals a better response.
To find out if ACC activity might also forecast response to glutamate-targeting medications, the NIMH researchers imaged the brain activity of 11 depressed patients and 11 healthy participants, using magnetoencephalography (MEG). This imaging technology can non-invasively detect brain electromagnetic activity lasting only milliseconds – the speed of communications in neural circuits – whereas other functional brain imaging techniques can only capture activity that last seconds or minutes, and some involve radiation exposure.
This precise timing enabled the MEG scanner to capture the brain's split-second responses to rapidly flashing pictures of fearful faces, a task known to activate the ACC. While healthy participants' ACC activity dropped off as they quickly habituated to the faces, patients' ACC activity showed an opposite trend. The more robust this increase, the more symptoms improved just four hours after a patient received a single infusion of ketamine.
"The ACC may be slow to respond, but not completely impaired, in patients who respond to ketamine," explained Cornwell.
While ketamine can lift depression very rapidly for some people ketamine does have side effects, especially at higher doses. Don't use it recklessly.
Here's another report on our role as puppets with genes as the puppeteers. A group of researchers has published a paper in Nature Genetics offering evidence that genes involved in calcium ion flow across nerve membranes might contribute to bipolar depression.
The largest genetic analysis of its kind to date for bipolar disorder has implicated machinery involved in the balance of sodium and calcium in brain cells. Researchers supported in part by the National Institute of Mental Health, part of the National Institutes of Health, found an association between the disorder and variation in two genes that make components of channels that manage the flow of the elements into and out of cells, including neurons.
"A neuron's excitability – whether it will fire – hinges on this delicate equilibrium," explained Pamela Sklar, M.D., Ph.D., of Massachusetts General Hospital (MGH) and the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard, who led the research. "Finding statistically robust associations linked to two proteins that may be involved in regulating such ion channels – and that are also thought to be targets of drugs used to clinically to treat bipolar disorder – is astonishing."
People with bipolar disorder have my sympathy. Until researchers can come up with better treatments for it a lot of people have to go thru a lot of suffering. Nature is a sadistic bastard.
Since researchers think many genes contribute to bipolar it is hard to pick out the genes that contribute from all the background noise. But the genes they suspect are involved in key functions done by neurons and the researchers had a large sample of bipolar and non-bipolar study participants for which they did DNA tests.
To boost their odds, Sklar and colleagues pooled data from the latter two previously published and one new study of their own. They also added additional samples from the STEP-BD study and Scottish and Irish families, and controls from the NIMH Genetics Repository. After examining about 1.8 million sites of genetic variation in 10,596 people – including 4,387 with bipolar disorder – the researchers found the two genes showing the strongest association among 14 disorder-associated chromosomal regions.
Variation in a gene called Ankyrin 3 (ANK3) showed the strongest association with bipolar disorder. The ANK3 protein is strategically located in the first part of neuronal extensions called axons and is part of the cellular machinery that decides whether a neuron will fire. Co-authors of the paper had shown last year in mouse brain that lithium, the most common medication for preventing bipolar disorder episodes, reduces expression of ANK3.
Variation in a calcium channel gene found in the brain showed the second strongest association with bipolar disorder. This CACNA1C protein similarly regulates the influx and outflow of calcium and is the site of interaction for a hypertension medication that has also been used in the treatment of bipolar disorder.
The fact that a hypertension medication works against bipolar is interesting though not unprecedented. Lots of drugs are originally developed for one reason and found to have benefits for other disorders.
Note that they looked at 1.8 million sites of known genetic variation. Ongoing projects aimed at identifying all sites where we genetically differ make this sort of study possible where it wouldn't have been possible even 5 years ago. Faster and cheaper ways to do DNA testing are going to cause a massive torrent of brain gene discoveries over the next 5 years.
Some people marvel at the supposed miracle of childbirth. Others claim that our bodies are evidence of intelligent design. Some arguments against the theory of evolution point to the eye as a supposedly amazing piece of engineering (even though a look at the cell layers that light has to pass thru to reach the rods and cones seem like poor engineering to me - to say nothing about widespread problems with sight and focus). Another example of poor human body engineering comes from a new report from the Medical College of Georgia that after giving birth to babies many women suffer from post partum depression as a result of an after effect of chemical signals that the fetus sent to ensure an adequate blood supply.
That crosstalk allows the mother's blood to flow out of the uterine artery and get just a single cell layer away from the fetus' blood, says Dr. Puttur D. Prasad, biochemist in the Medical College of Georgia School of Medicine.
That controlled exchange between the blood of mother and fetus is courtesy of the placenta regulating levels of serotonin, a neurotransmitter commonly associated with depression. But platelets that enable blood clotting also secrete serotonin which prompts platelets to aggregate and the placenta to want to get rid of it.
The same serotonic transporter mechanism that works in neurons gets used to control placental blood flow. This dual use of a component causes huge amounts of mental pain among new mothers.
"If there were no proper control here, blood leaving the mother's blood vessel would trigger release of serotonin, platelets would aggregate, vessels constrict and the fetus wouldn't get what it needs," says Dr. Prasad. An MCG research team led by Dr. Vadivel Ganapathy first reported evidence of serotonin transporter gene expression in the placenta back in 1989 in the Journal of Biological Chemistry. Now they know the gene plays an important role in the crosstalk that forestalls clotting until after birth.
If you were going to intelligently design an organism would you reuse the same transporter mechanism both for brain functioning and for feeding a developing fetus? The interleukin-1 beta that is used to stimulate serotonin transporters in the uterus also travels to the brain and as a side effect causes neurons all over the brain to make too many serotonin transporters.
When the fetus and placenta are gone, blood continues flowing from the mother's uterine artery until platelets move in to stop it, Dr. Prasad explains. Serotonin levels begin to rise and interact with receptors on the smooth muscle of the uterus. This stimulates production of interleukin-1 beta which the MCG researchers found regulates expression of serotonin-hoarding transporters. Interleukin-1 beta gets in the mother's bloodstream, crosses the blood brain barrier and creates more serotonin transporters on the neurons when they are not needed.
This lousy design is a product of evolution. The alternative is that the design is the product of an intelligent designer who isn't intelligent enough to make a really good design. It worked well enough to propagate the species and so the genetic sequences that code for this mechanism survived.
Until interleukin-1 beta levels normalize, there's too little communication between serotonergic neurons and moms get the blues, says Dr. Prassad. "We believe that 80 percent of women experience postpartum blues because of this effect of interleukin-1 beta. If our hypothesis holds true, lowering interleukin-1 beta levels may be a better treatment option." He notes that while serotonin reuptake inhibitors, commonly used for depression, work well in these women, transferring the drug to the baby during nursing can be problematic.
A woman pines to have a baby for many years. She finally finds Mr. Right, they work hard and save up enough money, get a decent house, they try to start a pregnancy, out comes the baby, and then due to poor genetic design of regulatory systems she spends weeks or even months suffering depression. Natural selection also brings us many genetic diseases too. Nature is cruel.
Major depressive disorder is a common and complex condition that impacts about 15% of the population of the United States, yet very little is known about the mechanisms behind the psychiatric disorder. What is known is that there are clinical parallels between depressive symptoms and the symptoms of certain inflammatory disorders.
In findings published electronically in Molecular Psychiatry, researchers from University of Miami found polymorphisms in inflammation-related genes that are associated with susceptibility to major depression and antidepressant response. Two genes critical for T-cell function in the immune system have been associated with susceptibility for major depressive disorder and antidepressant treatment response: PSMB4 (proteasome beta 4 subunit) and TBX21 (T-bet).
The study population was made up of 284 depressed Mexican-Americans from Los Angeles who were already enrolled in a pharmacogenetic study of antidepressant treatment response. The control group was made up of 331 individuals from the same community.
Does the immune system attack the brain to cause depression? Or perhaps T cells are involved in signalling systems that cause neural stem cells to replicate and form new neurons.
The point about depressive symptoms and inflammatory disorders is important as well. Possibly vitamin D and/or omega 3 fatty acids might dampen inflammation and thereby help to treat depression.
Some forms of a gene that controls the body's response to stress hormones appear to protect adults who were abused in childhood from depression, psychiatrists have found.
People who had been abused as children and who carried the most protective forms of the gene, called corticotropin-releasing hormone receptor one (CRHR1), had markedly lower measures of depression, compared with people with less protective forms, the researchers found in a recent study.
The findings could guide doctors in finding new ways to treat depression in people who were abused as children, says senior author Kerry Ressler, MD, PhD, assistant professor of psychiatry and behavioral sciences at Emory University School of Medicine.
This is not the first report of genetic variations of brain genes that affect how well developing children handle abuse and adversity. Previous research found that children who carry the low MAOA activity allele (MAOA-L) and who are abused demonstrate more aggressive and violent behavior as adults.
Some kids have genes that let them shrug off all sorts of abuse and basically keep trucking. Other kids aren't so lucky. Those latter kids become problems for the rest of us too. Violence prone adults pose a danger to whoever they come into contact with.
Early identification of kids with genetic vulnerabilities might some day get used to guide more aggressive state intervention into bad families. You can imagine social workers arguing to take a kid out of an abusive home more quickly if the has genes that make him or her vulnerable to permanent and problematic behavioral and personality alterations.
Once offspring genetic engineering becomes possible we can't assume parents should avoid giving offspring these genetic variations that make kids more vulnerable to abuse. There might be benefits to these alleles in more benign environments. Though I see a more compelling argument for discouraging the passing along of these alleles if either prospective parent has a genetic profile and brain scans that suggests he or she is likely to abuse kids.
Older men with lower free testosterone levels in their blood appear to have higher prevalence of depression, according to a report in the March issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
Depression affects between 2 percent and 5 percent of the population at any given time, according to background information in the article. Women are more likely to be depressed than men until age 65, when sex differences almost disappear. Several studies have suggested that sex hormones might be responsible for this phenomenon.
Osvaldo P. Almeida, M.D., Ph.D., F.R.A.N.Z.C.P., of the University of Western Australia, Perth, and colleagues studied 3,987 men age 71 to 89 years. Between 2001 and 2004, the men completed a questionnaire reporting information about demographics and health history. They underwent testing for depression and cognitive (thinking, learning and memory) difficulties, and information about physical health conditions was obtained from a short survey and an Australian health database. The researchers collected blood samples from the participants and recorded levels of total testosterone and free testosterone, which is not bound to proteins.
A total of 203 of the participants (5.1 percent) met criteria for depression; these men had significantly lower total and free testosterone levels then men who were not depressed. After controlling for other factors—such as education level, body mass index and cognitive scores—men in the lowest quintile (20 percent) of free testosterone concentration had three times the odds of having depression compared to men in the highest quintile.
I really want testosterone replacement to yield a net benefit in physical and mental health because I really want ways to slow up and delay the various deleterious effects of aging. We need prospective studies of its effects to know for sure.
A Plos Medicine meta-analysis of studes on 4 antidepressant drugs finds no benefit from their use for all but the most severely depressed. The 4 drugs are the selective serotonin reuptake inhibitors (SSRI) fluoxetine (Prozac), paroxetine (Seroxat, Paxil), venlafaxine (Effexor), and nefazodone (Serzone). Do these big name SSRIs really fail to help people?
What Did the Researchers Do and Find?
The researchers obtained data on all the clinical trials submitted to the FDA for the licensing of fluoxetine, venlafaxine, nefazodone, and paroxetine. They then used meta-analytic techniques to investigate whether the initial severity of depression affected the HRSD improvement scores for the drug and placebo groups in these trials. They confirmed first that the overall effect of these new generation of antidepressants was below the recommended criteria for clinical significance. Then they showed that there was virtually no difference in the improvement scores for drug and placebo in patients with moderate depression and only a small and clinically insignificant difference among patients with very severe depression. The difference in improvement between the antidepressant and placebo reached clinical significance, however, in patients with initial HRSD scores of more than 28—that is, in the most severely depressed patients. Additional analyses indicated that the apparent clinical effectiveness of the antidepressants among these most severely depressed patients reflected a decreased responsiveness to placebo rather than an increased responsiveness to antidepressants.
So then why do some people swear by the benefits they've gotten from Prozac and Paxil? Are they just lucky they started taking an SSRI just as their depression was about to lift? Or do SSRIs lift depression for short periods of time?
The researchers analyzed data from 35 clinical trials.
The dataset comprised 35 clinical trials (five of fluoxetine, six of venlafaxine, eight of nefazodone, and 16 of paroxetine) involving 5,133 patients, 3,292 of whom had been randomized to medication and 1,841 of whom had been randomized to placebo.
If you click through on the link you can read the full original paper. Plos Medicine is an open source scientific journal.
The SSRI drug makers find fault with this paper and claim it does not use more recent studies. However, the researchers who did this analysis claim they used the least biased among the available studies.
The more troubling question concerns what kind of data is appropriate for analyzing a drug's efficacy. The companies are correct in claiming there is far more data available on SSRI drugs now than there was 10 or 20 years ago. But Kirsch maintains that the results he and colleagues reviewed make up "the only data set we have that is not biased."
One point: The problem is that SSRIs seem to deliver a benefit but one not much better than placebos. Well, doctors can't get away with prescribing a placebo. So they might as well get their patients on SSRIs and get that beneficial placebo effect.
PITTSBURGH, Jan. 3 – Bright light therapy can ease bipolar depression in some patients, according to a study published in the journal Bipolar Disorders. Researchers from the University of Pittsburgh School of Medicine’s Western Psychiatric Institute and Clinic studied nine women with bipolar disorder to examine the effects of light therapy in the morning or at midday on mood symptoms.
“There are limited effective treatments for the depressive phase of bipolar disorder,” said Dorothy Sit, M.D., assistant professor of psychiatry and the study’s first author. “While there are treatments that are effective for mania, the major problem is the depression, which can linger so long that it never really goes away.”
In this study, women with bipolar depression were given light boxes and instructed on how to use them at home. The women used the light boxes daily for two-week stretches of 15, 30 and 45 minutes. Some patients responded extremely well to the light therapy, and their symptoms of depression disappeared. The responders to light therapy stayed on the light therapy for an additional three or four months. Four patients received morning light, and five used their light boxes at midday. Participants also continued to take their prescribed medications throughout the study period.
“Three of the women who received morning light initially developed what we call a mixed state, with symptoms of depression and mania that occur all at once – racing thoughts, irritability, sleeplessness, anxiety and low mood,” said Dr. Sit. “But when another group began with midday light therapy, we found a much more stable response.”
I am curious to know whether lights with high UVB would work better due to increased vitamin D synthesis and an anti-depressant effect from vitamin D. Also, light causes some endorphin release that might account for these results.
There's been controversy on whether those who take selective serotonin reuptake inhibitor (SSRI) antidepressants are at greater risk of thinking suicidal thoughts. It is a difficult effect to tease out since people depressed enough to take SSRIs are already at greater risk of depression and some of them probably become less at risk of suicide because SSRIs brighten their mood. But maybe others react to SSRIs by becoming more suicidal. Well, genetic testing might have allowed some scientists to discover who will be at greater risk of suicidal thoughts as a result of taking an SSRI. People taking the SSRI drug citalopram who have certain variants of glutamate receptor genes are at much higher risk of suicide thoughts.
Specific variations in two genes are linked to suicidal thinking that sometimes occurs in people taking the most commonly prescribed class of antidepressants, according to a large study led by scientists at the National Institutes of Health’s (NIH) National Institute of Mental Health (NIMH). Depending on the particular mix inherited, these versions increased the likelihood of such thoughts from 2- to15-fold, the study found. About 1 percent of adult patients were deemed to be at high genetic risk, 41 percent at elevated risk and 58 percent at lower risk.
If confirmed, the findings may hold promise for genetic testing, as more such markers are identified.
The "If confirmed" is important. They looked at many genes and so a false positive just by chance is possible.
Risk increased proportionately if a participant had two, as opposed to just one of the suspect versions. Both genes code for components of the brain’s glutamate chemical messenger system, which recent studies suggest is involved in the antidepressant response.
Overall, about 6 percent of 1,915 patients with depression reported that they started to have suicidal thoughts while taking an antidepressant. This rate soared to 36 percent among the few patients with both of the suspect gene versions; 59 percent of the patients who had suicidal thoughts had at least one of the versions.
Francis J. McMahon, M.D., Gonzalo Laje, M.D., NIMH Mood and Anxiety Disorders Program, and colleagues at the National Human Genome Research Institute (NHGRI), Mount Sinai School of Medicine, and the University of Texas Southwestern Medical Center, report on their findings in the October, 2007 issue of The American Journal of Psychiatry.
We are well within 10 years of widespread use of genetic testing when choosing between drugs and making other treatment decisions. Clinical practice will take a big turn when genetic tests can predict which drugs will cause which side effects in each patient.
The researchers found that certain versions of two genes that code for glutamate receptors – the receiving stations for the neurotransmitter’s chemical messages – were more prevalent in patients with suicidal thinking. How the newly identified versions affect the workings of glutamate receptors to confer increased risk remains to be discovered. It’s also not yet known whether the findings generalize to other antidepressants.
One percent of the study participants had a version of the kainate receptor gene, GRIK2, that increased the odds for suicidal thinking more than 8-fold. Forty-one percent of participants had a version of the AMPA receptor gene, GRIA3, that raised the odds nearly 2-fold. About one-half of 1 percent of participants had both high risk gene versions, boosting the odds 15 fold – but this was the case for only 11 participants, of whom four developed suicidal thinking.
The size of the observed effects makes it likely that their finding is real. It is the sort of result that could be confirmed pretty quickly with sufficient funding.
A discovery like this one is not just useful for making drug choices. It also provides clues about what causes people to become suicidal. A better understanding of the mechanisms which cause suicidal thoughts will lead to ways to stop suicidal thoughts.
In what may be the first study to use brain imaging to look at the neural circuits involved in emotional control in patients with depression, researchers at the University of Wisconsin-Madison have found that brains of people with clinical depression react very differently than those of healthy people when trying to cope with negative situations.
Depressed people and normal people were monitored for how their brains responded to negative pictures when they were told to try to imagine positive outcomes.
Participants were asked to consciously work to decrease their emotional responses to some of the negative images, using techniques such as envisioning a more positive outcome than the one implied or by imagining the situation was acted out rather than real.
"We ask them to reframe the content of what they're seeing," rather than divert their attention or distract themselves with unrelated thoughts, Johnstone says. "We hope to engage cognitive areas in re-interpreting the emotional content of a stimulus — to either increase or decrease its impact."
In both healthy and depressed individuals, they found that such efforts increased brain activity in prefrontal cortical areas known to help regulate the emotional centers of the brain, as they expected.
The big difference was seen in the reactions of the emotional centers themselves, including a small almond-shaped structure called the amygdala located deep in the brain.
In nondepressed individuals, high levels of regulatory activity correlated with low activity in the emotional response centers - in effect, the healthy subjects' efforts successfully quelled their emotional responses. In depressed patients, however, high levels of activity in the amygdala and other emotional centers persisted despite intense activity in the regulatory regions.
This finding suggests that healthy people are able to effectively regulate their negative emotions through conscious effort, but that the necessary neural circuits are dysfunctional in many patients with depression, the researchers say.
Attempts by depressed people to suppress their negative responses actually backfire. They think even more negative thoughts.
The difference becomes even more pronounced the harder the patients try.
"Those [healthy] individuals putting more cognitive effort into it are getting a bigger payoff in terms of decreasing activation in these emotional centers," Johnstone explains. "In the depressed individuals, you find the exact opposite relationship - it seems the more effort they put in, the more activation there is in the amygdala."
Depressed people should avoid negative images and negative information. Maybe depressed people shouldn't watch the news. I also wonder whether distraction could work as a strategy against depression. Thinking about something negative? Watch a comedy movie or TV show. Or play a game that is very engrossing. Just leave no room for the negative thoughts.
What the depressed people of the world need: A happy news channel. All happy, all the time. But that might not work. The depressed might resent happy news.
“I met a girl who sang the blues, And I asked her for some happy news; But she just smiled and turned away”.
The selective serotonin reuptake inhibitor (SSRI ) antidepressant drugs (e.g. Paxil, Zoloft, Prozac) are known to stimulate replication of brain stem cells to produce new neurons. The delay in the antidepressant action of SSRIs might be due to the delay before they start causing substantial neuron creation. Well, exercise has an antidepressant effect and perhaps not coincidentally exercise also causes new neuron generation in the brain.
Exercise has a similar effect to antidepressants on depression. This has been shown by previous research. Now Astrid Bjørnebekk at Karolinska Institutet has explained how this can happen: exercise stimulates the production of new brain cells.
In a series of scientific reports, she has searched for the underlying biological mechanisms that explain why exercise can be a form of therapy for depression and has also compared it with pharmacological treatment with an SSRI drug.
The experiment studies were conducted on rats. The results show that both exercise and antidepressants increase the formation of new cells in an area of the brain that is important to memory and learning. Astrid Bjørnebekk’s studies confirm previous research results, and she proposes a model to explain how exercise can have an antidepressant effect in mild to moderately severe depression. Her study also shows that exercise is a very good complement to medicines.
“What is interesting is that the effect of antidepressant therapy can be greatly strengthened by external environmental factors,” she says.
There's a practical question here for people suffering from depression: Do exercise and SSRI add up together to an antidepressant effect that is greater than either of them alone?
What I want to know: How does exercise stimulate brain cell growth? Blood pressure changes? Increased oxygen into the brain? Other?
Also, does exercise increase memory formation even in the non-depressed?
Treatment of mice with a ‘friendly’ bacteria, normally found in the soil, altered their behavior in a way similar to that produced by antidepressant drugs, reports research published in the latest issue of Neuroscience.
These findings, identified by researchers at the University of Bristol and colleagues at University College London, aid the understanding of why an imbalance in the immune system leaves some individuals vulnerable to mood disorders like depression.
Dr Chris Lowry, lead author on the paper from Bristol University, said: "These studies help us understand how the body communicates with the brain and why a healthy immune system is important for maintaining mental health. They also leave us wondering if we shouldn’t all be spending more time playing in the dirt."
This discovery was an accident. Dr. Lowry was experimenting with the use of M. vaccae to treat lung cancer and found that the mood and cognitive function of lung cancer patients were also boosted by the M. vaccae vaccination.
Interest in the project arose after human cancer patients being treated with the bacteria Mycobacterium vaccae unexpectedly reported increases in their quality of life. Lowry and his colleagues reasoned that this effect could be caused by activation of neurons in the brain that contained serotonin.
When the team looked closely at the brains of mice, they found that treatment with M. vaccae activated a group of neurons that produce the brain chemical serotonin. The lack of serotonin in the brain is thought to cause depression in people, thus M. vaccae’s effects on the behavior of mice may be due to increasing the release of serotonin in parts of the brain that regulate mood.
As expected, cytokine levels rose. They then looked directly in their animals' brains for the effect of those cytokines.
Cytokines actually act on sensory nerves that run to the brain from organs such as the heart and the lungs. That action stimulates a brain structure called the dorsal raphe nucleus. It was this nucleus that Dr Lowry focused on. He found a group of cells within it that connect directly to the limbic system, the brain's emotion-generating area. These cells release serotonin into the limbic system in response to sensory-nerve stimulation.
The consequence of that release is stress-free mice. Dr Lowry was able to measure their stress by dropping them into a tiny swimming pool. Previous research has shown that unstressed mice enjoy swimming, while stressed ones do not. His mice swam around enthusiastically.
It is worth noting that this work fits in a larger context: the argument (known as the hygiene hypothesis) that humans are suffering more auto-immune diseases such as allergies and asthma due to a lack of exposure to bacteria, digestive tract worms (which might be key to prevention and treatment of inflammatory bowel disease- also see here), and other pathogens. According to this theory people living in modern clean industrialized societies with purified water, refrigerators, automated farms, flush toilets, warm showers, and hand soap the immune system doesn't get exposed to pathogens it is designed to handle. The immune system is designed to work properly only in the presence of those pathogens. So it goes awry and starts attacking things it ought not attack. Considerable amounts of evidence (see here and here) supports the idea that getting dirty might be good for you.
This latest result suggests that other functions of the immune system (e.g. interactions with the nervous system) aren't getting sufficiently stimulated in modern society. So maybe we are suffering from an epidemic of depression (and other mental illnesses while we are at it?) due to excessive purity of our environments. Well, I'm sure glad as a kid that I liked to go out in the yard and build dirt castles and mud walls. City kids didn't have that advantage.
What I'd like to know: Do kids with dogs have a lower risk of getting depressed when they grow up? Do kids who grow up on pig and cow farms similarly have lower risks of adult depression? Also, does depression vary by country due to different vaccination regimes used in different countries?
The larger lesson: We are not in our ancestral environments which we are genetically adapted to. So all bets are off. We need to develop technologies that adapt us to our new environments. Speaking of which: In addition to vaccinations that give our immune systems needed exercise we also need to reshape our work environments to give ourselves more exercise in cubicle land. My suggestion: move exercise bicycles and steppers into meeting rooms and training rooms so that we can get exercise while getting training and giving project status reports.