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.
This seems an important observation:
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 kids have genes that make them better able to handle abuse with fewer long term repercussions.
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.
Would testosterone replacement with age lower the risk of depression?
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?
Vaccination of mice with Mycobacterium vaccae (M. vaccae) boosts their mood.
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.
Vaccination of mice with M. vaccae boosts immune system cytokines and the mice acted less stressed.
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.