• The Gut, Microbes & Mental/Emotional Health: Infected with Insanity

    From 23x@21:1/5 to All on Sat Apr 1 04:12:55 2017
    On Friday, April 26, 2013 at 7:32:57 AM UTC-5, 23x wrote:
    Scientific American published a great article this year on depression
    and the microbial link as a possible cause.

    http://www.sciam.com/article.cfm?id=infected-with-insanity&print=true Scientific American Mind - April 17, 2008

    Infected with Insanity: Could Microbes Cause Mental Illness?

    Viruses or bacteria may be at the root of schizophrenia and other
    disorders

    By Melinda Wenner

    Schizophrenia is a devastating illness. One percent of the world's
    population suffers from its symptoms of hallucinations, psychosis and impaired cognitive ability. The disease destroys relationships and
    renders many of its sufferers unable to hold down a job. What could
    cause such frightening damage to the brain? According to a growing
    body of research, the culprit is surprising: the flu.

    If you are skeptical, you are not alone. Being condemned to a lifetime
    of harsh antipsychotic drugs seems a far cry from a runny nose and
    fever. And yet studies have repeatedly linked schizophrenia to
    prenatal infections with influenza virus and other microbes, showing
    that the children of mothers who suffer these infections during
    pregnancy are more likely to be diagnosed with schizophrenia later in
    life. In 2006 scientists at Columbia University asserted that up to
    one fifth of all schizophrenia cases are caused by prenatal
    infections.

    Doctors have known for many years that microbes such as syphilis and Streptococcus can, if left untreated, lead to serious psychiatric
    problems. Now a growing number of scientists are proposing that
    microbes are to blame for several mental illnesses once thought to
    have neurological or psychological defects at their roots. The
    strongest evidence pertains to schizophrenia, but autism, bipolar
    disorder and obsessive-compulsive disorder have also been linked to bacterial, viral or parasitic infections in utero, in childhood or in maturity. Some of these infections can directly affect the brain,
    whereas others might trigger immune reactions that interfere with
    brain development or perhaps even attack our own brain cells in an
    autoimmune mistake.

    As scientists tease out the link between infections and psychiatric disorders, they anticipate opening the door to a new world of
    preventive measures. In the most immediate cases, a simple vaccine or
    regimen of antimicrobial drugs could rid the body of an infection
    before it damages the brain. And if our immune system is responsible,
    we might be able to develop drugs that stifle the effect of the immune response in the brain. The bottom line is, the more we know about the
    complex roots of mental illness, the better we can fight it.

    What Causes Mental Illness?
    In 1896 Scientific American published an editorial entitled "Is
    Insanity Due to a Microbe?" The question seemed logical, given that
    microbes were starting to be implicated in other diseases. In the
    editorial, two doctors described how they had injected cerebrospinal
    fluid of mentally ill patients into rabbits, which later got sick. The doctors concluded that "certain forms of insanity" could be caused by infectious agents, "similar to typhoid, diphtheria and others."

    But when Freudian psychoanalysis became popular in the 1930s, the idea
    was more or less put to rest. Then, in the 1950s, the discovery of DNA
    as hereditary material sparked a rising interest in genetics as a
    cause of illness, including mental disorders. Several papers reported
    a clear hereditary component to diseases such as schizophrenia, but
    genes were obviously not the whole story—as a number of studies have
    found, the identical twin of someone with schizophrenia has only about
    a one-in-two chance of developing schizophrenia himself.

    Certain environmental influences therefore probably interact with
    genes to trigger mental illness in a person with a genetic
    predisposition. Scientists began investigating everything from diet
    and lifestyle to parental nurturing and geographical location. In 1973
    E. Fuller Torrey, now a research psychiatrist at the Stanley Medical
    Research Institute in Chevy Chase, Md., published an article in the
    British journal Lancet that revived an idea that had been set aside
    for decades—could microbial infection cause mental illness?

    For the next 20 years, a few rogue scientists dominated the field,
    searching for connections between infections and psychiatric disorders—
    and the closer they looked, the more they found.

    The most compelling evidence is for schizophrenia. More than 200
    studies have suggested that schizophrenia occurs between 5 and 8
    percent more frequently than average in children born in the winter or spring. Scientists realized that viruses, which are most prevalent in
    the cold, dry winter months, could be one of the factors influencing
    this correlation.

    In 2004 Alan S. Brown, a psychiatrist at Columbia University, analyzed
    blood samples collected from 1959 through 1966 from 189 pregnant
    women, 64 of whom had later given birth to children who became
    schizophrenic. The women had had their blood drawn multiple times
    during pregnancy, allowing Brown and his colleagues to compare if and
    when the women had been exposed to the flu. "We showed that if [flu] infection occurred in the early to middle part of pregnancy, the risk
    of schizophrenia was increased three times," Brown explains. "For first-trimester exposure, it was increased seven times."

    Brown had also found in a 2001 study that children born to mothers who
    were exposed to the viral infection rubella, known as German measles,
    during the 1964 U.S. epidemic were 10 times more likely than other
    children to develop schizophrenia. Most people today are vaccinated
    against rubella during childhood, so the risk from this infection is
    now negligible. But Brown also showed a link between schizophrenia and Toxoplasma gondii, a single-celled parasite that infects about 40
    percent of the human population through contaminated water and
    uncooked meat. One of his studies suggests that if T. gondii antibodies —the human immune system's soldier cells that are a sure sign of
    ongoing or previous infection—are elevated in a mother's blood, her
    child is 2.5 times more likely than other children to develop
    schizophrenia.

    Although the case is strongest for schizophrenia, prenatal infections
    with rubella and several types of herpes have been linked less
    conclusively with psychiatric disorders, including autism, bipolar
    disorder and even Alzheimer's disease. To date, most of the
    correlations found between infections and psychiatric conditions are
    just that—correlations. There is no conclusive evidence that
    infections actually cause these diseases; it could be, for example,
    that carrying the genes for mental illness makes a person more likely
    to behave in a way that exposes him or her to a virus.

    But animal studies lend powerful support to the idea that prenatal
    infections can affect an offspring's brain. In 2003 California
    Institute of Technology biologist Paul H. Patterson showed that mice
    born to mothers infected with flu during gestation are much more
    fearful than normal mice, reluctant to explore novel objects and
    interact with other mice. Neural development also appears to be
    disrupted in these animals: postmortem investigation reveals vast
    differences in the distribution of their neurons.

    As the evidence mounts, many experts are beginning to think that a
    causal link indeed exists between prenatal infections and psychiatric disorders. Now a new question arises: What exactly are these
    infections doing to the fetal brain?

    The Immune Factor
    Although a developing fetus is protected by the placenta—the organ
    that transfers nutrients and waste between mother and fetus and
    prevents their blood from mixing—some microbes can cross this hurdle.
    T. gondii has this ability during its initial, or acute, infection of
    a pregnant woman. If an acute infection during early pregnancy is left untreated, it can cause severe birth defects or miscarriage. But the
    picture is less clear for acute infections in late pregnancy and
    dormant infections, in which the parasite hibernates quietly in the
    body and does not cross the placenta. Brown's antibody study suggests
    that these types of infections, once thought to be harmless, may lead
    to schizophrenia.

    T. gondii is also one of the few microbes that can cross the blood-
    brain barrier, a protective membrane separating brain cells from the
    rest of the body. Once in the brain, T. gondii affects its hosts'
    behavior. Infected rats and mice lose their fear of cats, making the
    rodents more likely to approach and be eaten by a cat, which is in the parasite's best interest—it can reproduce only in a feline. In people,
    T. gondii appears to subtly alter personality, making its hosts more
    neurotic and insecure and making men more cautious and women more kind
    and openhearted.

    The parasite probably instigates these behavioral changes by affecting
    the levels of certain brain chemicals. One study, for example, found
    that T. gondii increases the production of dopamine, an important neurotransmitter involved in a variety of brain processes, including
    motor activity, sleep, attention and reward. In a fetus, changes in
    dopamine levels can wreak havoc on normal brain development, and
    scientists have long known that schizophrenia is associated with an overabundance of dopamine in specific parts of the brain.

    But a dormant T. gondii infection, which may also be correlated with
    an increased risk of schizophrenia in the fetus, does not cross the
    placenta and therefore cannot directly affect the fetal brain. The
    influenza link is equally difficult to understand, because flu does
    not usually infect the fetus. Something else, then, may be at play.

    Some studies suggest that infections per se are not responsible for disrupting brain development; rather the body's immune response to
    infection affects the nervous system and does the damage. "When the
    immune system becomes activated, it can influence the functioning of
    the brain and, in turn, emotional and behavioral responses," explains Christopher L. Coe, a psychologist at the University of Wisconsin–
    Madison who studies the effects of psychological and environmental
    factors on the immune system.

    For example, recall how you typically feel the day before you come
    down with the flu. "You just don't feel right—you're more achy, you
    lose your appetite, you have a sense of fatigue," Coe says. It is not
    the flu making you feel that way—it is your immune response to it.
    "You're feeling cytokines," he says, referring to the small molecules produced by many cell types, including immune cells, for signaling
    purposes.

    Cytokines are produced in large numbers during infection, but their
    functions are not limited to the immune system—they are also important
    for brain development. When scientists culture neurons in the lab and
    then add cytokines to them, the neurons do not grow properly. "We know
    that high levels of cytokines interfere with growth and connections of neurons," Coe says. "A maternal infection—could that affect the
    immature brain in a way that sets the stage for mental illness?"

    It is possible, according to Coe; a pregnant mother's immune response
    may affect the way the placenta functions. The placenta's job is to
    pass hormones and nutrients to the fetus, but when the mother's body
    is fighting an infection the placenta likely behaves slightly
    differently. In some cases, it may prompt the fetus to produce its own cytokines; in other cases, the mother's cytokines will cross the
    placenta themselves. "There's sort of a reverberation, a harmonic—so
    as the mother is responding, it causes the baby to respond, even
    though there's no virus there," Coe explains.

    Bolstering the idea that cytokines play a key role are a number of
    studies showing that the levels of certain cytokines, such as one
    called interleukin-8, were markedly increased in the blood of mothers
    who gave birth to schizophrenic children, based on blood samples taken
    from pregnant women decades ago and the psychiatric profiles of their
    adult children. Genetic research has uncovered two genes associated
    with schizophrenia that are also involved in cytokine function, and
    animal research has lent support as well. Patterson of Caltech
    recently performed an experiment in which he injected pregnant mice
    not with a flu virus but with a dose of synthetic double-stranded RNA. Although this molecule of viral genetic material does not behave like
    a virus on its own, it is recognized as foreign by the body, eliciting
    an immune response without other infection-related effects. He found
    that the mice born of mothers injected with RNA behaved exactly like
    the offspring of flu-infected mothers—suggesting that the immune
    response, not the virus, is what actually affects the brain.

    Defense on the Offense
    The immune system may inadvertently harm the brain in another way, too—
    and not only in a fetus. Although current scientific evidence most
    strongly links mental illness to prenatal infections, many researchers
    are also investigating the possibility that childhood or even adult infections could cause psychiatric conditions by triggering an
    autoimmune reaction. Similar to the way the body attacks insulin-
    producing pancreas cells in type 1 diabetes, certain infections may
    trick the immune system into attacking brain cells.

    One such infection may result from Streptococcus, the same organism
    that causes strep throat. In 1998 doctors who were performing long-
    term studies of children who had obsessive-compulsive disorder (OCD)
    noticed that a small percentage of the children had suddenly developed
    OCD and a tic disorder following an infection with group A beta-
    hemolytic Streptococcus. Typical OCD will "just kind of come on
    gradually," says Susan E. Swedo, a senior neuroscience investigator at
    the National Institute of Mental Health. "But with these kids, it was
    24 to 36 hours between absolutely no symptoms and peak." In other
    words, these children literally woke up one day with OCD or serious
    tics.

    Swedo and her colleagues named the new mental disorder PANDAS, for
    pediatric autoimmune neuropsychiatric disorders associated with
    streptococcal infections. They believe PANDAS develops because the
    immune system begins attacking the brain after infection. The
    Streptococcus bacterium displays certain proteins on its surface that resemble proteins made by humans—a strategy that helps the bacterium
    evade detection by its host. Eventually, however, the body discovers
    the bacterium and attacks it. In that process of defense, the body
    also may begin attacking its own proteins. Some studies have found
    antibrain antibodies in PANDAS ­patients, and other studies have found temporal associations between a strep diagnosis and OCD onset.

    Other research, however, has failed to replicate these findings, and
    PANDAS is still a highly controversial diagnosis. Many experts doubt
    that such a clear cause-and-effect relation exists between strep
    infection and OCD. "We feel very strongly that the data support that infections will make tics worse but not cause them," says neurologist
    and pediatrician Harvey Singer of Johns Hopkins University. In 2005
    Singer and his colleagues analyzed blood samples from similar numbers
    of PANDAS patients and healthy people and did not find any major
    antibody differences between the two groups.

    Although PANDAS remains a subject of debate, many scientists consider
    it an important piece of the puzzle. Whether through an auto­immune
    reaction or the disruption of fetal brain development, if the immune
    system, rather than the infections themselves, is to blame for infection-related mental illness, it would surely simplify the
    problem. It would also explain why so many different infections seem
    to be implicated in mental illness. Flu, rubella, strep, herpes, T. gondii—these infections do quite different things to our bodies, yes.
    But they do have us in common.

    Stopping Illness before It Starts
    Researchers hope that as they continue to unravel the complex causes
    of mental illness, they will also keep moving closer to the ultimate
    prize: a cure. "The most important thing, if you want to deal with
    mental disorders, is to prevent them from happening in the first
    place," Columbia's Brown says. If infections do play a causal role,
    then we have a number of new solutions at our fingertips. "I think
    that this may just be the tip of the iceberg," he says.

    Even the small body of work that now exists could have immediate
    policy implications. The Centers for Disease Control and Prevention
    currently recommend that all pregnant women get flu shots—a dangerous proposition if immune response, rather than infection itself, is
    responsible for harming the fetal brain. "I don't think they have
    considered this risk. In fact, I know they haven't considered this
    risk," Patterson says, referring to the CDC. "If you take it seriously
    and vaccinate everybody, then what's going to happen?" Researchers
    cannot yet predict how often a prenatal immune response might lead to
    fetal brain damage, but even if it happens less than 1 percent of the
    time, vaccinating an entire population of pregnant women could affect thousands of children.

    Scientists also hope these new insights will help them develop
    preventive drug regimens, even perhaps using medications that exist
    today. A handful of studies have suggested that antipsychotic drugs
    have subtle effects on the immune system; Ina Weiner, a psychologist
    at Tel Aviv University, took this idea one step further. She wondered
    whether antipsychotics might be able to prevent schizophrenia—not just treat some of its symptoms. As Weiner explained at the 2007 conference
    of the International Brain Research Organization, she exposed mice in
    utero to an immune chemical that caused many of them to develop
    symptoms and brain abnormalities resembling schizophrenia's effects in humans. As in humans, the mice showed early signs of cognitive decline
    around the age of puberty, before developing full-blown schizophrenia. Administering antipsychotic medication as soon as these early symptoms appeared not only prevented future schizophrenic behavior but also
    protected the brain from the physical changes, such as a shrinking hippocampus, that accompany schizophrenia.

    Future drugs and vaccines may target the infections directly or go
    after the immune system, controlling its interference with the
    developing brain or preventing an autoimmune attack on brain cells.
    "There are many, many things that can be done," Brown says—the more we learn about the impact of infections on the brain, the better we will
    be able to prevent the damage that leads to mental illness. Last
    century scientists cured a broad range of physical diseases caused by infections; many hope that the 21st century will bring cures for the infections ailing our minds.


    Read More:
    http://curezone.com/forums/am.asp?i=1277847


    II

    --- SoupGate-Win32 v1.05
    * Origin: fsxNet Usenet Gateway (21:1/5)