Main article: Managing mental symptoms
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The existence of a blood-brain barrier has been historically touted as a reason why microbes could not possibly have caused any number of neurological diseases. However, with the accumulation of additional evidence, this concept has progressively lost meaning. An increasing number of studies show microbes persist in the brain and affect health.
Many chronic mental diseases are inflammatory conditions. As such, it seems like they are driven by the same pathogenesis as the rest of the body. This means that an activated immune response on an immunostimulatory therapy such as the Marshall Protocol will elicit mental symptoms.
This article presents a broad overview of the role microbes may play in causing and driving mental and neurological conditions. However, the Knowledge Base contains more in-depth articles on the following mental and neurological diseases and symptoms:
When patients on the MP kill bacterial pathogens, they experience a reaction called immunopathology. Immunopathology is an increase in one's present symptoms of Th1 inflammation, or a return of previous Th1 inflammatory symptoms, that is caused largely by cytokines generated by the immune response and endotoxins released from dying bacteria.
Like physical symptoms, mental symptoms such as anxiety, depression, cognitive dysfunctionThe loss of intellectual functions such as reasoning; memory loss; and other neurological abilities that is severe enough to interfere with daily functioning. (brain fogThe loss of intellectual functions such as reasoning; memory loss; and other neurological abilities that is severe enough to interfere with daily functioning.), insomnia and apathy are exacerbated during effective treatment with the MP.
Doctors should understand is that in the case of nearly every patient, immunopathology occurs in the brain. This means that during much of the treatment, patients are not thinking properly and have psychological issues. These mental reactions should not cause doctors to question the stability of the patient, but instead it should be understood that every patient will experience a certain level of confusion, anxiety and neurological symptoms while on the MP.
Greg Blaney, MD
At least one early study has suggested that olmesartan is neuroprotective. A 2002 in vitro study by Iwasaki et al. found that olmesartan improved regrowth of neurons in cultures of ventral spinal cord. On this basis, the team concluded that olmesartan has promise in treating diseases that involve degeneration and death of motor neurons, such as motor neuropathy and amyotrophic lateral sclerosis.1)
Main article: Managing mental symptoms
The symptoms of mental immmunopathology include apathy, sluggishness, cognitive dysfunction (brain fog), feeling paralyzed by misery, anxiety and depression. Managing these symptoms of microbial die-off is a challenge, particularly when those symptoms are mental. For one, mental immunopathology is difficult to recognize as such.
There are variety of ways to limit the discomfort of mental symptoms on the Marshall Protocol. These include restricting light, taking antidepressants or anti-anxiety medications, and seeking out social and faimly support. Patients have also reported that a proper attitude, if not always cheerful, attitude has allowed them to do the MP safely and effectively.
The existence of a blood-brain barrier has been historically touted as a reason why microbes could not possibly have caused any number of neurological diseases. However, with the accumulation of additional evidence, this concept has progressively lost meaning.
A range of bacteria and bacterial toxins… establish intimate interactions with endothelial cells [cells that comprise the membrane], triggering inflammatory responses and coagulation processes and modifying endothelial cell plasma membranes and junctions to adhere to their surfaces and then invade, cross and even disrupt the endothelial barrier.
E. Lemichez et al., Breaking the wall: targeting of the endothelium by pathogenic bacteria 4)
One prominent example of a microbe that passes the blood-brain barrier is Borrelia.5)
According to John Bienenstock of McMaster University, “Bacteria and bacterial products can clearly have an effect on the brain and pathways leading to the brain” while Knight, Gordon, and Turnbaugh have concluded the following:
One of the striking features of a variety of neuropsychiatric diseases (e.g., affective disorders) is their variance, with differences observed across individuals in terms of their susceptibility, in the combination of systems that are disturbed, and in the therapeutic and adverse responses to various medications. [We put forth] the possibility that the microbiome represents a source of this observed variance.
A. Gonzalez, The mind-body-microbial continuum6)
The following offers the evidence to support such statements:
Other evidence includes:
Infection and inflammation lead to changes in mood and cognition. Although the “classic” sickness behavior syndrome, involving fatigue, social withdrawal, and loss of appetites are most familiar, other emotional responses accompany immune activation, including anxiety. Recent studies have shown that gastrointestinal bacterial infections lead to enhanced anxiety-like behavior in mice. The bacteria-induced signal is most likely carried by vagal sensory neurons, and occurs early on (within 6h) during the infection. These signals induce evidence of activation in brain regions that integrate viscerosensory information with mood, and potentiate activation in brain regions established as key players in fear and anxiety.
L.E. Goehler et al.21)
The 100 trillion bacteria which together make up the intestinal microbiome are engaged in all the complex interactions with each other and the local tissue and in a balanced manner maintain normal homeostasis. They synthesize a vast array of biologically and neuroactive molecules including an almost complete array of neurotransmitters such as GABA, and through fermentation, a panoply of short chain fatty acids all of which have known and unknown effects on the nervous system. The direct and indirect effects of the intestinal microbiome on the intestinal epithelium, the local mucosal immune system and their cytokines, as well as the enteric nervous system, conspire to affect the afferent neuronal pathways to the brain. In turn, through complex interactional effects upon the HPA axis and especially central nervous system target structures affected by tractus solitarius activation in the brain stem, increasing evidence is pointing towards an influence by the intestinal microbiota upon cognition and mood.22)
Collectively, the human gut microbiome contributes 36% of the small molecules that are found in human blood.23)
The surprisingly high compositional variation in gut bacteria across individuals stands in stark contrast to the small amount of genetic diversity uncovered in the sequencing of our human genomes.24) Differences in our microbial communities may thus be one of the most important factors in differences in the metabolites that individuals extract from similar diets.
Related article: Psychosomatic explanations for disease
Sigmund Freud and Jean-Martin Charcot were born 150 years ago, but their ideas about the effect of the subconscious on disease continue to resonate in the scientific community.25) Freud and colleagues argued that unconscious mental processes such as sublimated rage could manifest as physical symptoms. However, with the advent of superior technology, one by one, many diseases once supposed to be caused by psychological stress have since been attributed to other factors including infections.
According to the Marshall PathogenesisA description for how chronic inflammatory diseases originate and develop., chronic fatigue syndrome, multiple chemical sensitivity and other chronic inflammatory diseases are likely caused by pathogens, yet many physicians consider these diseases to be “medically unexplained.” Medically unexplained diseases are widely prevalent26) but at the same time have few discernible markers or objectively measurable symptoms. While a lot of Freudian ideas have fallen out of favor, one legacy remains: difficult-to-explain diseases are still routinely attributed to psychological causes. The process by which patients supposedly manifest psychological problems as a disease has been named and renamed, classified and reclassified: hysteria, psychosomatic disorder, somatoform disorder, conversion disorder, functional disorder, etc. In each of these diagnoses, however, the stated origin of disease is unchanged: symptoms that cannot be explained are ultimately “all in a patient's head.”
While there is no denying the existence of some sort of “mind-body connection,” there is minimal compelling evidence that as the 19th century Swiss physician Georg W. Groddeck claimed: “Illness has a purpose; it has to resolve the conflict, to repress it, or to prevent what is already repressed from entering consciousness.”27) Despite the stark absence of evidence supporting these views, it is not unusual to read papers describing how patients with long-term so-called psychological illnesses may be subconsciously manifesting them, because it would allow them to have more “care, attention, disengagement, or even financial benefits.”28) Nor, is it uncommon for new theories to spring up along these lines. In one example, a 2008 continuing medical education publication taught physicians that when a celebrity becomes ill, healthy people are suggestible enough to develop long-term illnesses consistent with the celebrity's descriptions of their conditions. Such claims are recklessly speculative, harming patients and stalling needed research.
Treating patients who complain of so-called medically unexplained symptoms with cognitive behavioral therapy or, in the case of chronic fatigue syndrome, graded exercise therapy, may do more harm than good.29) The emergence of metagenomic technologies offers a more sophisticated set of tools for detecting and characterizing microbes in these disease states. Perhaps it is only the use of this technology that will finally relegate the notion of patient as attention-seeking victim to historical relic.
I have nooooooooo incentive but yet I don't feel depressed. I just feel like my brain has shut down. Also, I am having more difficulty finding the right words. Been having trouble sleeping lately.
Sometimes (when I talk faster than my brain is working) I stutter. I never used to stutter and have always been a good speaker. Sometimes I will stop what I'm saying mid-sentence because I forget what I was saying or the effort of completing the sentence or thought (by finding the right words and putting things in the right sequence) just seems too exhausting. I often will start talking and then say “oh never mind.” This irritates people after a while.
This teacher explained how the amygdala part of the brain is like the “guard shack” that everything has to get past before it is processed by the rest of the brain. And if the amygdala is on heightened alert, then we “forget to act like ourselves.”
So, if we are in “threat mode” we will act uncharacteristically immature emotionally. We will be responding to others in a self-preservation orientation, when usually we are more than happy to be considerate of others (along with other more mature behaviors).
I'm at 3.5 years on the MP and frankly cannot believe some of the changes in my mind…. I know that there is still a long way to go, but some of the clarity of mind and equanimity I experience now… it's just astonishing.
And I have tried many of the other 'options' before the MP (for my anxiety and depression) - CBT, psychoanalysis, antidepressants, meditation. All except psychoanalysis definitely gave some benefit. But when I compare them to what I am experiencing now, I would describe them more as management tools and giving symptomatic relief.
What I am experiencing now through the MP absolutely different. I could not conceive of this state of mind before, that it could exist. It is tricky because it is like trying to describe colour to someone who is blind. I read posts like this (i.e. the one I'm writing now) when I was sicker and was cynical and doubtful. I doubt I would have believed it if I hadn't gone through it myself.
The candy is definitely multiplying for me.
Keep hanging in there!
Eur J Neurosci. 2010 Jul;32(2):298-309. doi: 10.1111/j.1460-9568.2010.07349.x. Epub 2010 Jul 14. Mechanisms underlying autoimmune synaptic encephalitis leading to disorders of memory, behavior and cognition: insights from molecular, cellular and synaptic studies. Moscato EH, Jain A, Peng X, Hughes EG, Dalmau J, Balice-Gordon RJ. Source
Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6074, USA. Abstract Recently, several novel, potentially lethal and treatment-responsive syndromes that affect hippocampal and cortical function have been shown to be associated with auto-antibodies against synaptic antigens, notably glutamate or GABA-B receptors. Patients with these auto-antibodies, sometimes associated with teratomas and other neoplasms, present with psychiatric symptoms, seizures, memory deficits and decreased levels of consciousness. These symptoms often improve dramatically after immunotherapy or tumor resection. Here we review studies of the cellular and synaptic effects of these antibodies in hippocampal neurons in vitro and preliminary work in rodent models. Our work suggests that patient antibodies lead to rapid and reversible removal of neurotransmitter receptors from synaptic sites, leading to changes in synaptic and circuit function that in turn are likely to lead to behavioral deficits. We also discuss several of the many questions raised by these and related disorders. Determining the mechanisms underlying these novel anti-neurotransmitter receptor encephalopathies will provide insights into the cellular and synaptic bases of the memory and cognitive deficits that are hallmarks of these disorders, and potentially suggest avenues for therapeutic intervention. © The Authors (2010). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd. PMID: 20646055
Coughs and sneezes spread mind diseases
06 November 2004, Janet Ginsburg, Newscientist.com, Magazine issue 2472
IT WAS hell on earth. “I was in a concentration camp. I could smell the burning bodies,” recalls Stephanie Diers. But it was 1975, the second world war was long over, and Diers was in Martinez, California, thousands of miles from Auschwitz. The 19-year-old was locked up, but in a mental ward.
Diers's psychotic break was just the latest in a string of illnesses that had plagued her and puzzled her parents for the better part of a decade. No one could figure out what had happened to the bright little girl who loved riding horses and playing in the woods. Her list of ailments was as baffling as it was extensive: headaches, dizziness, fatigue, pain in her teeth, tingling in her toes, sore throats, flu-like illnesses, chest pains, pains in her spleen and liver, poor balance, sensitivity to light and sound, memory lapses. And now psychosis.
After six months in hospital, Diers was released and struggled on with her life, eventually earning a college degree and working as a teacher. But it would take another 14 years of serial illness before any of her doctors thought to test for Lyme disease, a tick-borne illness identified in the late 1970s.
Like its distant cousin syphilis, Lyme is caused by corkscrew-shaped bacteria called spirochaetes that are able to burrow into tissue, including the brain. There they can lie dormant and harmless for months, even years. But once active, they can stir up a devil's brew of symptoms, including conditions that match the clinical diagnoses for schizophrenia, bipolar disorder and depression.
Diers, of course, tested positive, and was put on a long course of antibiotics. “I had so many psychiatrists and psychologists tell me it was all in my head,” she says. They just didn't know how right they were.
Borrelia burgdorferi, the Lyme bacterium, is now widely accepted as a cause of psychiatric disease. And in recent years several other bugs have come to light that are able to trigger symptoms of mental illness, ranging from behavioural problems to depression and full-blown psychosis. In fact, so many potential “mind germs” have now been unearthed that some researchers are ready to challenge the conventional wisdom about the principal causes of mental illness.
When it comes to causes, genes have always been the prime suspects, with environmental triggers poorly understood and infectious disease an afterthought. Infectious disease is “maybe 5 per cent as important as genes”, claims Richard Straub of the Genes, Cognition, and Psychosis Program at the US National Institute of Mental Health in Bethesda, Maryland. Straub, who has identified several genes tentatively associated with schizophrenia, thinks that among environmental causes, peer groups, drug experiences and other social factors are far more significant targets for research.
But according to evolutionary biologist Paul Ewald of the University of Louisville in Kentucky, that ignores some obvious facts. “The biggest breakthrough in the history of psychiatry was recognising that syphilis causes insanity and that it can be prevented with antibiotics,” he says. The same mistake is being repeated today with Lyme disease and other infectious agents, Ewald believes.
If diagnosed quickly, before the bacterium gets a foothold, Lyme disease can be cured with a round of antibiotics. But spotting it can be tricky. Not everyone gets the telltale “bull's eye” rash and antibody tests can be unreliable, especially early on. That presents a dilemma for doctors concerned about overprescribing antibiotics. If they wait too long - as little as a few months after infection - the spirochaetes begin to attack the central nervous system with devastating consequences. This “late stage” Lyme is very hard to cure, often requiring months or years of antibiotics.
At Columbia University in New York, neuropsychiatrist Brian Fallon is in the middle of a series of studies designed to see what actually goes on inside the brains of chronic Lyme patients. One finding so far is that patients show significant reduction in blood flow in brain regions associated with memory and visuospatial organisation. Fallon has also looked at children, who are especially at risk because they tend to play outside, where the ticks are. He found significant cognitive and psychiatric problems in children who had been diagnosed late, on average a year after infection. They scored low on memory and perception tests and were also depressed, with some having suicidal thoughts.
In 2003, more than 21,000 cases of Lyme disease were reported to the Centers for Disease Control in Atlanta, Georgia, making it the most common vector-borne disease in the US. Yet as few as 1 in 10 cases are documented, so the true tally might be more than 200,000. And in 1996, another bacterium, Borrelia lonestari, which is carried by the lone star tick common throughout the American south, was linked to Lyme-like symptoms. So far there are no tests for it, so no case statistics.
Lyme isn't just a problem in the US. “You really have a pandemic,” says Raphael Stricker, a San Francisco physician specialising in chronic Lyme. “It's all over the US. It's all over Europe. It's in parts of Asia. It's everywhere.”
Beyond Lyme disease, the evidence linking infections to psychiatric disorders becomes a little more hazy. Ironically, though, some of the most tantalising clues are found in the very same data used to prove the case for genetic links: twin studies.
Identical twins, who have 100 per cent of their genes in common, are much more likely to both develop schizophrenia than are fraternal twins or full siblings, who share just 50 per cent of their genes. Clearly, then, genes are important. But the data is more complicated, explains Ewald. “People saw these associations without thinking about alternative explanations,” he says. For example, when one identical twin develops schizophrenia, half the time the other does not. If schizophrenia were strictly genetic, concordance (meaning both twins get sick) should be 100 per cent. This holds true even if many genes are involved in the disorder, as geneticists now believe.
But when the environment inside the womb is taken into account, the story begins to shift. Fetuses develop inside two porous sacs, the inner chorion and the outer amnion. Nearly 70 per cent of identical twins share a chorion, a feature that can be determined after birth by the presence of subtle physical traits such as mirror-image fingerprints. Those twin pairs are nearly six times as likely to be concordant for schizophrenia as identical twins with separate chorions.
Meanwhile, the concordance rate for non-identical twins is nearly twice that of full siblings, even though the genetic relationship is the same: 50 per cent. Fraternal twins rarely share sacs, but they do share a womb. That, says Ewald, points to an environmental factor - though not necessarily an infection.
To look for evidence that a prenatal infection could be linked to the development of schizophrenia years later, a team of Columbia University epidemiologists led by Ezra Susser and Alan Brown sifted through the medical records of 20,000 women who were pregnant in Alameda county, California, between 1959 and 1966. The women, all patients at Kaiser-Permanente, the largest healthcare provider in the region, were part of a massive child health and development study. But the real stroke of luck was that most of their children have remained in the Kaiser-Permanente system. “We could follow them right up to age 40,” says Susser.
The researchers first determined which children had been diagnosed with schizophrenia spectrum disorders. Then they tested their mothers' blood samples for antibodies to the strains of influenza virus that had been circulating during their pregnancies, and compared the results with blood tests from a set of matched controls - the mothers of mentally healthy children from the same Kaiser-Permanente group.
The results, which are published in the Archives of General Psychiatry (vol 61, p 774), are dramatic. Maternal exposure to flu during the first half of pregnancy tripled the child's risk of developing a schizophrenia spectrum disorder. “It's far higher than any single gene in terms of what we call relative risk,” says Brown.
Brown points out, however, that some of the healthy children's mothers were exposed to flu during the first half of pregnancy, too, so exposure doesn't guarantee schizophrenia. What's more, schizophrenia is rare, affecting just 1 per cent of the population. Still, if the results of the Columbia study can be duplicated, a significant number of cases - perhaps as many as 14 per cent, according to Brown - may turn out to be preventable.
So how might a virus cause schizophrenia? According to Paul Patterson at the California Institute of Technology in Pasadena, the virus may not be doing the damage directly. He injected pregnant mice with a molecular mimic of the flu virus, which generates an immune response without causing infection. Nevertheless, offspring mice developed behavioural abnormalities reminiscent of schizophrenia, suggesting that the stress of a maternal immune response alone may be enough to affect neurodevelopment.
More information on how viruses attack the brain is coming from work on Borna virus, which was first seen in horses in the late 1800s. Borna affects a number of bird and mammal species, including non-human primates, causing a broad range of movement and behaviour disorders. There are also tentative links to human psychiatric illnesses, most notably schizophrenia, bipolar disorder and depression, based largely on the presence of Borna virus antibodies in some patients' blood.
In rats infected with Borna in the lab, symptoms resemble autism, with delayed growth, learning disabilities and repetitive behaviours. And there are now some clues as to what the infection is doing to the brain. When rats are infected shortly after birth (the neurodevelopmental equivalent of a human prenatal infection), neurons critical for cognitive, emotional and motor development either die off or miss key developmental cues. If rats are infected during adolescence, when their brains are more developed, Borna appears to kill neurons both directly and through an overzealous immune response.
Yet another pathogen that has been linked to psychiatric conditions is the protozoan parasite Toxoplasma gondii. It infects everything from cats and cattle to sea otters and people. Human infection rates range from 15 per cent in the US to more than 80 per cent in some countries. Hundreds of millions of people have it, usually having caught it from undercooked meat or contact with cat faeces. Most of the time, toxo causes no more than a mild flu-like illness, but, like Lyme spirochaetes, the parasites can burrow into tissue and lie dormant for long periods of time.
Some studies have found that people with schizophrenia are three times as likely as the general population to be infected with toxo (New Scientist, 26 October 2002, p 41). Meanwhile, using the same Kaiser-Permanente data as in the influenza study, Susser and Brown have found a correlation between high maternal levels of anti-toxo antibodies and schizophrenia in the corresponding children. According to their calculations, toxo more than doubles the risk.
In the pantheon of mind-altering microbes, toxo is unique in its mission: it must alter the behaviour of its intermediate host, usually a rodent, to get itself back inside its reproductive host, a cat. In a series of experiments, Joanne Webster at the University of Oxford discovered that toxo-addled wild rats not only lost their natural fear of wandering into open spaces, but were actually attracted to cat smells. They practically delivered themselves for dinner.
Infected humans don't end up as cat food, but acute toxo can cause hallucinations and other psychotic behaviours. In fact, both rats and people may be tripping: studies from the 1950s and 60s suggest that toxo can trigger the production of LSD-like substances in the brain.
The most insidious mind germ of all could be an inside operator: a germ that behaves like a gene. Human endogenous retroviruses (HERVs) infect egg and sperm cells. Like genes, they are then copied into all the cells of the body, although they only become active under specific circumstances.
Virologist Robert Yolken at Johns Hopkins University in Baltimore has discovered one called HERV-W reproducing in the cerebrospinal fluid of some people with schizophrenia, but not in healthy controls. He suspects that a second, conventional pathogen, possibly a herpesvirus or Toxoplasma, may trigger HERV-W to switch on, and the combination somehow triggers symptoms. In a study published last year in The American Journal of Psychiatry (vol 160, p 2234), Yolken's team reported improvement in the symptoms of people with schizophrenia who were treated for cytomegalovirus, a common herpesvirus.
The idea that you can catch a mental illness from something as innocuous as a bug bite or a sneeze may seem the stuff of nightmares, but it also holds hope for new ways to fight back. For one thing, it suggests that treating mental illness can sometimes be as simple as tackling an underlying infection.
That's exactly what Borna researchers Liv Bode of the Robert KochAuthor of Koch's postulates, a set of rules for establishing a relationship between a causative microbe and a disease. Koch's belief that only one pathogens causes one disease has now been called into question as multiple postulates are increasingly considered out of date. Institute and Hans Ludwig at the Free University, both in Berlin, Germany, found in clinical trials of the antiviral drug amantadine. A majority of Borna-positive patients diagnosed with major depression or bipolar disorder showed significant improvement in as little as seven weeks on the drug.
There are also hints that some existing psychiatric drugs work because they eradicate infections. For example, Yolken reports that the antipsychotic haloperidol and the mood stabiliser valproic acid appear to inhibit the growth of Toxoplasma, at least in cell culture.
And for those of us lucky enough to be free from mental illness, there's a lesson to be learned, too. Good mental health may be as basic - and as cheap - as avoiding cat litter and undercooked meat, and checking for ticks.
Obsessive-compulsive sore throat?
It's not always infectious agents themselves that do the damage. More than a century ago doctors made the link between “strep throat” - a sore throat caused by the common bacterium Streptococcus - and the development of the heart condition rheumatic fever a few weeks later. The immune system gets confused, mistakes heart cells for bacteria, and attacks.
A similar autoimmune response seems to be causing behavioural problems ranging from Tourette-like tics and obsessive-compulsive disorder to attention-deficit hyperactivity disorder and anorexia. The syndrome, called PANDAS (Paediatric Autoimmune Neuropyschiatric Disorders Associated with Streptococcus), strikes about once in 1000 cases of strep infection.
PANDAS is a strep-induced autoimmune attack on an area of the brain called the basal ganglia, which helps control numerous behaviours. High levels of anti-strep antibodies have been linked to enlargement of the basal ganglia in PANDAS patients. As the levels go down, the brain recovers and symptoms fade away.
In an experiment at the National Institutes of Health in Maryland, researcher Susan Swedo removed antibodies from the blood plasma of 30 children with PANDAS. More than a year later, 80 per cent remained symptom-free.
Though PANDAS is technically a childhood condition, there are reports of adults with similar abrupt-onset behavioural problems. And a team from the UK's Institute of Child Health in London found that a PANDAS-like condition may be behind the mystery of von Economo's disease, the “sleepy sickness” that devastated thousands around the time of the 1918 flu pandemic (New Scientist, 18 October 2003, p 34). Of 20 contemporary patients with a similar illness, more than half had had a sore throat before developing the sickness, and 95 per cent tested positive for antibodies reactive against the basal ganglia.
Infectious Triggers of Mental Illness
Jill Neimark wrote an article in the 25th Anniversary Issue of Discover Magazine (Frontiers of Science) on infectious triggers of mental illness. It is out on the news stands now and will soon be on the Discover website at http://www.discover.com/
Diseases of the Mind
Bacteria, viruses and parasites may cause mental illnesses like depression and perhaps even autism and anorexia
By Janet Ginsburg Newsweek International
Dec. 1 issue - Olga Skipko has had the good fortune to live most of her adult life in the Polish village of Gruszki, in the heart of the Puszcza Bialowieska, one of Europe's most beautiful forests and home to wolves, lynxes and the endangered European bison. Unfortunately, the forest is also a breeding ground for disease-carrying ticks. Skipko, 49, thinks she was bitten about 10 years ago, when she began having the classic symptoms of Lyme borreliosis, a tickborne nervous-system disease: headaches and aching joints. She didn't get treatment until 1998. “I was treated with antibiotics and felt a bit better,” she says.
That was only the beginning of her troubles. A few years later, she began to forget things and her speaking grew labored. It got so bad that she had to quit her job in a nursery forest and check herself in to a psychiatric clinic. “I hope they will help me,” she says. “I promised my children that when I come back home, I will be able to do my favorite crosswords again.” Doctors ran a battery of tests and concluded that her mental problems were the advanced stage of the Lyme disease she had contracted years ago.
Scientists have long known that some diseases can cause behavioral problems. When penicillin was first used to treat syphilis, thousands of cured schizophrenics were released from mental asylums. Now, however, scientists have evidence that infections may play a far bigger role in mental illness than previously thought. They've linked cases of obsessive-compulsive disorder, bipolar disorder and schizophrenia to a variety of infectious agents, and they're investigating autism, Tourette's and anorexia as well. They're beginning to suspect that bad bugs may cause a great many other mental disorders, too. “The irony is that people talked about syphilis as the 'great imitator',” says University of Louisville biologist Paul Ewald, “but it may be the 'great illustrator'-a model for understanding the causes of chronic diseases.”
Mental illnesses constitute a large and growing portion of the world's health problems. According to the World Health Organization, depression is one of the most debilitating of diseases, on a par with paraplegia. Psychiatric illnesses make up more than 10 percent of the world's “disease burden” (a measure of how debilitating a disease is), and are expected to increase to 15 percent by 2020. Much of this may be the work of viruses, bacteria and parasites. Psychiatrist E. Fuller Torrey, of the Stanley Medical Research Institute in Maryland, has found from studying historical asylum records that hot spots-higher-than-normal incidences-of mental illness can shift, much like infectious-disease outbreaks, which lends credence to the notion that infectious agents play a big role. “Mental disorders are the major chronic recurrent disorders of youth in all developed countries,” says Harvard policy expert Ronald Kessler, who directs the WHO's mental-health surveys.
Perhaps the most well known disease that's been linked to mental disorders is Lyme disease, which is caused by the Borrelia burgdorferi germ. First identified in the mid-1970s among children near Lyme, Connecticut, the disease has long been known to cause nervous-system problems and achy joints if left untreated. Now scientists are finding that Lyme disease can also trigger a whole smorgasbord of psychiatric symptoms, including depression. One New York man (we'll call him Joe) found out firsthand how debilitating the disease can be. When he began having bouts of major depression back in 1992, he had forgotten all about the tick bite he had gotten four years earlier. He spent two years in a blur of antipsychotic drugs, mental institutions, jails and suicide attempts. On a hunch, a doctor at a psychiatric hospital in New Jersey had Joe tested for Lyme disease. After an intensive course of antibiotics, Joe's improvement was dramatic and immediate. “I started to have this fog lift,” he recalls. Still, he will probably have to be on psychotropic drugs for the rest of his life.
Some psychiatrists fret that there may be thousands of people suffering from Lyme-induced depression without knowing why. Not only is Lyme disease tricky to diagnose-not everybody gets the circular rash, and lab tests still aren't wholly reliable-it can take a decade or more for mental disorders to set in. The U.S. Centers for Disease Control says that nine out of 10 cases of Lyme diseases remain unreported. There are 15 species of borellias-making them the most common tickborne disease-producing bacteria in the world.
For its part, the parasite Toxoplasma gondii, which can be found in undercooked meat and cat feces, can lead to full-blown psychotic episodes. Some studies suggest that the parasite stimulates the production of a chemical similar to LSD, producing hallucinations and psychosis. Even when the parasite lies dormant in muscle and brain tissue, it can affect attention span and reaction time in otherwise healthy people. Researchers at Charles University in Prague have discovered that people who test positive have slightly slower-than-average reaction times and-possibly as a result-are almost three times as likely to have car accidents. That's a disturbing prospect, considering that the disease is so widespread: billions of people are thought to be infected.
Even a simple sore throat can lead to psychiatric problems. Few children avoid coming down with a streptococcus infection, also known as strep. Scientists now think that one in 1,000 strep sufferers also develops abrupt-onset obsessive-compulsive disorder (OCD) in a matter of weeks. Strep bacteria trigger OCD by igniting an overzealous response from the immune system, which attacks certain types of brain cells, causing inflammation. Symptoms generally die down after a few months but can flare up again, especially if there's another bout of strep, says Susan Swedo, a childhood-disease expert at the National Institutes of Health. The most effective treatment, still experimental, is to filter out the misbehaving antibodies from the blood. Best is to treat strep early on.
The specter of a depression germ or contagious obsessive-compulsive disorder is unnerving, but it also opens up many more treatment options-antibiotics, vaccines, checking for ticks. Geneticists believe that diseases may trigger the onset of inherited mental illnesses by activating key genes. Avoiding and treating infection may be just as important as the genes you inherit, and a whole lot easier to do something about.
With Joanna Kowalska In Warsaw
© 2005 Newsweek, Inc. © 2005 MSNBC.com
Neurological symptoms may include:
I guess the simple reply to the “science” behind these symptoms is that our brains, cranial nerves, spinal cord and nerves emerging from our cord; as well as peripheral nerves(the whole dang system) are infected with CWD organisms. I suspect there are a number of errant feedback loops and “short circuits” in our brains as well as primary nerve involvement. There is a neurologic syndrome caller Barre-Lieou that involves pinched or inflamed nerves in the cervical spine having effects on the rest of the system.
Some people have reported improvement with skilled osteopathic manipulation or prolotherapy if it is just a post whiplash type injury effecting the neck; but I feel the root of our problem is CWD infection. An MRI can not show cwd infection and can not cure you, but if expense is affordable it does rule out some possibilities like bulging disk and spinal stenosis (for peace of mind) But I feel the little beasties are most likely the problem.
Phase three continues to amaze me. I just went through a series of herxs in my upper spine that the best ways to describe them are very MS like. I had a lot of neuropathy and paralysis in my hands and my legs. I had no strength in my hands and my legs became real heavy and rigid feeling real difficult to walk. I've had this before but just not as bad and it always followed with a lot of joint pain in my legs and hips. This time it pretty much left my joints alone just mild joint pain which has been great.
I even had the lightning flashes and the spots of light that people with MS get and Major chronic fatigue for a couple days. This took a little over two weeks to run its course and I feel fine now. The best thing about it I was able to stay on the full dose of Phase Three meds the whole time.
That has been a long time coming and I'm excited to say that I've been able to stay at the full dose and get through a herxs. I could have slowed it down by lowering the Clind but I did not have to do.
My oldest sister has MS and she has had some of these very same symptoms over the years. It is so obvious once you start this protocol how all of these diseases are related. I came down with rheumatoid arthritis but one or two different species or just catching them in a different order and I could've had multiple sclerosis or Sarcoidosis.
I definitely feel like I'm running out of bacteria and my herxs are going to be background nuisance before too long. ~Ival
J Neuropsychiatry Clin Neurosci. 2011 Fall;23(1):90-7.The emerging link between autoimmune disorders and neuropsychiatric disease. Kayser MS, Dalmau J.
Department of Psychiatry, University of Pennsylvania, Philadelphia, PA 19104, USA. firstname.lastname@example.org Abstract Abnormal autoimmune activity has been implicated in a number of neuropsychiatric disorders. In this review, the authors discuss a newly recognized class of synaptic autoimmune encephalitides as well as behavioral and cognitive manifestations of systemic autoimmune diseases.
Infectious moods: Bugs that cause bizarre behaviour 13:53 12 January 2011 by Linda Geddes Magazine issue 2795. Subscribe and save Read more: “Infectious moods: How bugs control your mind” Sometimes it takes antibiotics, not a psychologist, to cure strange obsessions Sammy Maloney was a healthy, outgoing 12-year-old, who played in the school band, and liked nothing better than to dump his backpack after school and hang out with his friends in Kennebunkport, Maine. Then, in 2002, Sammy's personality began to change. “The first thing I noticed was that he was walking around the backyard with his eyes closed,” says Sammy's mother, Beth Maloney. “I asked him what he was doing, and he said he was memorising.” In rare cases streptococcus infections can cause severe personality changes (Image: Juergen Berger/SPL) The next day, Sammy was again walking with his eyes closed and would only use the back door. Then he progressed to holding his breath while doing it, only wearing certain coloured clothes, and refusing to allow the windows to be opened, or the lights to be switched off. “Every single day was a new behaviour,” says Beth. “We went from baseline to completely dysfunctional within a period of four to six weeks.” Sammy was diagnosed with obsessive compulsive disorder, and then Tourette's syndrome. When he continued to deteriorate, a friend suggested testing Sammy for streptococcus - a common childhood bacterial infection that usually causes no more than a sore throat. “By this point he was totally emaciated and he was covered with scabs from scratching himself,” says Beth. Sammy hadn't shown any signs of streptococcal infection, but it turned out he was infected. When doctors prescribed antibiotics, his symptoms began to improve. Within a few weeks he was playing board games with his brothers. “After six months of treatment, I knew that he would recover,” says Beth. Sammy remained on antibiotics for four years, as every time the dose was reduced he had a relapse. Now aged 20, Sammy has none of the compulsions that blighted his youth. Madeline Cunningham at the University of Oklahoma in Oklahoma City says that, although extreme, Sammy's story isn't that unusual. She has spent years investigating behavioural disorders linked to childhood streptococcal infection, including Tourette's syndrome, an OCD-like disorder called PANDAS, and the movement disorder Syndenham's chorea, which is associated with tics and an inability to control emotions. Cunningham has shown that, at least as far as Sydenham's chorea is concerned, antibodies against one group of streptococcal bacteria can bind to receptors in an area of the brain that controls movement. Here they mimic the effects of natural signalling molecules, triggering the ADVERTISEMENTrelease of the neurotransmitter dopamine, which may explain the tics and emotional problems experienced by children with the disorder (Autoimmunity, vol 39, p 21). Not every child with PANDAS has similar antibodies, but for those that do antibiotics or drugs that suppress the immune system are effective treatments, says Cunningham. Preliminary evidence also links such antibodies to Tourette's syndrome. Cunningham stresses that there is no evidence that vaccination can trigger disorders like PANDAS. “You're more likely to get this from not being immunised,” she says. Meanwhile, Betty Diamond of the Feinstein Institute for Medical Research in Manhasset, New York, has also shown that antibodies associated with the autoimmune disease lupus can get into the brain and kill neurons by binding to NMDA receptors. This might partly explain the mood changes and cognitive decline associated with the disease. Mouse studies suggest how behaviour is affected depends on what makes the blood-brain barrier leak, as well as on the antibodies themselves. When the barrier is compromised by inflammation, lupus-related antibodies damage the hippocampus, impairing memory. When the barrier is breached by stress hormones (adrenaline), the antibodies damage the amygdala, making individuals more fearful. The results were presented at a meeting of the American Association of Immunologists in Baltimore in May last year. “This could change the way we treat mental disorders forever,” says Cunningham, who thinks antibodies influence the behaviour even of apparently healthy individuals. “Your immune system develops based on what organisms it sees, and it could be that your brain does too.” Diamond agrees: “We have tonnes of antibodies even when we don't have clinical disease. I'm sure that some of these are having an effect on the brain.” Read more: “Infectious moods: How bugs control your mind” Linda Geddes is a New Scientist reporter based in London
Infectious moods: The happiness injection 13:55 12 January 2011 by Linda Geddes Magazine issue 2795. Subscribe and save The investigators could tell who had been injected with the bacteria because their whole attitude changed ADVERTISEMENT Read more: “Infectious moods: How bugs control your mind” Down in the dumps? A shot of friendly bacteria could give you the boost you need It was meant to be a new way to fight cancer. The idea was that injecting a certain bacterium into people would stimulate their immune systems to destroy tumours. Unfortunately, the treatment had little effect on the survival of the terminally ill lung cancer patients in the first trial. It did have one unexpected effect, though: those injected with the bacterium experienced a radical improvement in their mood and quality of life. A boost of serotonin (Image: Michael W. Davidson/SPL) “It was supposed to be a double-blind study, but the investigators could nearly always tell who was on the genuine treatment because their whole attitude, their demeanour, changed,” says Charles Akle, chair of Immodulon Therapeutics in London, UK. “They just looked better.” How can injecting a bacterium brighten someone's mood? We don't yet know all the details, but animal studies suggest that the immune response triggered by Mycobacterium vaccae causes neurons in the prefrontal cortex to release large amounts of serotonin, boosting mood and well- being (Neuroscience, vol 146, p 756). This might seem odd, given that immune stimulation can also lead to depression (see opposite), but our relationship with M. vaccae goes back a long way. Such “old friends” are thought to prime the immune system in interesting ways. “We think M. vaccae is inducing regulatory cells which will dampen down and terminate unwanted inflammatory responses,” says Graham Rook of the Royal Free and University College Medical School in London. Whatever the mechanism, the discovery adds to the growing evidence that bacteria affect our mind as well as our body. “Bacteria and bacterial products can clearly have an effect on the brain and pathways leading to the brain,” says Bienenstock. “There are quite a few papers now suggesting that you can influence behaviour, and that the microbiome has something to do withcortisol production, which are pretty hard-core, basic human reactions to stress and things like that.” In fact, Rook recently proposed that one reason depression is so prevalent in western countries is because people are no longer routinely exposed to organisms like M. vaccae during early life. The “hygiene hypothesis” was originally proposed to explain soaring rates of asthma and allergies, but Rook believes it could also be implicated in psychiatric disorders (Trends in Immunology, vol 29, p 150). So could M. vaccae be used to make people happy? It is much harder to get approval to inject live bacteria into people with depression than those with terminal cancer, so Immodulon's next trial will be in people with prostate cancer. If there is a strong mood-boosting effect again, the company may focus more on its potential for treating depression. Ultimately, if the precise mechanism can be uncovered, it might be possible to develop drugs that mimic the bacterium's effect.
already covered this above
CytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system.-Associated Emotional and Cognitive Disturbances in Humans
In summary, sufficient evidence is now available to indicate that pro-inflammatory cytokines released in the periphery by activated monocytes and macrophages activate peripheral afferent nerves to induce the synthesis and release of pro-inflammatory cytokines in the brain.
Centrally produced cytokines then act on key neural circuits that regulate sleep patterns and other sickness behavior responses, including body temperature, metabolism, psychological status and behavior. Brain cytokines induced in key neural circuits mediate the brain-controlled responses of the host to infection.
Glucocorticoids released by the adrenal cortex in response to the hypothalamic effects of pro-inflammatory cytokines then regulate the expression and actions of cytokines in the periphery. Similarly, SNS pathways activated in response to hypothalamic effects of pro-inflammatory cytokines also regulate synthesis and release of peripheral cytokines.
These two pathways, the HPA axis and the SNS, act via negative-feedback regulation to dampen production of proinflammatory and promote expression of anti-inflammatory cytokines and to restore immune system homeostasis as the infection is cleared or the injury has healed.
The existence of an interactive brain-cytokine system that alters sleep patterns, perception and other behaviors of the host in response to activation of the peripheral innate immune system is an important finding that is critical for health and well-being and that has many clinical implications.
Activation of this system allows individuals to efficiently respond in a coordinated manner to infectious pathogens. However, activation of this system inadvertently in vulnerable individuals can have pathological consequences that lead to sleep disturbances and other nonspecific symptoms.
Evidence suggests that repeated activation of this system by cytokines released in chronic diseases or induced by some treatments are responsible for nonspecific symptoms that include sleep disorders, pain, cachexia, fatigue and cognitive alterations.
-It seems you are still trying to understand if the lesions indicated on your brain MRI could have been from sarcoidosis. This article cited a couple of sources in stating, “MRI findings of CNS [central nervous system] sarcoidosis including white matter, periventricular, periacuaductal or leptomengial lesions, have often been reported.”
Keep in mind that while inflammation is central to numerous diseases, it is also an important part of the body's repair processes. This report says inflammation is pivitol for repair of peripheral nerve damage, for instance. So signs of inflammation can be related to disease as well as to healing and repair.
Sarcoidosis can result in brain involvement even in pediatric patients, so you are not too young. This abstract says, “Among inflammatory conditions, granulomatous diseases such as sarcoidosis have predilection for involvement of the suprasellar regions and can spread along perivascular spaces deep within the parenchyma.”
Inflammation in the inner ear can make you have vertigo - a feeling you are moving, even spinning, or that your environment is moving when in fact they are not. Or you may feel like you are floating or falling. OR these may be due to neurological inflammation. The sensation may occur during sleep (waking a person from sleep) or while awake.
While these symptoms can seem disturbing, at least they are not painful and are relatively trivial as long as you are not falling or constantly nauseated. Mentally reassuring yourself may help. Keep in mind that *feeling anxious* can be a neurological symptom. If you don't have a family member around to help you identify anxiety as neurological immunopathologyA temporary exacerbation of neurological symptoms due to bacterial death. Requires careful management by physicians., you are left with having to try to remind yourself. Take heart that these do get better in later portion of treatment. ~Belinda Fenter
The mind-body-microbial continuum
Cognitive and emotional disturbances have been associated with Brucella suis infection21; manic and psychotic symptoms resistant to antipsychotics but treatable with antibiotics during infection with Leptospira22; baseline depression and anxiety caused by Mycobacterium tuberculosis23; and24,25
22. Semiz UB, Turhan V, Basoglu C, Oner O, Ebrinc S, Cetin M. Leptospirosis presenting with mania and psychosis: four consecutive cases seen in a military hospital in Turkey. Int J Psychiatry Med. 2005;35:299-305. 23. Vega P, Sweetland A, Acha J, et al. Psychiatric issues in the management of patients with multidrug-resistant tuberculosis. Int J Tuberc Lung Dis. 2004;8:749-759. 24. Snider LA, Lougee L, Slattery M, Grant P, Swedo SE. Antibiotic prophylaxis with azithromycin or penicillin for childhood-onset neuropsychiatric disorders. Biol Psychiatry. 2005;57:788-792. 25. Swedo SE, Leonard HL, Rapoport JL. The pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) subgroup: separating fact from fiction. Pediatrics. 2004;113:907-911. 26. Neufeld KM, Kang N, Bienenstock J, Foster JA. Reduced anxiety-like behavior and central neurochemical change in germ-free mice. Neurogastroenterol Motil. 2011;23;255-e119.
Jerking and tremors
-There are times too, when I am having “all over jerks and tremors” that last for so long and include such dramatic jerking of the head, neck, trunk, and limbs that a prescription is neccesary for this, as it becomes very painful on the muscles with all this non stop action, not to mention interferring with fluid intake, eating, speaking, etc.
One of the triggers for “Myoclonus” is infection, as you will find in this Fact Sheet on Myoclonus. You may want to speak with the staff and your physician on medication when this becomes debilatating. ~hrts4me
Interdiscip Perspect Infect Dis. 2010;2010:273573. Epub 2010 Feb 21.Chlamydophila pneumoniae Infection and Its Role in Neurological Disorders. Contini C, Seraceni S, Cultrera R, Castellazzi M, Granieri E, Fainardi E. Source Section of Infectious Diseases, Department of Clinical and Experimental Medicine, University of Ferrara, Via Fossato di Mortara, 23, 44100 Ferrara, Italy. Abstract Chlamydophila pneumoniae is an intracellular pathogen responsible for a number of different acute and chronic infections. The recent deepening of knowledge on the biology and the use of increasingly more sensitive and specific molecular techniques has allowed demonstration of C. pneumoniae in a large number of persons suffering from different diseases including cardiovascular (atherosclerosis and stroke) and central nervous system (CNS) disorders. Despite this, many important issues remain unanswered with regard to the role that C. pneumoniae may play in initiating atheroma or in the progression of the disease. A growing body of evidence concerns the involvement of this pathogen in chronic neurological disorders and particularly in Alzheimer's disease (AD) and Multiple Sclerosis (MS). Monocytes may traffic C. pneumoniae across the blood-brain-barrier, shed the organism in the CNS and induce neuroinflammation. The demonstration of C. pneumoniae by histopathological, molecular and culture techniques in the late-onset AD dementia has suggested a relationship between CNS infection with C. pneumoniae and the AD neuropathogenesis. In particular subsets of MS patients, C. pneumoniae could induce a chronic persistent brain infection acting as a cofactor in the development of the disease. The role of Chlamydia in the pathogenesis of mental or neurobehavioral disorders including schizophrenia and autism is uncertain and fragmentary and will require further confirmation. PMID: 20182626
Gut Bacteria Linked to Behavior: That Anxiety May Be in Your Gut, Not in Your Head
New study suggests link between Toxoplasma gondii parasite and suicide attempts (press release): New research ap… bit.ly/SwMlwF
Early Gut Bacteria Regulate HappinessInbox
ScienceDaily (June 12, 2012) — UCC scientists have shown that brain levels of serotonin, the 'happy hormone' are regulated by the amount of bacteria in the gut during early life. Their research is being published June 12 in the international psychiatry journal, Molecular Psychiatry.
Schizophr Res. 2012 Mar 23. [Epub ahead of print]
Gastrointestinal inflammation and associated immune activation in schizophrenia.
Severance EG, Alaedini A, Yang S, Halling M, Gressitt KL, Stallings CR, Origoni AE, Vaughan C, Khushalani S, Leweke FM, Dickerson FB, Yolken RH.
Stanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Blalock 1105, Baltimore, MD, 21287-4933, United States.
Immune factors are implicated in normal brain development and in brain disorder pathogenesis. Pathogen infection and food antigen penetration across gastrointestinal barriers are means by which environmental factors might affect immune-related neurodevelopment. Here, we test if gastrointestinal inflammation is associated with schizophrenia and therefore, might contribute to bloodstream entry of potentially neurotropic milk and gluten exorphins and/or immune activation by food antigens. IgG antibodies to Saccharomyces cerevisiae (ASCA, a marker of intestinal inflammation), bovine milk casein, wheat-derived gluten, and 6 infectious agents were assayed. Cohort 1 included 193 with non-recent onset schizophrenia, 67 with recent onset schizophrenia and 207 non-psychiatric controls. Cohort 2 included 103 with first episode schizophrenia, 40 of whom were antipsychotic-naÃ¯ve. ASCA markers were significantly elevated and correlated with food antigen antibodies in recent onset and non-recent onset schizophrenia compared to controls (pâ‰¤0.00001-0.004) and in unmedicated individuals with first episode schizophrenia compared to those receiving antipsychotics (pâ‰¤0.05-0.01). Elevated ASCA levels were especially evident in non-recent onset females (pâ‰¤0.009), recent onset males (pâ‰¤0.01) and in antipsychotic-naÃ¯ve males (pâ‰¤0.03). Anti-food antigen antibodies were correlated to antibodies against Toxoplasma gondii, an intestinally-infectious pathogen, particularly in males with recent onset schizophrenia (pâ‰¤0.002). In conclusion, gastrointestinal inflammation is a relevant pathology in schizophrenia, appears to occur in the absence of but may be modified by antipsychotics, and may link food antigen sensitivity and microbial infection as sources of immune activation in mental illness.