Well, in answering that question, I often find myself saying that it propagates every single situation, every decision that I make on a daily basis, even as far as to go, the very undertones of my existence.
As much as I try to hide my schizophrenia away from those around me that I would prefer not to know about it, there is no possible way to not demonstrate, in every facet of my existence, that I suffer from the insufferable. However, to many people, it would just be what they would say is me just being myself.
Does the medication help? No question that it does, but does it make me symptom free? Definitely not! In fact, sometimes it just adds to the confusion of whether the symptoms are part and parcel of the disorder itself, or an un-intentional side effect of the medication that I take for it.
I do consider myself lucky to be such a highly motivated, successful, and caring and loving person, which really is another reason that upbringing is so important. It is not just genes that determine who we are and what we become, but the environment of learned values over time, that shape and mold us over time.
Thursday, March 3, 2011
Friday, February 18, 2011
Got fired from my job today because of the disorder
Hello All,
I just got fired today because I didn't use good judgement because of my disorder! Oh man, this sucks!
My boss had it in for me from the beginning. She is a mega bitch!
Oh well, I am going to pull on through this.....just hope that I don't have a major psychotic break too!
I just got fired today because I didn't use good judgement because of my disorder! Oh man, this sucks!
My boss had it in for me from the beginning. She is a mega bitch!
Oh well, I am going to pull on through this.....just hope that I don't have a major psychotic break too!
Tuesday, February 1, 2011
Such are life's litle inequities
I am continually hounded at work to do the best job that I can do in a politically charged work force, and know that I have and want to be the best dad that I can be to my two sons--all the while on two separate neuroleptic medications and suffering from Schizo-Affective Disorder. Is it fair, I say no.
But what can one expect in the realm of equity for all? Not much. There are many things in this life that are inequitable and not fair, but we don't always address them. When it comes to the stigma of mental illness, I end up acting like a jerk half the time, not because I mean to, but just because I am experiencing one or the other of the symptoms of my disorder.
I have to constantly remind myself that the only person that you have to ultimately be accountable to in this life is yourself. And in the end, depending on your faith-base, you are accountable to God. You see, your family is the only one who loves you unconditionally, and no one else can bear that responsibility nor will they for you.
Shea
But what can one expect in the realm of equity for all? Not much. There are many things in this life that are inequitable and not fair, but we don't always address them. When it comes to the stigma of mental illness, I end up acting like a jerk half the time, not because I mean to, but just because I am experiencing one or the other of the symptoms of my disorder.
I have to constantly remind myself that the only person that you have to ultimately be accountable to in this life is yourself. And in the end, depending on your faith-base, you are accountable to God. You see, your family is the only one who loves you unconditionally, and no one else can bear that responsibility nor will they for you.
Shea
Sunday, January 16, 2011
Post from Psyche Central
I realize that around my age and older is when symptoms of schizophrenia begin to show. I am extremely concerned that I may have it. I hear voices and see things all the time. The voices in my head introduce themselves to me, and sometimes speak in different languages. I have a friend that has Schizophrenia and she said it is usually obvious, and that it looks as if I am showing early signs. I feel as if I can read other people’s minds. The voices in my head tell me things. Sometimes good, more often bad. It’s affecting my school work because they will shout things at me in Italian. I have done extensive research on schizophrenia, and I have many of the symptoms. Such as delusions and disorganized speech. So far I’ve counted 29 voices in my head. Do I need to check in to a mental hospital? Or do I not even have Schizophrenia. Please help.
A. I do not believe that you have to “check in” to a psychiatric hospital at this point but you should have a psychiatric evaluation. You can do this several ways. One way is to go to the hospital and request a psychiatric evaluation. Generally, an individual would utilize this option if he or she is experiencing significant or severe distress or there is an emergency. Typically, an individual would be admitted to the hospital if the evaluators suspect that they are a danger to themselves or to others.
Another way to have a psychiatric evaluation is to make an appointment with a psychiatrist. You would choose this option if there was no immediate psychiatric emergency. Your parents can call the local community mental health center and schedule an appointment with a psychiatrist. Your parents can also speak to your primary care physician who may be able to recommend a psychiatrist. Another option, if you have health insurance, is to call the telephone number on the back of your insurance card. The insurance company typically has a list of mental health professionals they recommend and who are “in network.”
As I mentioned above, it is imperative that you are evaluated as soon as possible. Auditory hallucinations are not a common occurrence. It is a symptom that should be investigated very thoroughly. Hallucinations, both visual and auditory, are associated with schizophrenia but they can also be brought on by drug use, fever, organic brain disorders, dementia, and on rare occasions, parasitic infection.
Please speak with your parents immediately about having a psychiatric evaluation. It is best not to assume that you have schizophrenia or any other condition. You will not know what, if any, disorder you have until you have been thoroughly screened by medical and mental health professionals. In the meantime, it is important to remain calm. To the best of your ability, try to engage in activities that are stress-free and that you find relaxing. If the voices are worse during certain times, for instance when you are alone, try to distract yourself either by watching television, listening to music or by being in the presence of others. Other stress reducing activities include physical exercise, deep breathing, meditation, and yoga. I am not suggesting that you engage in these activities as a way to treat a possible diagnosis of schizophrenia. I am simply recommending that you reduce your stress levels as much as possible because increased levels of stress might exacerbate your symptoms.
The next step for you is to speak your parents and to be evaluated. I know it may be difficult but please try not to worry. Worrying increases stress and at this point, you want to focus on stress reduction. Effective treatments exist for virtually every mental health condition. Please do not hesitate to write again if you have any additional questions. I wish you the best of luck.
Dr. Kristina Randle
A. I do not believe that you have to “check in” to a psychiatric hospital at this point but you should have a psychiatric evaluation. You can do this several ways. One way is to go to the hospital and request a psychiatric evaluation. Generally, an individual would utilize this option if he or she is experiencing significant or severe distress or there is an emergency. Typically, an individual would be admitted to the hospital if the evaluators suspect that they are a danger to themselves or to others.
Another way to have a psychiatric evaluation is to make an appointment with a psychiatrist. You would choose this option if there was no immediate psychiatric emergency. Your parents can call the local community mental health center and schedule an appointment with a psychiatrist. Your parents can also speak to your primary care physician who may be able to recommend a psychiatrist. Another option, if you have health insurance, is to call the telephone number on the back of your insurance card. The insurance company typically has a list of mental health professionals they recommend and who are “in network.”
As I mentioned above, it is imperative that you are evaluated as soon as possible. Auditory hallucinations are not a common occurrence. It is a symptom that should be investigated very thoroughly. Hallucinations, both visual and auditory, are associated with schizophrenia but they can also be brought on by drug use, fever, organic brain disorders, dementia, and on rare occasions, parasitic infection.
Please speak with your parents immediately about having a psychiatric evaluation. It is best not to assume that you have schizophrenia or any other condition. You will not know what, if any, disorder you have until you have been thoroughly screened by medical and mental health professionals. In the meantime, it is important to remain calm. To the best of your ability, try to engage in activities that are stress-free and that you find relaxing. If the voices are worse during certain times, for instance when you are alone, try to distract yourself either by watching television, listening to music or by being in the presence of others. Other stress reducing activities include physical exercise, deep breathing, meditation, and yoga. I am not suggesting that you engage in these activities as a way to treat a possible diagnosis of schizophrenia. I am simply recommending that you reduce your stress levels as much as possible because increased levels of stress might exacerbate your symptoms.
The next step for you is to speak your parents and to be evaluated. I know it may be difficult but please try not to worry. Worrying increases stress and at this point, you want to focus on stress reduction. Effective treatments exist for virtually every mental health condition. Please do not hesitate to write again if you have any additional questions. I wish you the best of luck.
Dr. Kristina Randle
Saturday, November 6, 2010
Something I found on Twitter
Sexual Abuse Tied To Schizophrenia
‘Children May Become Auxious, Withdrawn’
NEW YORK, Nov 3, (RTRS): Sexually abused children are at increased risk of developing schizophrenia later in life, Australian researchers have found.
Although child abuse has been firmly tied to other mental health problems — including depression, anxiety and suicide — the link to psychotic illnesses has long been a subject of debate.
The new study shows sexual assaults more than doubled the odds that a child would develop schizophrenia as an adult — from less than 1 in 100 (0.7 percent) in the general population to nearly 2 in 100 (1.9 percent) among the abuse victims.
The risk was higher still if the assault involved penetration or multiple perpetrators, or took place in the early teenage years.
Nearly one in five adults who had been raped by more than one person between ages 13 and 15 developed schizophrenia or another psychotic illness, Margaret Cutajar, of Monash University in Victoria, and colleagues found.
In their report, published in the Archives of General Psychiatry, they say the new results cannot prove a cause-and-effect relationship between the abuse and the later psychoses, but at the very least they may help point to a group of people who would benefit from professional help.
The researchers linked three decades’ worth of data from police and medical examinations to a mental health register in the Australian state of Victoria.
Then they compared the rates of psychotic illnesses between people who’d been abused before age 16 and a control group of people drawn from voting records.
That design makes the study stand out, because the intersection between mental health problems and childhood abuse is a difficult area to investigate, said Mark Shevlin, a professor of psychology at the University of Ulster in Londonderry, Northern Ireland.
“Many of the studies to date have relied on retrospective recall of traumatic experiences,” said Shevlin, who was not involved in the new research. And recall, he added, is not always trustworthy.
He stressed the findings don’t necessarily mean the abuse triggers later psychosis directly, because it may reflect other risk factors such as poverty or a difficult family situation.
Still, he said, children who experience sexual assaults, especially by a family member, may become anxious and withdrawn and perceive the world as a threatening place.
“These things could maybe explain things like paranoid beliefs,” said Shevlin. “Environmental factors are obviously very important in the development of serious health problems.”
Craig Steel, an expert in psychological trauma at Reading University in the UK, said the new paper made a strong case for going beyond drugs when treating people with schizophrenia.
Although both US and UK government guidelines recommend using cognitive behavioral therapy in addition to medication, he said, psychiatrists tend not to focus on patients’ personal histories.
‘Children May Become Auxious, Withdrawn’
NEW YORK, Nov 3, (RTRS): Sexually abused children are at increased risk of developing schizophrenia later in life, Australian researchers have found.
Although child abuse has been firmly tied to other mental health problems — including depression, anxiety and suicide — the link to psychotic illnesses has long been a subject of debate.
The new study shows sexual assaults more than doubled the odds that a child would develop schizophrenia as an adult — from less than 1 in 100 (0.7 percent) in the general population to nearly 2 in 100 (1.9 percent) among the abuse victims.
The risk was higher still if the assault involved penetration or multiple perpetrators, or took place in the early teenage years.
Nearly one in five adults who had been raped by more than one person between ages 13 and 15 developed schizophrenia or another psychotic illness, Margaret Cutajar, of Monash University in Victoria, and colleagues found.
In their report, published in the Archives of General Psychiatry, they say the new results cannot prove a cause-and-effect relationship between the abuse and the later psychoses, but at the very least they may help point to a group of people who would benefit from professional help.
The researchers linked three decades’ worth of data from police and medical examinations to a mental health register in the Australian state of Victoria.
Then they compared the rates of psychotic illnesses between people who’d been abused before age 16 and a control group of people drawn from voting records.
That design makes the study stand out, because the intersection between mental health problems and childhood abuse is a difficult area to investigate, said Mark Shevlin, a professor of psychology at the University of Ulster in Londonderry, Northern Ireland.
“Many of the studies to date have relied on retrospective recall of traumatic experiences,” said Shevlin, who was not involved in the new research. And recall, he added, is not always trustworthy.
He stressed the findings don’t necessarily mean the abuse triggers later psychosis directly, because it may reflect other risk factors such as poverty or a difficult family situation.
Still, he said, children who experience sexual assaults, especially by a family member, may become anxious and withdrawn and perceive the world as a threatening place.
“These things could maybe explain things like paranoid beliefs,” said Shevlin. “Environmental factors are obviously very important in the development of serious health problems.”
Craig Steel, an expert in psychological trauma at Reading University in the UK, said the new paper made a strong case for going beyond drugs when treating people with schizophrenia.
Although both US and UK government guidelines recommend using cognitive behavioral therapy in addition to medication, he said, psychiatrists tend not to focus on patients’ personal histories.
Wednesday, October 20, 2010
Plug for an amazing product to help with schizophrenia
As I post this plug for Isagenix International's product, "Cleanse for Life" I must say, in regards to the previous post that I made on this site--if there ever was anything causing my psychosis such as toxoplasmosis, Cleanse for Life has knocked it right out of me for good, it seems.
There are many possible causes for schizophrenia and other mental illness issues, and I am not suggesting that the Isagenix products will work in all cases. However, it certainly has made a HUGE difference for me in my daily life. It is like night and day, that I haven't experienced ANY psychotic symptoms, much less any other types of symptoms, since I have been taking "cleanse for life."
There are many possible causes for schizophrenia and other mental illness issues, and I am not suggesting that the Isagenix products will work in all cases. However, it certainly has made a HUGE difference for me in my daily life. It is like night and day, that I haven't experienced ANY psychotic symptoms, much less any other types of symptoms, since I have been taking "cleanse for life."
Friday, October 15, 2010
I have posted articles on here before, but this one is by far the best
This article is in reference to potential causes of schizophrenia and published by E Fuller Torrey, one of the most trusted researchers in his field.
Schizophr Bull. 2007 May; 33(3): 727–728.
Published online 2007 April 9. doi: 10.1093/schbul/sbm026.
PMCID: PMC2526129
Copyright © The Author 2007. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.
Editors' Introduction: Schizophrenia and Toxoplasmosis
E. Fuller Torrey1,2 and Robert H. Yolken3
2The Stanley Medical Research Institute, Chevy Chase, MD
3Stanley Laboratory of Developmental Neurovirology, Johns Hopkins University Medical Center, Baltimore, MD
1To whom correspondence should be addressed; tel: 301-571-2078, fax: 301-501-0775, e-mail: torreyf@stanleyresearch.org
This article has been cited by other articles in PMC.
Other Sections▼
This issue of Schizophrenia Bulletin includes articles on a possible infectious cause of schizophrenia. This approach follows a lead suggested by Emil Kraepelin and Eugen Bleuler a century ago. In the 1896 edition of his textbook, Kraepelin speculated that dementia praecox might be caused by a focal infection of bodily organs that then affected the brain as an autointoxication.1 Fifteen years later, Bleuler, in his Dementia Praecox, or The Group of Schizophrenias, suggested that “the connection of the disease to infectious processes equally needs further study … many writers assume that schizophrenia is caused by some physical weakness or possibly even by some infectious disease.”2
Toxoplasma gondii has emerged as an interesting candidate as a possible cause of some cases of schizophrenia. Past infectious research on schizophrenia has focused almost exclusively on bacteria and viruses, but T. gondii is a protozoa. Other protozoa known to chronically infect human brain tissue and cause behavioral changes include Plasmodium (malaria) and Trypanosoma (sleeping sickness).
The meta-analysis by Torrey et al provides an overview of studies of T. gondii antibodies in individuals with schizophrenia.3 The number of such studies that have been carried out surprised even the authors; even as this article was going to press, we became aware of additional studies, such as the one by Yazar et al that accompanies this special section.4 Since most of the studies have been published in languages other than English, they provide a sobering reminder of the limitations of MEDLINE and other search engines. The odds ratio of 2.73, although modest, exceeds that for most genetic studies and suggests that T. gondii may play some etiological role in a large number of cases. The fact that the studies were done in many geographical areas suggests that T. gondii may be associated with the disease worldwide.
Dickerson et al provide additional information on one of the cohorts included in the meta-analysis.5 The individuals with schizophrenia who have antibodies against T. gondii were more likely to be female but otherwise did not differ clinically on the Positive and Negative Syndrome Scale or cognitively on repeatable battery for the assessment of neuropsychological status from those who do not have antibodies, suggesting that cases associated with T. gondii do not form a clinical or cognitive subgroup. Of note, however, is the significantly increased mortality associated with seropositive antibody status. If this study can be replicated, it will be an important milestone in helping explain the 20% increase in premature mortality among individuals with schizophrenia.
T. gondii has a known pernicious effect on the developing fetal central nervous system (CNS) when it infects women early in pregnancy; that is why pregnant women are advised to not change the cat litter. Possible delayed CNS effects of T. gondii infection later in pregnancy have been the subject of much speculation but with no definitive resolution of this issue.6,7 In this regard, the review of two studies by Mortensen et al is of special interest.8 One study showed that mothers having antibodies to T. gondii late in pregnancy, even though the infection was not necessarily recent, had an increased risk of giving birth to offspring who later were diagnosed with a schizophrenia spectrum disorder. The other study revealed that newborns who have antibodies to T. gondii have an increased risk of later being diagnosed with schizophrenia. A much larger replication of this latter study is in progress.
Carruthers and Suzuki contribute an elegant summary of T. gondii's life cycle and its ability to cause a chronic, latent infection in both neurons and glia.9 The outcome of such infections is determined by a variety of factors, including host genes and cytokine production. Of special interest are differences in T. gondii strains as well as the route of initial infection. Both these factors may contribute to the differences in levels of antibody observed by Hinze-Selch et al in the accompanying article in her large study of T. gondii in individuals with schizophrenia and major depression.10
The ability of T. gondii to alter rodent behavior has received considerable publicity. Much of this work has been carried out by Joanne Webster, who clearly summarizes it.11 Webster describes how the T. gondii infection causes a rat to lose its innate avoidance of cats, thus increasing the chances that the rat will be eaten by a cat, thereby enabling the T. gondii to complete its life cycle. Noteworthy was Webster's experiment showing that haloperidol apparently suppressed the T. gondii and reversed its effect on the rat.
Finally, Jaroslav Flegr summarizes his pioneering research demonstrating the effects of T. gondii on the personality and behavior of university students and military recruits.12 Such studies need to be replicated but are of great interest. Humans are reluctant to acknowledge the possibility that our behavior may be manipulated by infectious organisms; anyone who doubts that it is possible will no longer doubt, if they read Carl Zimmer's fascinating Parasite Rex13
Where do we go from here with this research? The facts that T. gondii is neurotrophic, affects neurotransmitters, is apparently suppressed by some antipsychotic drugs, and has predisposing genes make an etiological link between toxoplasmosis and schizophrenia inherently plausible. A major limitation of such a hypothesis is that it has been difficult to detect Toxoplasma organisms in the brains of individuals with schizophrenia. However, it is of note that Toxoplasma organisms can persist in very small numbers in the brains of immune competent individuals. It is also unclear why most individuals with Toxoplasma do not develop schizophrenia. Variables in terms of disease expression are likely to include the timing of infection, the strain of the infecting organism, and the genetic makeup of the infected individual.
If a causal relationship is to be established between toxoplasmosis and schizophrenia, it will most likely be established by treatment trials, specifically by demonstrating that medications that suppress T. gondii infections produce an improvement in the clinical symptoms of schizophrenia. This is the way in which the Helicobacter pylori bacteria was ultimately proven to cause gastric ulcers. Multiple treatment trials are in progress, and others are planned using various antitoxoplasmosis drugs as adjunct medication to treat individuals with schizophrenia. Combined with ongoing research on the neuropathology and strain differences in T. gondii, such research should help illuminate the validity of this approach to schizophrenia. And if a causal relationship can be established, it will open the door to new treatment approaches as well as to the ultimate possibility of prevention through vaccines.
Schizophr Bull. 2007 May; 33(3): 727–728.
Published online 2007 April 9. doi: 10.1093/schbul/sbm026.
PMCID: PMC2526129
Copyright © The Author 2007. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.
Editors' Introduction: Schizophrenia and Toxoplasmosis
E. Fuller Torrey1,2 and Robert H. Yolken3
2The Stanley Medical Research Institute, Chevy Chase, MD
3Stanley Laboratory of Developmental Neurovirology, Johns Hopkins University Medical Center, Baltimore, MD
1To whom correspondence should be addressed; tel: 301-571-2078, fax: 301-501-0775, e-mail: torreyf@stanleyresearch.org
This article has been cited by other articles in PMC.
Other Sections▼
This issue of Schizophrenia Bulletin includes articles on a possible infectious cause of schizophrenia. This approach follows a lead suggested by Emil Kraepelin and Eugen Bleuler a century ago. In the 1896 edition of his textbook, Kraepelin speculated that dementia praecox might be caused by a focal infection of bodily organs that then affected the brain as an autointoxication.1 Fifteen years later, Bleuler, in his Dementia Praecox, or The Group of Schizophrenias, suggested that “the connection of the disease to infectious processes equally needs further study … many writers assume that schizophrenia is caused by some physical weakness or possibly even by some infectious disease.”2
Toxoplasma gondii has emerged as an interesting candidate as a possible cause of some cases of schizophrenia. Past infectious research on schizophrenia has focused almost exclusively on bacteria and viruses, but T. gondii is a protozoa. Other protozoa known to chronically infect human brain tissue and cause behavioral changes include Plasmodium (malaria) and Trypanosoma (sleeping sickness).
The meta-analysis by Torrey et al provides an overview of studies of T. gondii antibodies in individuals with schizophrenia.3 The number of such studies that have been carried out surprised even the authors; even as this article was going to press, we became aware of additional studies, such as the one by Yazar et al that accompanies this special section.4 Since most of the studies have been published in languages other than English, they provide a sobering reminder of the limitations of MEDLINE and other search engines. The odds ratio of 2.73, although modest, exceeds that for most genetic studies and suggests that T. gondii may play some etiological role in a large number of cases. The fact that the studies were done in many geographical areas suggests that T. gondii may be associated with the disease worldwide.
Dickerson et al provide additional information on one of the cohorts included in the meta-analysis.5 The individuals with schizophrenia who have antibodies against T. gondii were more likely to be female but otherwise did not differ clinically on the Positive and Negative Syndrome Scale or cognitively on repeatable battery for the assessment of neuropsychological status from those who do not have antibodies, suggesting that cases associated with T. gondii do not form a clinical or cognitive subgroup. Of note, however, is the significantly increased mortality associated with seropositive antibody status. If this study can be replicated, it will be an important milestone in helping explain the 20% increase in premature mortality among individuals with schizophrenia.
T. gondii has a known pernicious effect on the developing fetal central nervous system (CNS) when it infects women early in pregnancy; that is why pregnant women are advised to not change the cat litter. Possible delayed CNS effects of T. gondii infection later in pregnancy have been the subject of much speculation but with no definitive resolution of this issue.6,7 In this regard, the review of two studies by Mortensen et al is of special interest.8 One study showed that mothers having antibodies to T. gondii late in pregnancy, even though the infection was not necessarily recent, had an increased risk of giving birth to offspring who later were diagnosed with a schizophrenia spectrum disorder. The other study revealed that newborns who have antibodies to T. gondii have an increased risk of later being diagnosed with schizophrenia. A much larger replication of this latter study is in progress.
Carruthers and Suzuki contribute an elegant summary of T. gondii's life cycle and its ability to cause a chronic, latent infection in both neurons and glia.9 The outcome of such infections is determined by a variety of factors, including host genes and cytokine production. Of special interest are differences in T. gondii strains as well as the route of initial infection. Both these factors may contribute to the differences in levels of antibody observed by Hinze-Selch et al in the accompanying article in her large study of T. gondii in individuals with schizophrenia and major depression.10
The ability of T. gondii to alter rodent behavior has received considerable publicity. Much of this work has been carried out by Joanne Webster, who clearly summarizes it.11 Webster describes how the T. gondii infection causes a rat to lose its innate avoidance of cats, thus increasing the chances that the rat will be eaten by a cat, thereby enabling the T. gondii to complete its life cycle. Noteworthy was Webster's experiment showing that haloperidol apparently suppressed the T. gondii and reversed its effect on the rat.
Finally, Jaroslav Flegr summarizes his pioneering research demonstrating the effects of T. gondii on the personality and behavior of university students and military recruits.12 Such studies need to be replicated but are of great interest. Humans are reluctant to acknowledge the possibility that our behavior may be manipulated by infectious organisms; anyone who doubts that it is possible will no longer doubt, if they read Carl Zimmer's fascinating Parasite Rex13
Where do we go from here with this research? The facts that T. gondii is neurotrophic, affects neurotransmitters, is apparently suppressed by some antipsychotic drugs, and has predisposing genes make an etiological link between toxoplasmosis and schizophrenia inherently plausible. A major limitation of such a hypothesis is that it has been difficult to detect Toxoplasma organisms in the brains of individuals with schizophrenia. However, it is of note that Toxoplasma organisms can persist in very small numbers in the brains of immune competent individuals. It is also unclear why most individuals with Toxoplasma do not develop schizophrenia. Variables in terms of disease expression are likely to include the timing of infection, the strain of the infecting organism, and the genetic makeup of the infected individual.
If a causal relationship is to be established between toxoplasmosis and schizophrenia, it will most likely be established by treatment trials, specifically by demonstrating that medications that suppress T. gondii infections produce an improvement in the clinical symptoms of schizophrenia. This is the way in which the Helicobacter pylori bacteria was ultimately proven to cause gastric ulcers. Multiple treatment trials are in progress, and others are planned using various antitoxoplasmosis drugs as adjunct medication to treat individuals with schizophrenia. Combined with ongoing research on the neuropathology and strain differences in T. gondii, such research should help illuminate the validity of this approach to schizophrenia. And if a causal relationship can be established, it will open the door to new treatment approaches as well as to the ultimate possibility of prevention through vaccines.
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