Posts Tagged ‘schizophrenia’
Posted on March 17, 2010 - by David
Does Flu During Pregnancy Raise Schizophrenia Risk?
The authors of a study recently published in the journal Biological Psychiatry claim that influenza infection during pregnancy may play a role in the development of schizophrenia later in life.
The study subjects were monkeys. 
According to the abstract, twelve pregnant rhesus monkeys were infected with influenza early in the third trimester, and 7 healthy subjects were used as a control group. The brains of the babies were scanned using MRI after one year, and the researchers found that “exposed offspring had significantly smaller cingulate and parietal cortical gray matter and left parietal white matter than nonexposed offspring. Bilaterally, cingulate white matter was greater in exposed offspring than in controls.” (Gellner, Journal Watch Psychiatry) It is this finding that gets translated into a sentence like “The results showed ‘a significant effect’ which mirrored brain changes in schizophrenic humans” which I read in a short news clip on the Dallas-Fort Worth Fox News affiliate website, under the (only slightly misleading) title ‘Scientists Find Link Between Pregnant Women with Flu and Schizophrenia.’
The study’s main author, Sarah Short, chose her words a little more carefully:
“This was a relatively mild flu infection, but it had a significant effect on the brains of the babies,” Short said. “While these results aren’t directly applicable to humans, I do think they reinforce the idea, as recommended by the Centers for Disease Control and Prevention, that pregnant women should get flu shots, before they get sick.”
But obviously, the object of the study wasn’t merely to reinforce the idea that pregnant women should get flu shots. The hypothesis that flu infection during pregnancy might play a role in the development in schizophrenia was first put forth over 20 years ago, in a study involving a Finnish cohort born during the 1957 influenza pandemic. They found that “those exposed to the viral epidemic during their second trimester of fetal development were at elevated risk of being admitted to a psychiatric hospital with a diagnosis of schizophrenia,” but the results of similar studies have varied considerably. To date, only about half of the 25 research papers examining this phenomenon have confirmed these findings. Those who support this hypothesis often cite one of the more recent and “scientific” studies, which looked at maternal blood tests to confirm when and if those diagnosed with schizophrenia were exposed to the flu. The 2004 investigation found that “the risk of schizophrenia was increased 7-fold for influenza exposure during the first trimester.” If this is indeed true, it’s easy to understand why the authors considered it significant, but the finding that “there was no increased risk of schizophrenia with influenza during the second or third trimester,” conflicts with the earlier studies which claimed that risk of schizophrenia was increased with second trimester exposure. Based on the available data, it’s impossible to draw any conclusions about the relationship between schizophrenia and prenatal exposure to the flu, but obviously, as the recent publication of the monkey study demonstrates, researchers are still actively pursuing this track.
A few questions/criticisms about this study from someone with an admittedly (very) limited knowledge of neurology…
Is there a difference between contracting the flu virus in the typical way and forced infection, in terms of effects on the fetus?
If the available data points to first or second trimester exposure as a risk factor, what is the comparative value of this study considering the pregnant monkeys were infected during the third trimester?
What are other health effects for children of mothers who have the flu while pregnant? Has there been any research examining the relationship between prenatal exposure to influenza and any other mental illnesses?
If this really is a significant risk factor, wouldn’t it suggest that in developing countries where the flu vaccine is less readily available, there should be higher rates of schizophrenia?
A summary of the study by Asian News International (available on many websites) says that “rhesus monkey babies born to mothers who had the flu while pregnant had smaller brains and showed other brain changes similar to those observed in human patients with schizophrenia.” To my knowledge, schizophrenics do not have “smaller brains,” and from what I’ve read, nearly every region of the brain and every neurotransmitter has been implicated by one study or another in the etiology or progression of schizophrenia. It seems a bit misleading then to represent the changes observed in the monkey’s brains as “similar to those observed in human patients with schizophrenia.” This may be the fault of the news article and not the study authors, but I feel it’s important to point out that despite all our technology and the proliferation of research into the “biological basis” of schizophrenia, there is no test or scan, no specific brain changes that can be identified and used to diagnose schizophrenia.
Because so many potential genetic and neurological risk factors are being investigated and written about, there can be a false sense that we are approaching an understanding of what causes schizophrenia. But risk and vulnerability are merely that: factors which increase the possibility that a person exposed to the cause of schizophrenia will go on to develop the disease. In the first chapter of a 2007 book called Recovery from Schizophrenia, Norman Sartorius, former President of the World Psychiatric Association and former Director of the World Health Organization’s Division of Mental Health, writes:
“Despite advances in our knowledge about schizophrenia in the past few decades, nothing allows us to surmise that the causes of schizophrenia will soon become known, or that the prevention of the disorder will become possible in the immediate future.” (3)
Sure, I like monkeys, and I understand how biologically similar we are, but if we want to understand schizophrenia, perhaps we should be looking in the realm of what makes us human.
Posted on February 22, 2010 - by David
More on the DSM-V Changes
I regret how spotty my posts have been lately, but if I’m not writing something new every day the best thing I can do is point you to someone else’s work. With the proposed changes for the DSM-V being made public last week, there are plenty of opinions floating around on the internet. I found this op-ed piece from the Wall Street Journal by Yale psychiatrist Dr. Sally Satel interesting.
She points out that many of the proposed changes, (as well as the opposition to those changes), have more to do with stigma, labels, and identity issues than actual advances in the understanding of mental illness. Satel also mentions the common overlap in symptoms and diagnoses within individual patients, and underlines our relative ignorance as to how genes are actually related to mental illness:
The other problem that confounds psychiatry is how to draw boundaries around diagnostic categories, given that we rarely know the cause of mental illness at the neural level. Mental illnesses are the product of numerous genes that interact with one another, with the environment and also with experience. (A recent study by the National Institute of Mental Health found that 80 genes could be associated with bipolar disorder.) Add to this the miasma of social and personal encounters that impinge upon the genetically vulnerable individual—stress, poverty, family instability, drug or alcohol use, and so forth—and the causal mechanisms of any mental illness become staggeringly complex and elusive. Moreover, the “psychopathological pie,” as a colleague calls it, is rarely divided up as tidily as the manual implies. Patients often have symptoms that sprawl across several diagnostic categories. For example, half of kids who receive the diagnosis of bipolar disorder also have ADHD.
Of course, if you’ve been a regular reader of this blog you won’t be surprised that I take slight issue with her explanation of mental illness, (even though it might not be totally fair to judge her based on one sentence in a WSJ op-ed piece). The inadequacy of her own definition is made clear when she mentions that “80 genes could be associated with bipolar disorder,” but says nothing about how these genes “interact with each other.” Also, what is meant by “environment” and “experience” is unclear and could be taken in a variety of ways. She seems to offer a broad explanation for mental illness and demonstrates well that there major issues with the way we classify symptoms as disorders which often overlap, but like a good psychiatrists she still locates cause with genetics or “at the neural level.”
MindHacks has an extensive summary of the DSM-V changes with links to other major media coverage. I found his comments on the restructuring of the schizophrenia diagnosis and the addition of ‘psychosis risk syndrome’ particularly interesting. His article suggests that a lot of the more subtle changes are aimed at “de-freuding” the DSM. Definitely worth your time to check this out.
Posted on February 17, 2010 - by David
Anemia During Pregnancy: Another Trigger for Schizophrenia?
At the close of a 20 year long study, researchers from the University Hospital of Copenhagen claim that “children of mothers who had been diagnosed with anemia during pregnancy, most likely due to iron deficiency, had a significantly elevated risk of developing the mental disorder. ” You can check out the article where I first read about the findings, or look at an abstract of the research paper, published in the Schizophrenia Bulletin.
Once again, I find myself less than impressed with the analysis of the data gathered and the conclusions drawn. I quote the Reuters news article:
To further investigate this potential link, Srensen and colleagues analyzed the psychiatric outcomes of a large group of Danish children born between 1978 and 1998 — the biggest cohort in which the relationship has been examined. Each child was followed from age 10 until the onset of schizophrenia, death or the study’s closure on December 31, 2008.
Among 1,115,752 newborns, 17,940 (1.6 percent) were exposed to anemia in the womb. A total of 3,422 — including 41 from the exposed group — went on to develop schizophrenia, according to the report published in the journal Schizophrenia Bulletin.
After accounting for differences between the two groups and other relevant factors, including the parents’ ages and history of mental illness, exposure to anemia in the womb was associated with a 60 percent increased risk of schizophrenia in offspring during the 20 years of the study.
The researchers further concluded that 0.58 percent of schizophrenia cases (a total of about 20 diagnoses) could have been prevented had there been no cases of anemia among the mothers.
Now I don’t claim to be a statistician. I took two semesters of stat in college to fulfill my math requirement, and let’s just say my attendance wasn’t great. Still, I can’t seem to resist doing some of my own number crunching…
- 41 schizophrenics in the exposed group / 17,940 exposed to anemia = a prevalence rate for schizophrenia of approximately 0.2% for those exposed to anemia in the womb
- 3,422 total cases of schizophrenia – 41 exposed cases= 3381 schizophrenics not exposed
- 1,115,752 total children – 17,940 children exposed to anemia = 1,097,812 children not exposed
- 3381 / 1,097,812 = a prevalence rate for schizophrenia of approximately 0.3% for those not exposed to anemia in the womb
Obviously, 0.3% is greater than 0.2%, but after adjusting for potentially confounding factors, the researchers still arrive at the conclusion that “exposure to anemia in the womb was associated with a 60 percent increased risk of schizophrenia in offspring.” According to my best reading, this adjustment leaves them with only 20 cases of schizophrenia among those exposed to anemia which could not be attributed to some other factor. If the adjustments cut the number of the exposed cases in half, and they still determine that this group has a 60% greater risk of developing schizophrenia, then obviously the total number of schizophrenic cases they are working with has also been drastically reduced. It seems pretty bold to make this claim about increased risk on the basis of 20 cases, but my lack of statistical expertise probably renders me unqualified to make this judgment. Still, the simple fact that adjustment for confounding factors dramatically altered the size of the group is a little reminder of how many and how varied are the explanations for the cause of schizophrenia. Even if it’s true that about one half of one percent of all cases of schizophrenia can be attributed to iron deficiency anemia, does this really get us any closer to understanding the origins of this destructive mental illness?
A few last thoughts. According to my admittedly brief google research conducted this afternoon, iron deficiency is probably the most common nutritional deficit in the world, and I would assume that iron deficiency, (and therefore iron deficiency anemia), is more common in less developed parts of the world. So, if Iron Deficiency Anemia during pregnancy is a significant cause or contributor to the development of schizophrenia, then why aren’t the rates of schizophrenia higher in less developed countries? This line of reasoning would also suggest that rates of schizophrenia should have been higher centuries ago when diets were poorer and fewer resources were available, but it appears that this is not the case.
Posted on February 2, 2010 - by David
Fish Oil the Latest in Psychiatric Treatment?
This article summarizes the results of a study from the University of Melbourne, which suggests that the omega-3 fatty acids found in fish oil may help prevent psychosis in adolescents and young adults who have been identified as “at-risk.”
The study involved 81 individuals ages 13-25 “who met at least one of the following three criteria: having low-level psychotic symptoms; having transient psychotic symptoms; or having a schizophrenia-like personality disorder or a close relative with schizophrenia, along with a sharp decline in mental function within the past year.”
For 12 weeks, half the group was given fish oil capsules and the other half recieved placebo. Participants were then monitored for next 40 weeks. Only 2 of the 41 people given fish oil developed a psychotic disorder compared to 11 of 40 of the placebo group. The omega-3 group also “also showed significant reductions in their psychotic symptoms and improvements in function.” The researchers hope to replicate the findings in a multicenter trial involving 320 people.
Certainly, the lack of adverse side effects compared to the commonly used anti-psychotic medications would make this treatment a much preferred choice for patients. While these findings are definitely positive, it was a very small and relatively short-term study, so further research is obviously needed to determine the value of fish oil as a treatment or preventitive measure for serious mental illness. Also, this once again highlights how little is understood about what is happening in the brain of the schizophrenic patient. The article mentions some of the potential reasons this novel treatment may be effective:
There are a number of mechanisms through which omega-3s could protect the brain, Amminger said; they are a major component of brain cells. They are also key to the proper function of two brain chemical signaling systems, dopamine and serotonin, which have been implicated in schizophrenia. Fish oil also boosts levels of glutathione, an antioxidant that protects the brain against oxidative stress.
In the quest to understand the cause and progression of this illness, nearly every neurotransmitter and every part of the brain has been implicated in some way or another. While hopefully this study will lead to new ways of dealing with the symptoms of schizophrenia without the devastating side-effects of many commonly prescribed drugs, it seems to be another example of a “scientific” answer which amounts to, “this might work, and if it does, these might be some of the reasons why.”
Posted on January 24, 2010 - by David
Crazy Like Us, Part 3: Schizophrenia in Zanzibar
Chapter 3- The Shifting Mask of Schizophrenia in Zanzibar
In the first two chapters of Ethan Watters’ new book, Crazy Like Us: The Globalization of the American Psyche, we encounter the idea that differences in source of identity and social integration between cultures may account for differences in the expression, (and prevalence), of mental illness. The third chapter suggests that cultural differences may also explain the rather enigmatic finding that those diagnosed with schizophrenia in the “developing” world seem to fare better than their Western counterparts. I found anthropologist Juli McGruder’s case studies particularly interesting, as they raise the possibility that the cause, or at least trigger, for schizophrenia may lie in cultural conditions.
I think it’s worth noting, as Watters points out, that despite the privileged position science has been given in the study of schizophrenia and all the technological advances of the last few decades, we still know very little about the causes of this strange affliction.
More than any other mental illness in the Western world, this one belonged to the “hard scientists” who looked for the causes in bad genes, biochemistry, and the structure of the brain. The advent of brain scans – allowing a researcher to see into the head of live patients – brought with it a seemingly endless series of theories about the root cause of the illness. Abnormalities supposedly key to schizophrenia have been reported in the frontal cortex, the prefrontal cortex, the basal ganglia, the hippocampus, the thalamus, the cerebellum – and pretty much every other corner of the brain as well. No firm consensus had emerged about the location or cause, but there was wide agreement that the exciting advances in understanding the disease were coming from the laboratories of brain researchers.(134)
In the meantime, there are others like Juli McGruder who, (like sociologist Liah Greenfeld), believes that “culture and social setting play a more complicated role in the disease than simply influencing the content of the delusions.” (136) Scholars on the cultural side of the fence point to the results of two international studies by the World Health Organization. The WHO research, which began in the 1960’s and lasted 25 years, suggests that the severity of schizophrenia is not the same worldwide. Watters summarizes the findings:
What they found was that those diagnosed with schizophrenia living in India, Nigeria, and Colombia often experienced a less severe form of the disease (had longer periods of remission and higher levels of social functioning) than those living in the United States, Denmark, or Taiwan. Whereas over 40 percent of schizophrenics in industrialized nations were judged to be “severely impaired,” only 24 percent of patients in the poorer countries ended up similarly disabled. (137)
Liah Greenfeld believes that anomie, which she considers a built-in feature of modern culture, causes problems with identity formation which often lead to mental illness. In Nationalism and the Mind, she describes this phenomenon and its effects on individuals:
Anomie, commonly translated as “normlessness,” refers to a condition of cultural insufficiency, a systemic problem which reflects inconsistency, or lack of coordination, between various institutional structures, as a result of which they are likely to send contradictory messages to individuals within them. On the psychological level anomie produces a sense of disorientation, of uncertainty as to one’s place in society, and therefore as to one’s identity: of what one is expected to do under the circumstances of one sort or another, of the limits to one’s possible achievement… (14)
The chronic, modern state of anomie may not (yet) be a built-in a feature of Zanzibari culture, but when we use the word “developing” to describe a country or culture, we imply that they are developing into something more like us, i.e moving towards modernity. This process of modernization is necessarily anomic:
Anomie, is, in fact, the ultimate cause of cultural change. It both breaks the old cultural routine and encourages the formation of a new one. The general pattern of human history can be imagined as an alteration between relatively brief and rare periods of widespread (though culturally localized) anomie and cultural routine. Widespread anomie, most commonly implying gross inconsistencies between elements of culture impinging on individual identities, specifically inconsistencies within the system of social stratification which defines a person’s position in the social world in general and vis-à-vis particular others, affects large groups of individuals and expresses itself in social turmoil. (14-15)
I wasn’t surprised, then, to see the title ‘Revolution and Madness’ above the section introducing McGruder’s first case study. Watters describes the state of affairs in the country at the time when Hemed began to experience symptoms of schizophrenia:
After years of being a British colony, Zanzibar embarked on the uncertain path to self-governance. There were three political parties, twenty-two trade unions, and sixteen partisan newspapers stirring up anger and resentment on all sides. Hemed’s first experience of derangement, McGruder believes, was sparked by the social upheaval of the time. (142)
Given what was going on in that moment in the history of Zanzibar, the amount of stress felt by Hemed must have been intense. He was a middle-class man from a high-profile Arab minority at a time of growing racial and class distrust. His curly dark hair and facial features made him identifiably Arab. There seemed to be no safe political refuge. Even the political party he belonged to, the Zanzibar Nationalist Party, was internally split between those who considered themselves African and those of Arab heritage. No one knew whom to trust. (143)
We can also see how conflicting cultural messages may have played a role in the experience of Kimwana, Hemed’s daughter who suffered from the same illness.
She was a happy child even though her early years were turbulent times for the island. Her mother and classmates remember her as the brightest student in the class. Particularly skilled with numbers, she graduated from secondary school and took a job with the Ministry of Finance. This was 1983, a time of rapid change for women on the island. To fill in for the many educated men who had fled the political upheaval, women were beginning to enter the professional workforce by the thousands. (144)
While we in the West would see these new opportunities for women aa a change for the better, there still existed traditional guidelines on behavior which seemed to contradict this elevation in social status. It was only a few months after Kimwana started her new job that she began to hear male voices “gossiping that she was a disloyal and disrespectful daughter and sister” (146). Before the cultural changes which led to an influx of women into the workplace, Kimwana’s identity would have been based primarily on her relationship to her family and in behaving according to the prescriptions of the Islamic religion.
Much of the torment of having these male presences in her head related to Islamic rules of female modesty. While the voices were with her, she felt she must respect the codes of conduct as is she were actually in the presence of a man. At such times she could not bathe or undress and she tried not to go to the bathroom. Although she sometimes found it helpful to argue with the voices when they became critical, her sense of decorum made it difficult to do this out loud. (146-147)
In this section of the chapter, Watters highlights McGruder’s amazement at the ability of Amina, the mother and effectively the head of the household, to care for the large family and its two sick members. Her daily activities seem to far surpass western notions of busyness, and she takes the extra load created by mental illness in stride. This is possible, I believe, because she is secure in her identity in a way that neither Hemed nor her daughter Kimwana could be. She was raised to serve her family and God, and that is what she does. McGruder compares the Western, Christian attitude towards adversity to Amina’s stance and sees an importance difference.
In the cosmology of Western Christians, life’s challenges provide opportunities to become stronger and to have a closer relationship with God. The burdens God sends to Christians in the Western world are incitements to self-improvement. The comforts that Amina found in her religious belief, by contrast, were not in an encouragement to overcome or learn from hardships. Rather, simply accepting her burden was a continuous act of penance. (155)
In other words, the challenge of caring for her sick relatives did not provide a reason to change her identity. Her identity was essentially unchanged since childhood, she was merely to continue behaving and believing as she always knew she should. Unfortunately for her daughter, the conflict between the new cultural value of work for women, and the traditional emphasis on family and religion proved too much for her mind to handle.
The chapter also describes the damage often done by family members’ emotional over-involvement in the lives of their schizophrenic loved ones. This cultural tendency, according to Watters, is closely related to the Western emphasis on individual identity and the belief that individuals should be able to control their own destinies. As in the previous two chapters, the resounding message is that the highly individualistic nature of identity in modern societies and the lack of clear, shared cultural beliefs and practices lead to more widespread and more severe forms of mental illness.

Exploring modern culture and its effects on the mind