Today I went back to school. Every fall, I help teach the introduction to psychiatry class for the second year medical students at my institution. I work with a small group, teaching basic interviewing and write-up skills. Today was a large lecture, though, so I got to be in the audience, thumbing through this month's stack of journals while the students were Introduced to Psychiatry.
There are a few interesting papers in the Archives of General Psychiatry this month, which isn't always the case. The Archives tends to have really tedious genetic polymorphism and functional MRI studies out the wazoo. You get paper headings like "Reduced brain white matter integrity in trichotillomania." Which, believe me, is not even as interesting as it sounds. Still, the Archives is an excellent journal and they don't accept horrible studies, just boring ones.
The first interesting one is "Modification of Cognitive Performance in Schizophrenia by Complexin 2 Gene Polymorphisms." (I know, it sounds really boring! But give it a chance.) Turns out this group in Germany put together a database of genetic data for schizophrenia research. 23 different research centers compiled the genetic data of 1071 patients with schizophrenia and 1079 controls. Then they threw the DNA into their big machines, and out pops loads of data. Over 3000 phenotypic data points for each patient! There's a specific gene, complexin 2, which codes for a type of protein that regulates how synaptic signaling happens in the brain. Specifically, complexin 1 and 2 control the release of the soluble-N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE). Differences in the complexin 2 proteins and mRNA have been noted in previous autopsy studies of schizophrenics, so the genes were an obvious place to look. In those autopsy studies, a significant decrease in complexin 2 was found in regions of the brain that are specifically damaged in schizophrenia (like the dorsolateral prefrontal cortex and the hippocampus). This same protein/gene expression was found to be decreased in studies of bipolar disorder, Alzheimer's, and Huntington's disease, but in different parts of the brain more affected by those other disorders. All of the disorders, though , have symptoms of cognitive impairment, meaning in the advanced stages of each disease, you just can't think as clearly as you once did. And, sure enough, when they traced the schizophrenia patients who had certain types of poorly expressed complexin 2 gene, they tended to have more cognitive impairment than the other schizophrenia patients
Okay, that's not particularly interesting, at least from an evolutionary medicine standpoint. Except I couldn't help but notice all those disorders up there (except bipolar disorder) are ones I've discussed in the blog who have some evidence to link them to wheat or to metabolic syndrome. Mice with knocked out complexin 2 genes have a few issues, but apparently not cognitive ones. Until you take those mice and deprive them of their mothers. Then the complexin 2 knockout mice get mouse dementia, of sorts. It's the genetic difference plus the stress that seems to cause the disease. Good old two-hit hypothesis.
Next up is one that will warm the cockles of your sun-worshiping hearts. "Neonatal Vitamin D Status and Risk of Schizophrenia: A Population-Based Case Control Study." Thank you, Netherlands, who apparently keeps dried blood samples from all the babies born there. The researchers took 424 individuals with schizophrenia and 424 sex and age matched controls, and pulled their blood samples from the big bank 'o blood, and figured out each neonate's vitamin D levels.
Vitamin D is a big suspect in schizophrenia for the following reasons - Vitamin D undoubtedly plays a role in the development of the brain. People born in winter and spring have higher risk for developing schizophrenia, and the farther you are born from the equator, the more likely your birth month will be a factor. Immigrants with dark skin who move to northern countries also have children with higher rates of schizophrenia. In addition, city kids are more likely to develop schizophrenia compared to country kids. This study is the first time someone was able to go back and directly check the vitamin D levels from neonatal blood of people who later get schizophrenia.
The average level of vitamin D (measured as 25 (OH) vitamin D3) varied widely from winter to summer, with babies born in March (cases and controls) having the lowest levels, around 26 (deficient), and babies born in August having an average level of nearly 50 (which is good). One caveat - the actual level may be misleading. The level might degrade over time, and these samples were up to 27 years old when tested. However, since there were matched controls of the same age for each patient, it was presumed that the degradation would be the same for both sets of data.
But now the key results - babies born with a vitamin D level of 46.5 had the lowest risk for schizophrenia (again, that might not be the actual level, measured so many years later). The babies within the lowest two quintiles (the lowest 40%) of vitamin D levels had significantly increased risk. Surprisingly, babies in the highest quintile, with the highest vitamin D levels, had higher risk too. The researchers were able to go back and check for all sorts of variables which might confound things - UV light therapy at birth for high bilirubin might affect vitamin D levels, for example, admission to the NICU, age, sex, etc. etc. and nothing seemed to change the overall U-shaped data curve, with the "sweet spot" between the 3rd and 4th quintiles of vitamin D levels. Now the researchers wisely emphasized caution when considering these results - it's an observational study, and there can be plenty of confounders nobody thought of. However, if the cause-effect relationship holds true, the researchers suggest that mere vitamin D supplementation in dark-skinned immigrants in northern countries could reduce the incidence of schizophrenia in those populations by "a staggering 87%."
A third study in this same issue is called "Birth Weight, Schizophrenia, and Adult Mental Disorder," where the researchers did pretty much what you might think, but on a very large scale. They followed 1.49 million single babies born in Sweden and Denmark between 1973 and 1986. Both countries have "comprehensive national registers of psychiatric treatment." In 2002 (Sweden) and 2005 (Denmark), these countries had 5,445 registered cases of schizophrenia and 57,455 cases of "any adult psychiatric disorder." (My first thought - 5445 cases of schizophrenia seems low out of 1.49 million, and it is only 0.37 %. There should be around 14,900 cases as the worldwide prevalence is right around 1%. Just something to keep in mind!)
The results - birth weight of less than 2500 grams (5 pounds, 8 ounces) in these babies translated into a higher risk for schizophrenia, and the risk actually decreases (for schizophrenia) as the birth weights go up. The heavier the kiddos were, the lower the risk, all the way up to >4500g (that's 9 pounds, 15 ounces). Low birth weight also translated into a higher risk for all mental disorders, including an aggregate "all diagnoses" group and for each subgroup of substance abuse, mood disorders (like major depression and bipolar disorder), and anxiety disorders. And, indeed, in the subgroups, the higher the birth weight (all the way up to the megababy 10 pounder and above group), the lower the risk.
Interesting! Obviously, very low birth weight is associated with all sorts of issues - premature delivery, infection, brain hemorrhages - any or all of these could have stress on the baby's forming brain. It is interesting that the heavy babies had lower risk than the so-called normal weight babies. I actually would have expected another "U-shaped" curve here. But no! Still, there could be huge confounders. High birth weights are associated with gestational diabetes, but I'm not sure how common that was in Sweden and Denmark back in the 70s and 80s, so maybe it wouldn't be as much of a factor as I would have thought.
One of those confounding factors could actually be vitamin D! This study showed maternal vitamin D intake associated with birth weight (low vitamin D = lower average birth weight), and it was postulated that adequate vitamin D intake protects moms from infections. This study is a little more interesting - white women with a vitamin D level from 60-80 had the lowest risk of having small for gestational age babies, but there was no relationship between vitamin D levels and birth weight in black women. And, of course Don Matesz blogged today about this study, showing that pregnant women who took 4000 IU vitamin D daily had a lower risk of preterm birth.
All told, several interesting findings this month. Don't get vitamin D deficient! But try not to go nuts with the supplementation either. Levels are best! Ask your doctor, or go to Grassroots Health to order a home test. I tend to aim for a level of 50, but perhaps pregnant women would want to go just a bit higher (Caucasian women may want to aim for that 60-80 range). Be sure you are getting your K2 also! I always use pastured butter, but I also have a vitamin D supplement that comes with K2 in it.
Believe it or not, there is another blog-worthy study in this month's Archives, but I will save it for later in the week. See you then!
Showing posts with label schizophrenia. Show all posts
Showing posts with label schizophrenia. Show all posts
Tuesday, September 14, 2010
Friday, September 3, 2010
Woe is Wheat
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| (Shirt available at Cafe Press) |
I don't eat wheat as a general rule, and the reasons I don't are circumstantial, to be sure. The most compelling reasons to me are all those healthy non-wheat eating cultures. Read enough of Food and Western Disease: Health and nutrition from an evolutionary perspective
, or The Primal Blueprint: Reprogram your genes for effortless weight loss, vibrant health, and boundless energy
, or Dangerous Grains: Why Gluten Cereal Grains May Be Hazardous To Your Health
, and wheat just doesn't seem tasty anymore. If it ever did. Well, maybe in a pizza.However, the beautiful Ms. Minger has used the (admittedly fairly useless) China Study data to make the smokey fire around wheat flare up again. The handsome Dr. Guyenet has a reasonable overview at his site. (Hmmm... there seems to be a strong correlation between non-wheat eating blogging and good health and good looks.)
And, very recently, Dr. Rodney Ford published a paper where he makes an argument that there should be a medical condition labeled "The Gluten Syndrome," and that everyone with many common neurological and psychiatric conditions (such as ataxia, hypotonia, developmental delay, migraine, depression, anxiety, etc.) be tested for gluten sensitivity via the IgG anti-gliadin antibody. His reasoning being that IgG antigliadin positive people can have negative intestinal biopsies (if they have latent disease or patchy involvement of the intestine), and they can also have negative IgA tTG testing (another pretty specific celiac antibody test) and still have improvement in symptoms on a gluten free diet.
While looking into the matter, I stumbled upon a very good paper called Neurological complications of coeliac disease: what is the evidence? If you have institutional access, I highly recommend checking this one out. It has some nice suggestions for teasing out biases and inaccuracies in research papers, and it has a good review of the pathophysiology of celiac disease. Neurologists are one of my favorite species of doctor, as they tend to be brilliant and cranky*, and these authors point out very fairly that the evidence linking gluten exposure to ataxias, certain types of epilepsy, and peripheral neuropathy is often poor and contradictory. Bless their clinical hearts, though, they end up recommending a trial of gluten-free diet for anyone who's game, educated about the type of data there is, and who has a positive celiac biopsy or positive celiac or gliadin antibody testing for those with certain neurologic conditions, recognizing that the harm of a gluten-free diet is minimal, and there are some case reports where going gluten-free improved ataxias, peripheral neuropathy, and seizures.
I have the same take with schizophrenia - the indirect evidence is damning, the direct not as much, but enough case studies and small studies to suggest that at least some (especially new onset) schizophrenics could really benefit from a gluten-free diet. And seeing as how we are dealing with a progressive, devastating brain illness with no cure, it seems fair to give patients and families the option and explaining the data. For most it won't make a difference, but for a few... I wouldn't hold off medication for a new onset psychosis to try a gluten-free diet, though.
I'm not sure about testing everyone with depression and anxiety (or schizophrenia) for IgG or IgA ani-gliadin, or even IgA tTG. I'd probably just recommend the gluten-free diet trial idea to anyone interested. Mostly it's the schizophrenia data that puts me in this mindset. All sorts of anti-wheat antibodies were found in the serum and urine of schizophrenics, after all, but most of them were entirely different than the celiac antibodies. Until we know more about what to test for, I think you risk giving someone with a negative test a false sense of security about gluten.
No classical music link this week. Nope. It's a holiday weekend and there's a hurricane coming, and that calls for something a little more modern.
I'll still be blogging over the weekend, though. Did you know that in a study of 52 patients with Huntington's disease (invariably fatal genetic autosomal dominant ataxia condition), 44% had a positive IgA or IgG (or both) anti-gliadin antibodies? The general population is about 4.8% positive. Wild, huh? (No, don't jump on that and say OMG WHEAT causes HUNTINGTON's because that might not be what it means at all. But still, pretty wild). This means a post on evolution, Iceland, genetics, anthropology, and even a mention of poor Dr. T. Colin Campbell. In the mean time, keep eating meat, fish, veggies, and a bit of fruit and nuts.
*Neurologists are almost always right handed. The field of psychiatry has more left handers (I have no source for this and it may be an urban medical myth). There was a Nova episode last year about Oliver Sachs (famous neurologist) and music. In it he admitted to preferring Bach to Beethoven. I think that is the very definition of a neurologist.
Saturday, June 19, 2010
Wheat and Schizophrenia
I'm in the middle of an introduction to vegetable oils post, but in the midst of tweaking that one, my youngest woke up from her nap, and I moved to the family room to observe her toddling about while I glanced at this seriously interesting paper, Genetic Hypothesis of Idiopathic Schizophrenia: It's Exorphin Connection. Free full text! Click the gray box on the upper right.
Schizophrenia is an unfortunate brain disease. Inherited often, progressive, presents usually with social withdrawal, paranoia, hearing voices, that sort of thing. After a while you get a kind of "burnout" effect where the voices and whatnot lessen, but the afflicted is left with all the negative symptoms of social withdrawal, thought blocking, and an inexpressiveness known as "flat affect." MRI of the brain will show "large ventricles" at this point, meaning cell death (brain damage) has caused the active, lively part of the brain to shrink. Dementia, basically. You'll see schizophrenia in any large public park in any major city. Go ask the guy on the bench with holey shoes if he wants a sandwich, and see what he says. If it's paranoid meaningless word salad, that's schizophrenia, most likely. He had parents, brothers, sisters, maybe even a college degree. There aren't enough group homes, even if he were willing to stay.
Anyway, most of the research is focused on dopamine and genetic polymorphisms of the receptor (yawn), some on acetylcholine, histamine, serotonin. The usual questions about ineffective brain chemistry. The usual treatment is neuroleptic medication (hopefully decreases excess dopamine in the right place and leaves it well enough alone in other corners of the brain). Read a popular press book called "The Food-Mood Connection" which sounds like my sort of book, really, until the the author (who has a PhD of some sort!) explained that schizophrenia in a certain case was caused by childhood teasing. Poor man was treated with horrible prescription medicine and his genetics were examined, but I suppose some serious teasing psychoanalysis would have cured that schizophrenia eventually...it must have been his mother, come to think of it.
Anyway, there's a funny thing about schizophrenia, turns out that quite a few of the adult schizophrenics on Handford's inpatient unit in 1967 happened to have a major history of celiac disease (gluten/wheat intolerance) as children. As in 50-100 times the amount of celiac disease that one would expect by chance. Celiac doctors also noticed their patients were schizophrenic about 10X as often as the general population. That's a lot!
Allow me to paraphrase and expand on Table 1 of this paper, "Major Evidence that Peptides from Grain Glutens Evoke Idiopathic Schizophrenia in Those with Its Genotype"
1) In the 1960s, many observations suggested celiac disease and schizophrenia shared some genes. The role of gluten in schizophrenia was examined.
2) Epidemiologic studies showed a strong, dose-dependent relationship between grain intake and schizophrenia (Pacific islanders who ate no wheat had extremely rare occurence of schizophrenia - 2 in 65,000 rather than about 1 in 100 as we have in the grain-eating West. Then the same islanders changed their diet and began eating wheat - and schizophrenia became common).
3) Clinical trials and showed that gluten made new-onset acutely ill schizophrenics worse. Only occasional long-term patients responded to gluten restriction (remember, the affected brain cells of the long-term schizophrenics are already dead, so getting rid of the possible poison that killed the cells won't make much difference).
4) NIH investigators looked for poisonous protein fragments derived from gluten, gliadin, and casein. They found them - potent opiate (yes, opiate as in morphine. Or heroin) analogs they called "exorphins." They did these studies in rats, and I've read several of them. Very creepy. Turns out, you take wheat gluten, add stomach enzymes, and you end up with fragments of proteins that are potent opiates (1). The cute thing is these fragments aren't digested by the small intestine and definitely end up in the body and brain of rats that are fed gluten orally. Inject these same proteins directly into the brains of poor unfortunate rats, and you get rat seizures.
5) People with schizophrenia have a lot of these opioid-like small gluten-derived peptides in their urine. Way more than people without schizophrenia.
Let me review what is perhaps the most important part of the paper - a gluten-free diet definitely improved some of the new-onset schizophrenics on the inpatient unit. Not all of them. But 2 out of 17 or so. Putting back the wheat made the affected a lot worse. 115 patients on a locked ward were all given a gluten free milk free diet (remember the casein issue). They were released into the community (got better?) on average twice as fast as the similar patients on another, diet as usual ward (p=.009). It is of note that repeat studies didn't show the same thing, but instead of 17 or 115 patients, these studies had 4 or 8 patients, and they used chronic schizophrenics (end stage, when the brain cells are already gone).
Historically, prior to WWII, when grain consumption was super-high and neuroleptics (those medications, as you recall, which affect brain dopamine levels and are used to treat schizophrenia) did not yet exist, there are reports of schizophrenics having marked, unexplained fluctuations in weight and gut symptoms, poor iron absorption just like celiac sufferers, and "post-mortem abnormalities like those subsequently discovered in celiac patients." Why aren't these found now? Well, it turns out that a side effect of neuroleptics is that they decrease the permeability of the gut. Meaning gluten may not be able to weasel through quite so easily.
Which begs the question, is that the side effect? Or perhaps the principle effect?
Who knows?
Not psychiatrists in 2010. The paper (from 1988) finishes by suggesting a number of methods to investigate this connection further. One of the suggestions was morally bankrupt (feed the identical twins of schizophrenics a high gluten diet to see what happens!), but intriguing. That study wasn't done (fortunately). Nor, looking at pubmed (via eCommons), were any others (that I could find. I'm not the wiliest research paper discoverer so I might have missed one). The article is mentioned in a few review articles, and schizophrenics were left to eat wheat in peace.
Edit: I shouldn't be such a cynic, and I should search harder before I post - Here are more recent studies, including one from last month (Thanks to the commenter for the link - why I love blogging. Interactive! Editable! We can all stand on eachother's shoulders and the shoulders of past giants). All told, they throw out some more "biochemical smoke" about the link between schizophrenia and gluten:
Markers of Gluten Sensitivity and Celiac Disease in Recent-Onset Psychosis and Multi-Episode Schizophrenia: Conclusions - Individuals with recent-onset psychosis and with multi-episode schizophrenia who have increased antibodies to gliadin may share some immunologic features of celiac disease, but their immune response to gliadin differs from that of celiac disease.
Novel immune response to gluten in individuals with schizophrenia: The researchers here looked at all sorts of different anti-gliadin antibodies and celiac disease associated biomarkers (meaning some different antibodies and also specific celiac MHC genes - basically genetic predispositions to have autoimmune response to wheat). They also did some fancy chromatography to find if the schizophrenic's blood reacted to other wheat proteins, and then it sounds like they used "peptide mass mapping" to figure out what the wheat proteins were that the schizophrenics were reacting to - and the results were... schizophrenics of the wheat-reactive subtype had lots of anti-wheat protein immune response, and a lot of them were completely different than those found in celiac disease.
A Case Report of the Resolution of Schizophrenic Symptoms on a Ketogenic Diet That link is to the full text. It doesn't need much translating to make it more understandable - the title says it all.
This article from 2006 is also cited often, and I did look at it before I posted the first time, but it doesn't add that much: The gluten connection: the association between schizophrenia and celiac disease. Basically it says there are case reviews in the literature that show dramatic improvements in schizophrenia on a gluten-free diet (these studies were the same ones commented on in the original paper that I reviewed in detail at the top of the post) and that only a subset of schizophrenics are affected. (The researchers in residency would always refer to them as "the schizophrenias" rather than "schizophrenia." It is several different diseases, lumped into a similar symptom cluster because we don't fully understand the pathology, and in psychiatry, lumping is done by symptoms, as that made the most sense for research purposes.)
I would love to take a look at this one, but my institutional access won't get me there for the moment - A PILOT STUDY OF THE KETOGENIC DIET IN SCHIZOPHRENIA
PACHECO et al. Am J Psychiatry.1965; 121: 1110-1111. We'll track it down eventually.
The bottom line? Schizophrenia is a progressive and destructive psychotic mental illness that, at the moment, can sometimes be managed with medications and community therapeutic support, but does not have a cure. Some people with schizophrenia are bound to have the gluten-sensitive variety, and a few lucky souls apparently have been cured among the case reports. A gluten-free diet is safe and doesn't have side effects - I don't see a good argument against giving it a try for anyone with schizophrenia who is willing to give it a go, at least for a few months (how long? 3? 5? I'll look more into that one), while more data is being gathered. (You *might* get even better results with stabilizing your GABA receptors and whatnot via a ketogenic (very low carbohydrate) diet. More on this later! Very little research in psychiatry...) The worst thing that happens is you find you are not one of the gluten-sensitive schizophrenics, and you've gone without bread for a little while. The best thing that happens is that your symptoms get better, possibly quite a lot better.
Schizophrenia is an unfortunate brain disease. Inherited often, progressive, presents usually with social withdrawal, paranoia, hearing voices, that sort of thing. After a while you get a kind of "burnout" effect where the voices and whatnot lessen, but the afflicted is left with all the negative symptoms of social withdrawal, thought blocking, and an inexpressiveness known as "flat affect." MRI of the brain will show "large ventricles" at this point, meaning cell death (brain damage) has caused the active, lively part of the brain to shrink. Dementia, basically. You'll see schizophrenia in any large public park in any major city. Go ask the guy on the bench with holey shoes if he wants a sandwich, and see what he says. If it's paranoid meaningless word salad, that's schizophrenia, most likely. He had parents, brothers, sisters, maybe even a college degree. There aren't enough group homes, even if he were willing to stay.
Anyway, most of the research is focused on dopamine and genetic polymorphisms of the receptor (yawn), some on acetylcholine, histamine, serotonin. The usual questions about ineffective brain chemistry. The usual treatment is neuroleptic medication (hopefully decreases excess dopamine in the right place and leaves it well enough alone in other corners of the brain). Read a popular press book called "The Food-Mood Connection" which sounds like my sort of book, really, until the the author (who has a PhD of some sort!) explained that schizophrenia in a certain case was caused by childhood teasing. Poor man was treated with horrible prescription medicine and his genetics were examined, but I suppose some serious teasing psychoanalysis would have cured that schizophrenia eventually...it must have been his mother, come to think of it.
Anyway, there's a funny thing about schizophrenia, turns out that quite a few of the adult schizophrenics on Handford's inpatient unit in 1967 happened to have a major history of celiac disease (gluten/wheat intolerance) as children. As in 50-100 times the amount of celiac disease that one would expect by chance. Celiac doctors also noticed their patients were schizophrenic about 10X as often as the general population. That's a lot!
Allow me to paraphrase and expand on Table 1 of this paper, "Major Evidence that Peptides from Grain Glutens Evoke Idiopathic Schizophrenia in Those with Its Genotype"
1) In the 1960s, many observations suggested celiac disease and schizophrenia shared some genes. The role of gluten in schizophrenia was examined.
2) Epidemiologic studies showed a strong, dose-dependent relationship between grain intake and schizophrenia (Pacific islanders who ate no wheat had extremely rare occurence of schizophrenia - 2 in 65,000 rather than about 1 in 100 as we have in the grain-eating West. Then the same islanders changed their diet and began eating wheat - and schizophrenia became common).
3) Clinical trials and showed that gluten made new-onset acutely ill schizophrenics worse. Only occasional long-term patients responded to gluten restriction (remember, the affected brain cells of the long-term schizophrenics are already dead, so getting rid of the possible poison that killed the cells won't make much difference).
4) NIH investigators looked for poisonous protein fragments derived from gluten, gliadin, and casein. They found them - potent opiate (yes, opiate as in morphine. Or heroin) analogs they called "exorphins." They did these studies in rats, and I've read several of them. Very creepy. Turns out, you take wheat gluten, add stomach enzymes, and you end up with fragments of proteins that are potent opiates (1). The cute thing is these fragments aren't digested by the small intestine and definitely end up in the body and brain of rats that are fed gluten orally. Inject these same proteins directly into the brains of poor unfortunate rats, and you get rat seizures.
5) People with schizophrenia have a lot of these opioid-like small gluten-derived peptides in their urine. Way more than people without schizophrenia.
Let me review what is perhaps the most important part of the paper - a gluten-free diet definitely improved some of the new-onset schizophrenics on the inpatient unit. Not all of them. But 2 out of 17 or so. Putting back the wheat made the affected a lot worse. 115 patients on a locked ward were all given a gluten free milk free diet (remember the casein issue). They were released into the community (got better?) on average twice as fast as the similar patients on another, diet as usual ward (p=.009). It is of note that repeat studies didn't show the same thing, but instead of 17 or 115 patients, these studies had 4 or 8 patients, and they used chronic schizophrenics (end stage, when the brain cells are already gone).
Historically, prior to WWII, when grain consumption was super-high and neuroleptics (those medications, as you recall, which affect brain dopamine levels and are used to treat schizophrenia) did not yet exist, there are reports of schizophrenics having marked, unexplained fluctuations in weight and gut symptoms, poor iron absorption just like celiac sufferers, and "post-mortem abnormalities like those subsequently discovered in celiac patients." Why aren't these found now? Well, it turns out that a side effect of neuroleptics is that they decrease the permeability of the gut. Meaning gluten may not be able to weasel through quite so easily.
Which begs the question, is that the side effect? Or perhaps the principle effect?
Who knows?
Not psychiatrists in 2010. The paper (from 1988) finishes by suggesting a number of methods to investigate this connection further. One of the suggestions was morally bankrupt (feed the identical twins of schizophrenics a high gluten diet to see what happens!), but intriguing. That study wasn't done (fortunately). Nor, looking at pubmed (via eCommons), were any others (that I could find. I'm not the wiliest research paper discoverer so I might have missed one). The article is mentioned in a few review articles, and schizophrenics were left to eat wheat in peace.
Edit: I shouldn't be such a cynic, and I should search harder before I post - Here are more recent studies, including one from last month (Thanks to the commenter for the link - why I love blogging. Interactive! Editable! We can all stand on eachother's shoulders and the shoulders of past giants). All told, they throw out some more "biochemical smoke" about the link between schizophrenia and gluten:
Markers of Gluten Sensitivity and Celiac Disease in Recent-Onset Psychosis and Multi-Episode Schizophrenia: Conclusions - Individuals with recent-onset psychosis and with multi-episode schizophrenia who have increased antibodies to gliadin may share some immunologic features of celiac disease, but their immune response to gliadin differs from that of celiac disease.
Novel immune response to gluten in individuals with schizophrenia: The researchers here looked at all sorts of different anti-gliadin antibodies and celiac disease associated biomarkers (meaning some different antibodies and also specific celiac MHC genes - basically genetic predispositions to have autoimmune response to wheat). They also did some fancy chromatography to find if the schizophrenic's blood reacted to other wheat proteins, and then it sounds like they used "peptide mass mapping" to figure out what the wheat proteins were that the schizophrenics were reacting to - and the results were... schizophrenics of the wheat-reactive subtype had lots of anti-wheat protein immune response, and a lot of them were completely different than those found in celiac disease.
A Case Report of the Resolution of Schizophrenic Symptoms on a Ketogenic Diet That link is to the full text. It doesn't need much translating to make it more understandable - the title says it all.
This article from 2006 is also cited often, and I did look at it before I posted the first time, but it doesn't add that much: The gluten connection: the association between schizophrenia and celiac disease. Basically it says there are case reviews in the literature that show dramatic improvements in schizophrenia on a gluten-free diet (these studies were the same ones commented on in the original paper that I reviewed in detail at the top of the post) and that only a subset of schizophrenics are affected. (The researchers in residency would always refer to them as "the schizophrenias" rather than "schizophrenia." It is several different diseases, lumped into a similar symptom cluster because we don't fully understand the pathology, and in psychiatry, lumping is done by symptoms, as that made the most sense for research purposes.)
I would love to take a look at this one, but my institutional access won't get me there for the moment - A PILOT STUDY OF THE KETOGENIC DIET IN SCHIZOPHRENIA
PACHECO et al. Am J Psychiatry.1965; 121: 1110-1111. We'll track it down eventually.
The bottom line? Schizophrenia is a progressive and destructive psychotic mental illness that, at the moment, can sometimes be managed with medications and community therapeutic support, but does not have a cure. Some people with schizophrenia are bound to have the gluten-sensitive variety, and a few lucky souls apparently have been cured among the case reports. A gluten-free diet is safe and doesn't have side effects - I don't see a good argument against giving it a try for anyone with schizophrenia who is willing to give it a go, at least for a few months (how long? 3? 5? I'll look more into that one), while more data is being gathered. (You *might* get even better results with stabilizing your GABA receptors and whatnot via a ketogenic (very low carbohydrate) diet. More on this later! Very little research in psychiatry...) The worst thing that happens is you find you are not one of the gluten-sensitive schizophrenics, and you've gone without bread for a little while. The best thing that happens is that your symptoms get better, possibly quite a lot better.
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