Celiac.com 10/06/2010 - Do you know where LSD comes from? It is made from gluten grains. In 1938 Albert Hofmann, a Swiss chemist, discovered LSD, having refined it from a mold that grows on grains. However, it was not until 1943 that he discovered its psycho-active properties. In his own words Hofmann states: “I synthesized the diethylamide of Iysergic acid with the intention of obtaining an analeptic.” The expectation of such a drug was based on its source—ergot—which grows on gluten grains and causes ergotism, also known as ergotoxicosis, ergot poisoning, holy fire, and Saint Anthony’s Fire.
This poisonous mold has long been known to infect gluten grains. It was to prevent the development of these molds that the Romans invented central heating systems. They stored their grains on the lowest floor of residences and other buildings that were centrally heated and well ventilated. Their fears of ergot were based on the powerful and bizarre symptoms that developed in people who ate grains that had become moldy with ergot. Some afflicted individuals began to hallucinate, often becoming so mentally disturbed that they injured or killed themselves. Others experienced loss of blood circulation to their extremities which became gangrenous. Their digits and limbs sometimes fell off before these people died. Some experienced a combination of these two sets of symptoms. Animals sometimes display similar symptoms after consuming moldy grains.
- Last Friday, April 16, 1943, I was forced to stop my work in the laboratory in the middle of the afternoon and to go home, as I was seized by a peculiar restlessness associated with a sensation of mild dizziness. On arriving home, I lay down and sank into a kind of drunkenness which was not unpleasant and which was characterized by extreme activity of imagination. As I lay in a dazed condition with my eyes closed (I experienced daylight as disagreeably bright) there surged upon me an uninterrupted stream of fantastic images of extraordinary plasticity and vividness and accompanied by an intense, kaleidoscope-like play of colors. This condition gradually passed off after about two hours. From http://www.psychedelic-library.org/hofmann.htm.
Several days later Dr. Hofmann intentionally ingested 250 µg of LSD which he hypothesized would be a threshold dose. Here is what he said about his second ingestion:
- April 19, 1943: Preparation of an 0.5% aqueous solution of d-lysergic acid diethylamide tartrate.
- 4:20 P.M.: 0.5 cc (0.25 mg LSD) ingested orally. The solution is tasteless.
- 4:50 P.M.: no trace of any effect.
- 5:00 P.M.: slight dizziness, unrest, difficulty in concentration, visual disturbances, marked desire to laugh...
- At this point the laboratory notes are discontinued: The last words were written only with great difficulty. I asked my laboratory assistant to accompany me home as I believed that I should have a repetition of the disturbance of the previous Friday. While we were cycling home, however, it became clear that the symptoms were much stronger than the first time. I had great difficulty in speaking coherently, my field of vision swayed before me, and objects appeared distorted like images in curved mirrors. I had the impression of being unable to move from the spot, although my assistant told me afterwards that we had cycled at a good pace. http://www.psychedelic-library.org/hofmann.htm
The difficulty Hofmann experienced with speaking coherently is reminiscent of a 1988 case report from Massachusetts General Hospital in which a patient was admitted for investigation of bowel complaints. While in the hospital he became unable to speak coherently. Eventually diagnosed with celiac disease, he was placed on a gluten free diet. After several months on the diet, his speech was fully returned. But I’m getting ahead of myself. We were talking about Hofmann’s discovery.
LSD arrived in the USA in 1948 and was used to gain a better understanding of the schizophrenic experience:
- In psychiatry, the use of LSD by students was an accepted practice; it was viewed as a teaching tool in an attempt to enable the psychiatrist to subjectively understand schizophrenia. http://en.wikipedia.org/wiki/History_of_LSD
These students who tried LSD apparently failed to consider that the connection between the symptoms of LSD ingestion and schizophrenia might be due to a common source—psycho-active peptides from gluten grains.
About a decade after LSD had crossed the Atlantic, and from a very different research perspective, Dr. Curtis Dohan began investigating the possibility that gluten grains might be a factor in schizophrenia. He had found that people with celiac disease and those with schizophrenia both excrete increased quantities of specific groups of indoles in their urine. Some such indoles are known to be psychoactive and some psychoactive alkaloids also contain such indoles.
Having learned about this connection between celiac disease and schizophrenia, Dr. Dohan then undertook a study in which he examined hospital admission rates for schizophrenia both during periods of plenty and during World War II grain shortages. He found that there was, indeed, a reduction in admissions during grain shortages, which normalized when ample grains became available again.
Dohan’s next step, along with several colleagues, was to design and conduct a single-blind cross-over study of schizophrenic patients in a locked ward. They found that symptoms of schizophrenia abated on a gluten-free, dairy-free diet. These same patients relapsed on re-introduction of these foods. These data were published in The British Journal of Psychiatry in 1969. Dohan’s findings were replicated and published in the January1976 issue of Science by Man Mohan Singh and Stanley Kay.
Three years later, Christine Zioudrou and her colleagues demonstrated the presence of psychoactive peptides in the incomplete digests of gluten grains, including some with morphine-like properties, which they named “exorphins”. Subsequent research by Fukudome and Yoshikawa has shown that there are five separate sequences from gluten grains that have psycho-active properties. They named these exorphins A4, A5, B4, B5, and C.
At some point in this process, Dohan may have learned about the pseudo-hallucinations sometimes reported in celiac patients. The primary difference between the schizophrenic’s hallucinations and those associated with celiac disease is that the celiac patient can exercise conscious control to stop them. The schizophrenic appears unable to do this.
As he continued to accumulate more such data, Dohan went on to publish 16 more papers and letters over the next twenty years demonstrating an impressive body of evidence to support his suspicion that psychoactive peptides from gluten and possibly dairy proteins had a powerful impact on many cases of schizophrenia. Yet, to an even greater extent than today, most people simply could not believe that such supposedly healthful foods as gluten grains and dairy products could be causing illness. It was probably this paradigm that helped lead to subsequent publications and a period of dormancy in this area of research.
Several reports of very small numbers of schizophrenic patients, chronic patients, which Dohan had specifically identified as unlikely to respond to the diet, showed no benefit from a gluten-free diet. Other studies were improved through double-blinding but weakened by extremely limited dietary control, permitting visitors to bring food to patients participating in that study, essentially abrogating the value of the entire study. Some researchers ignored Dohan’s assertions that celiac disease could serve as a model for studying schizophrenia. They chose, instead, to produce data that discredited the possibility that schizophrenia is identical to celiac disease by showing that most schizophrenic patients do not show signs of malabsorption. Other work, conducted in the same vein, showed that celiac antibodies are not found in most schizophrenic patients.
Despite all the powerful evidence compiled by Dohan and others, this wave of studies and letters discredited Dohan’s work by contradicting notions that Dohan had never voiced. For instance, he never expressed the notion that schizophrenia was celiac disease. He simply asserted that there were compelling similarities and a small but significant overlap between schizophrenia and celiac disease, suggesting the need to explore gluten as a possible contributing factor in schizophrenia. Considerable data support that notion but Dohan’s vigorous and persistent pursuit of this important discovery was soon depicted as a personal quest. For instance, in a private email with one of Dohan’s contemporaries, Dohan was repeatedly called “unscientific.” Yet, fifteen years later, this same researcher has since participated in a published study that supports Dohan’s hypothesis.
Fortunately for all of us, the last dozen years have seen a resurgence of interest in the gluten hypothesis regarding schizophrenia, beginning with a case report by De Santis et al. They described a patient with schizophrenia and a SPECT scan showing abnormal blood flow patterns in the brain typical of schizophrenia. This patient developed symptoms of celiac disease and was placed on a gluten free diet. Not only did this patient’s celiac symptoms disappear, her/his symptoms of schizophrenia disappeared and blood flow patterns in her brain normalized. The gluten-free diet was the only plausible explanation for these changes.
A list of reports suggest important reasons to investigate the impact of gluten on our brains. For instance, Dr. Knivsburg reported the discovery of two cases of celiac disease and one of milk protein sensitivity among 15 dyslexic children. That is a huge increased incidence over the general population. Similarly, Dr. Kozlowska found that almost 70% of celiac children have ADHD that normalizes on a gluten-free diet. The Massachusetts General Hospital case study mentioned earlier reported celiac-associated aphasia that resolved on a gluten free diet. Dr. Hu and colleagues report a laundry list of cognitive impairments in association with celiac disease including amnesia, acalculia, confusion, and personality changes. Many of these disabilities wax and wane according to the gluten content of the diet.
However, the notion of gluten-driven cognitive deficits, including learning disabilities, and behavioral abnormalities in association with non-celiac gluten sensitivity, has only recently gotten some research attention. For instance, Alexandra Blair of The TimesOnline in the United Kingdom reported on an informal study conducted at a small school for dyslexic children in Northumberland. They got some startlingly positive improvements in students’ performance after placing them on a gluten free diet. Dr. Marios Hadjivassiliou et al. at the Royal Hallamshire Hospital in Sheffield, U.K. have repeatedly reported that a majority of patients with neurological disease of unknown origin are also gluten sensitive while only about one third of these patients have celiac disease.
Kalaydjian et al. reviewed the medical literature to about 2005 and called for large, controlled studies of the connection between gluten and schizophrenia because it is clear that some schizophrenic patients benefit enormously from a gluten free diet. Similarly, earlier this year, Kraft et al. reported on a schizophrenic patient who was diagnosed at seventeen years of age. Fifty three years later, at her doctor’s suggestion, she undertook a ketogenic diet to lose weight. Not only did she lose weight, she also lost all signs and symptoms of schizophrenia.
As 2009 comes to a close, two more publications have made this year into something of a turning point for this research. Cascella et al. state that “Our results confirm the existence of a subgroup of patients with antibody characteristics associated with the presence of a specific immune response to gluten.”
Similarly, Samaroo et al. report that their findings “…. indicate that the anti-gliadin immune response in schizophrenia has a different antigenic specificity from that in celiac disease…” they go on to assert that the genetic HLA markers for celiac disease were not found in the schizophrenic patients they studied.
At the most basic level, we know that gluten causes increased intestinal permeability among a wide range of genetically susceptible individuals. We also know that substances from moldy grains will cause schizophrenic symptoms in any of us. It is not a great leap to suggest that, in the context of gluten-induced increased intestinal permeability, similarities in hallucinations, altered brain perfusion, and a range of cognitive deficits found in schizophrenia, celiac disease, and gluten sensitivity might all be rooted in the commonest food in our diets from which hallucinogenic drugs can be produced.
Institutional nutrition and food programs for the needy and/or homeless include large proportions of inexpensive gluten-laden foods. Such diets, often provided charitably for those at the lowest socio-economic strata, are at least self-defeating. Further, such foods are often consumed at this economic level despite visible molds growing on them. I have heard stories of homeless persons scavenging through dumpsters located at or near bakeries. There can be little doubt that such eating practices perpetuate the very psychiatric conditions that have reduced many of these people to a state of homelessness.