This isn't directly about autism but since schizophrenia and autism seem to have some biological mechanisms in common I think it is still relevant -
Prevention and Schizophrenia — The Role of Dietary Factors
Adequate prenatal nutrition is essential for optimal brain development. There is a growing body of evidence from epidemiology linking exposure to nutritional deprivation and increased risk of schizophrenia. Based on studies from the Netherlands and China, those exposed to macronutrient deficiencies during famine have an increased risk of schizophrenia. With respect to micronutrients, we focus on 3 candidates where there is biological plausibility for a role in this disorder and at least 1 study of an association with schizophrenia. These nutrients include vitamin D, folic acid, and iron. While the current evidence is incomplete, we discuss the potential implications of these findings for the prevention of schizophrenia. We argue that schizophrenia can draw inspiration from public health interventions related to prenatal nutrition and other outcomes and speculate on relevant factors that bear on the nature, risks, impact, and logistics of various nutritional strategies that may be employed to prevent this disorder.
Full Text
The idea that correcting nutriental deficiencies can help a person with a mental disorder is actually common in the bio-medical part the autism community. This journal article takes it one step further and suggests that a mental disorder - in this case schizophrenia - might be able to be prevented by correcting these deficiencies.
Hi MJ -
ReplyDeleteThe idea that correcting nutriental deficiencies can help a person with a mental disorder is actually common in the bio-medical part the autism community.
I think a lot of the time semantics is a problem here, if we want to 'help' someone, that seems to invoke a lot less anger than wanting to 'cure' someone. Nicely done.
This journal article takes it one step further and suggests that a mental disorder - in this case schizophrenia - might be able to be prevented by correcting these deficiencies.
The full version is unavailabe right now (do you have a copy?), but I think it's important to note that the abstract indicates that the time period of effect is prenatal.
There are also some animal models (insert caveat here), that indicate other prenatal supplementations, i.e., NAC, might be able to reduce autism in the offspring by attenuating the immune response.
Late N-acetylcysteine treatment prevents the deficits induced in the offspring of dams exposed to an immune stress during gestation
Prenatal infection is a major stressful experience leading to enhanced susceptibility for mental illnesses in humans. We recently reported in rats, that oxidative stress and glutathione (GSH) shortage occurred in fetal male brain after lipopolysaccharide (LPS) to the dams and that these responses might be involved in the neurodevelopmental deficits observed in adolescent offspring. Furthermore, pretreatment with N-acetylcysteine (NAC) before LPS avoided both delayed synaptic plasticity and mnesic performance deficits. Since NAC is one of the few medications permitted in pregnant women, this study evaluated the ability of NAC to serve as a protective therapy even after the LPS challenge. Pregnant rats received a single ip injection of E. coli LPS, two days before delivery, and were given NAC in their tap water after the LPS. GSH was evaluated at the time of its expected drop in the hippocampus of male fetuses, whereas long-term potentiation (LTP) in the CA1 area of the hippocampus and spatial memory in the water-maze were recorded in 28-day-old male offspring. Post-treatment with NAC, four hours after the LPS challenge fully prevented the drop in the GSH hippocampal content. LTP, as well as spatial learning were completely protected. NAC administration at delivery also partially restored the LTP whereas post-treatment two days later was inefficient. Another set of dams were supplemented with alpha-tocopherol prior to LPS exposure, enhancing the alpha-tocopherol levels in fetal hippocampus. This treatment did not prevent the LPS-induced synaptic plasticity impairment. These results point to fetal hippocampal GSH as a major target of the detrimental effects of in utero LPS challenge. The therapeutic window of NAC extends up to birth, suggesting that this drug might be clinically useful even after an immuno-inflammatory episode.
It's a long way to humans, of course, but still a very interesting line of experimentation. I have wondered aloud on more than one occassion, if this type of intervention would be permissible by the orthodox neurodiverse, without any response.
Regarding schizophrenia, there are some studies that you can affect behavioral severity by affecting the immune system; but you don't have to do it prenatally.
http://www.ncbi.nlm.nih.gov/pubmed/20492850 [double blind, placebo control, randomized study finding adjuvant aspirin treatment improved schizophrenia]
http://www.ncbi.nlm.nih.gov/pubmed/17208413 [similar methodologies and findings using cox-2 inhibitors]
There is often an intense desire to ignore these types of findings due to their basis in immunology for obvious reasons, but the data is the data.
- pD
[Last attempt to post. If this double posts (or worse), please nuke all but one. damn you, blogger!]
Hi Pd,
ReplyDeleteBlogger never seems to like your comments for some reason. I wish I could turn off the spam filter but Google, in all of its wisdom, has decided that there is no need for that option.
I can see the study text using the link above and selecting the "full text (html)" link but I can't get it in pdf without paying for it. You are right though that the study focuses on prenatal deficiencies rather than deficiencies that are observed in the person after they are born.
But I think autism might be different than schizophrenia in that regard. I am wondering if post-natal deficiencies play a larger role than prenatal ones in autism
There are a few interesting things about autism that make me say that. Such as the idea that it is more common in more affluent people. I would think that the more affluent would be less likely to have these sorts of deficiencies.
Or consider some of the other strange, non-intuitive, results like the one in the most recent Bearman paper on interpregnacy intervals that showed that the risk of autism increased for shorter IPIs. Yet if you look at the data table in the paper, you can see that for a given IPI range the risk of autism went down as the parents got older. You would think that older women would stand a higher chance of having these deficiencies, especially in the face of two pregnancies in a very short period of time.
And at the same time, you have numerous results showing that children with autism suffer from a wide variety of nutrient deficiencies. I know that my children were deficient in a good number of nutrients - including iron - at a very young age.
None of this is in any way conclusive but it is interesting. I would love to see a good paper that examines (and actually measures) basic nutrient levels in a large population of children with autism. I have seen a few that looked just at food intake or just at one or two nutrients but nothing really comprehensive.
Apologies for being a bit late to this. There is quite a lot of talk about diet and mental health over at Evolutionary Psychiatry - no I am not paid to suggest the link!:
ReplyDeletehttp://evolutionarypsychiatry.blogspot.com/
A recent posting on NAC and the wide research net being spread around it is also included:
http://evolutionarypsychiatry.blogspot.com/2011/03/problems-i-have-nac-for-that.html
With regards to schizophrenia and nutrition/diet perhaps also important to take on board the work of Faith Dickerson and colleagues.