Kimmelie skrev:Så det är bara att härda ut tills gifterna går ur kroppen igen. Jag har för mig att jag började känna mig piggare efter ca 3 dagar sist.
Fråga: Vilka ämnen är det som du anmärker vara toxiska och i vilka mängder per kg kroppsvikt då?
Kimmelie skrev:Så ett tips till de som lider av liknande symptom: Prova att utesluta allt spannmål förutom ris (kom ihåg att majs räknas som spannmål) och alla baljväxter, och ev även mjölkprodukter, i minst 3 veckor. Sen kan man prova att lägga tillbaka en sak i taget för att se vad man tål.
Ypperligt sätt OM en misstänker födoämnesöverkänslighet eller allergi - subjektiva spekulationer är dock inte att helt förlita sig på - rådgöra med legitimerad vårdpersonal bör ingå.
Kimmelie skrev:Tänk på att gliadinet i glutenet är en opiat, så jag rekommenderar att trappa ner det under en vecka. Jag provade först att klippa tvärt, men klarade inte av det. Abstinensen blev så stark att det var outhärdligt.
Gliadin är inte beroendeframkallande dock - att folk moffar i sig ex bröd, är till större del av bekvämliga anledningar (enkelt att fixa).
Utesluta gluten är rekommenderat om en har överkänslighet -
har en inte detta, så är det ingen fara att äta glutenprodukter, dock är det alltid bra att alternera sin kost.Sammanfattande text finns [urlhär[/url] (Gluten- and casein-free dietary intervention for autism spectrum conditions, 2012):
Conclusions
Experimental studies on the use of a GFD, CFD, or combinatorial GFCF diet for ASCs have suggested an amelioration of symptoms and improved developmental outcome for at least a proportion of people on the autistic spectrum. That being said, various methodological issues potentially biasing results remain which, combined with a lack of generalizable information on mode of action and best-responder data, have limited the impact of such findings over the years.
More recent controlled longitudinal studies examining group dietary effectiveness alongside an increasing recognition of individual cases of food-related co-morbidity and evidence of more consolidated biological mechanisms potentially at work, offer a favorable evidence base for at least a partial effect of diet on some cases of ASCs.
There is a continued requirement for further study on the potential role of dietary intervention for ASCs. Future controlled trials including blinded and placebo elements are necessary carrying appropriate power of study by sample size and duration. Based on the significant heterogeneity present in ASCs and the likelihood of various “autisms” manifesting similar presentation, further thought should also be given to the concept of best- and non-responders to this type of intervention. So for example, (1) screening for GI and/or potentially relevant pathogenic comorbidity, (2) measuring gut hyperpermeability, (3) examining gut microbial populations and food-related enzyme activities, and (4) ascertaining the presence of inflammatory processes, either peripherally in GI tissue or more centrally, might all be included as parameters for future dietary investigations. Similarly, measuring any relationship between behavior and GI function over the course of dietary intervention may offer some information about any connection between these factors.
Given the evidence hinting at neurological changes following the implementation of dietary intervention in related conditions, future research might also benefit from looking at brain structural and biochemical changes in cases of ASCs adopting dietary intervention. Indeed, the gut-brain relationship, seemingly so important to explaining the role of dietary intervention in best-responder cases, is a woefully under-researched area with ASCs in mind.
Finally but perhaps just as important, is a need to focus on the measurement of clinical changes to symptoms alongside statistical changes to psychometric or other assessment tools in view of the restrictiveness of the dietary regime. This point in particular reflects the fact that not everyone who might potentially benefit from dietary intervention will necessarily be able to implement such a restrictive regime, or indeed, want to.
The growing emphasis on various phenotypes for ASCs provides a template for conceptual changes to the way ASCs are viewed; where a ‘diet-related autism phenotype’ may be a target for future research and indeed a marker for efficacy of dietary intervention. Further discussions on whether such dietary intervention should form part of best practice guidelines for ASCs and onward representative of an autism dietary-sensitive enteropathy is warranted.
En annan studie (påbörjad) från 2010 visar att det *kan* finnas visst belägg för att utesluta mjölk -och gluten i kosten för människor med AST, dock behövs fler studier, större urval etc:
Abstract
There is increasing interest in the use of gluten- and casein-free diets for children with autism spectrum disorders (ASDs). We report results from a two-stage, 24-month, randomised, controlled trial incorporating an adaptive 'catch-up' design and interim analysis. Stage 1 of the trial saw 72 Danish children (aged 4 years to 10 years 11 months) assigned to diet (A) or non-diet (B) groups by stratified randomisation. Autism Diagnostic Observation Schedule (ADOS) and the Gilliam Autism Rating Scale (GARS) were used to assess core autism behaviours, Vineland Adaptive Behaviour Scales (VABS) to ascertain developmental level, and Attention-Deficit Hyperactivity Disorder - IV scale (ADHD-IV) to determine inattention and hyperactivity. Participants were tested at baseline, 8, and 12 months. Based on per protocol repeated measures analysis, data for 26 diet children and 29 controls were available at 12 months. At this point, there was a significant improvement to mean diet group scores (time*treatment interaction) on sub-domains of ADOS, GARS and ADHD-IV measures. Surpassing of predefined statistical thresholds as evidence of improvement in group A at 12 months sanctioned the re-assignment of group B participants to active dietary treatment. Stage 2 data for 18 group A and 17 group B participants were available at 24 months. Multiple scenario analysis based on inter- and intra-group comparisons showed some evidence of sustained clinical group improvements although possibly indicative of a plateau effect for intervention. Our results suggest that dietary intervention may positively affect developmental outcome for some children diagnosed with ASD. In the absence of a placebo condition to the current investigation, we are, however, unable to disqualify potential effects derived from intervention outside of dietary changes. Further studies are required to ascertain potential best- and non-responders to intervention.
...
och så har vi det som är väldokumenterat att det faktiskt fungerar:
Abstract
There is currently controversy regarding the need for and the effectiveness of behavior modification for children with attention-deficit hyperactivity disorder (ADHD) despite years of study and multiple investigations reporting beneficial effects of the intervention. A meta-analysis was conducted by identifying relevant behavioral treatment studies in the literature. One-hundred seventy-four studies of behavioral treatment were identified from 114 individual papers that were appropriate for the meta-analysis. Effect sizes varied by study design but not generally by other study characteristics, such as the demographic variables of the participants in the studies. Overall unweighted effect sizes in between group studies (.83), pre-post studies (.70), within group studies (2.64), and single subject studies (3.78) indicated that behavioral treatments are highly effective. Based on these results, there is strong and consistent evidence that behavioral treatments are effective for treating ADHD.