Talk:Attention deficit hyperactivity disorder/Archive 25

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Gluten and ADHD

Break

Hi, Doc James. Perhaps you didn't read my last message. You proposed summarize this as "A gluten free diet in those with CD and ADHD may improve the symptoms of both." and I proposed something like this, to adjust and be more precise: A few studies in patients with an undiagnosed celiac disease showed an improvement of symptoms of ADHD when starting a gluten-free diet.[1] Which of the two we choose?
The Psychiatric Quarterly is a peer-reviewed medical journal that was established in 1915, with an impact factor of 1.26 (5-year impact: 1.39).
Best regards. --BallenaBlanca (talk) 10:01, 3 April 2016 (UTC)
Added. Doc James (talk · contribs · email) 14:16, 3 April 2016 (UTC)
I've gotten the full paper of the newly added source PMID 26825336. It is a good source, published on Journal of Attention Disorders (current impact factor of 3.78). I will expand, supported by this source, and I will try to be as brief as possible. The text I will add is on the same line that the text has been discussed and approved above, that led to the inclusion of this text by Doc James: [1] (There is no clear relationship betwen ADHD and CD, but is not incompatible with the fact that CD patients with ADHD improve with GFD). I hope you agree and I wait your opinions. Best regards. --BallenaBlanca (talk) 10:38, 13 April 2016 (UTC)
Have adjusted it some. Let me know what you think. Remember to use "person with ADHD" rather than "ADHD patient" per the WP:MEDMOS.Doc James (talk · contribs · email) 19:09, 13 April 2016 (UTC)
Remember to use "person with ADHD" Oops...! Sorry! I will remember.
I like the adjustments you made, minus the last sentence: "People with ADHD and a broad range of physical symptoms should be tested. [158]" This implies that people with CD and ADHD have always a large number of other symptoms. The meaning is very different. The authors say literally: "Therefore, it is recommended for clinicians to assess a broad range of physical symptoms, in addition to typical neuropsychiatric symptoms, when evaluating patients with ADHD" because they previously explained the wide variety of symptoms (digestive and/or extra-digestive) that can present CD and make it difficult to identify. What it means is that physicians have to evaluate a wide range of symptoms, because the presence of any of them (perhaps only one, or two, or more... all is possible) may be the track to identify an undiagnosed CD. I realize that my previous text was confused, wanting to do so shortly.
It is clear that it is better to add a clarification, for everyone can understand it, without reading the entire reference, because out of context it is confusing.
I will adjust. Tell me if you like the result.
Best regards. --BallenaBlanca (talk) 21:10, 13 April 2016 (UTC)
The exact symptoms of celiacs belongs in the celiac article IMO as those symptoms are complicated. How about "In people with ADHD, those with any of a range of physical symptoms should be tested to identifying unrecognized celiac disease"? Doc James (talk · contribs · email) 12:47, 14 April 2016 (UTC)

People with symptoms of any mental health problem should always see their PCP to rule out likely physical ailments first. Celiacs is not unique in having some overlapping symptoms with ADHD and it's far from the most common. It not in the top 5. This reads like doctors have no idea ADHD symptoms could be caused by something else. We can't/shouldn't attempt to address every other issue that might present like ADHD and if we're going to mention some things that should be ruled out first, it should be the most common: seasonal allergies, asthma hearing or vision disorders, anemia, hashimotos/thyroid issues, tonsil/adenoid issues, sleep apnea and other sleep disorders, brain injury, elevated lead levels...[2][3] and that's not even mentioning things like learning disabilities, other mental illnesses, and having crappy parents. If your pediatrician isn't ruling out other likely possibilities before officially diagnosing your kid with anything, you need a new pediatrician. As far as celiacs goes, it would encompassed with due weight in sentence like, "doctors should always rule out potential physiological explanations for attentional issues as part of a thorough ADHD evaluation." More sources talking about common things to rule out in patients with ADHD symptoms that don't mention celiacs:[4][5][6][7][8] PermStrump(talk) 15:02, 14 April 2016 (UTC)

Hi, Permstrump. Your comments are very interesting and you are quite right. There is already a Differential diagnosis section which mentions most of the diseases that you are listing Attention_deficit_hyperactivity_disorder#Differential_diagnosis but I agree your observation: "doctors should always rule out potential physiological explanations for attentional issues as part of a thorough ADHD evaluation." IMO, this sentence should be on first place in the Diagnosis section, because it must be the first step, prior to psychiatric evaluation and ADHD diagnosis, searching a good source to support it. What do you think?
In the case of the section Diet, the objetive is to reflect the results of the studies with neutrality, explaining all conclusions. Perhaps the best thing is to modify a little again, to reflect what the authors mean in other words, compatible with the existence of a differential diagnosis section. I will do it. Let me know if you agree.
If your pediatrician isn't ruling out other likely possibilities before officially diagnosing your kid with anything, you need a new pediatrician. It could not have said it better! How right you are! And not only pediatrician, ADHD affects both children and adults.
Best regards. --BallenaBlanca (talk) 18:09, 14 April 2016 (UTC)
Doc James thanked me by this edit [2], reverted by Garzfoth [3] "Uh, this is even more incorrect and misleading... " I don't understand why this is "even more incorrect and misleading". It seems that the problem is to say that celiac disease "may present with mild or absent gastrointestinal complaints". Currently, it has changed the understanding of the presentation of CD. Non-classical CD presentation (with mild or absent gastrointestinal symptoms and extra-intestinal manifestations) is more common than classical presentation (with malabsorption and chronic diarrhea). Really, is even more adjusted to say that often present with mild or even absent gastrointestinal symptoms. Let's see two sources (NOTE: Non-classical and atypical refer to the same presentation and are interchangeably. Also, classical and typical are synonymous):
World Gastroenterology Organisation Global Guidelines on Celiac Disease
Many patients with CD have few symptoms or present atypically, whereas a minority of patients have malabsorption (classical CD).
Diagnosis and management of adult coeliac disease: guidelines from the British Society of Gastroenterology
Traditionally patients with CD presented with malabsorption dominated by diarrhoea, steatorrhoea, weight loss or failure to thrive (‘classical CD’),7 but over time the proportion of newly diagnosed patients with malabsorptive symptoms has decreased,31 and ‘non-classical CD’7 and even asymptomatic CD have gained prominence. Newly diagnosed patients with CD can present with a wide range of symptoms and signs, including anaemia,32 vague abdominal symptoms (often similar to irritable bowel syndrome (IBS)33), neuropathy,34 ,35 ataxia,36 depression,37 short stature,38 osteomalacia and osteoporosis,39 liver disease,40 adverse pregnancy outcomes41 and lymphoma.42
And let's see part of the text of the source used in ADHD.[9] Really, the text currently included is very summarized, as there is much that can be written about it:
Quotation from Ertürk et al.: (Edited to fix layout and create a box)
Untreated, CD has a wide range of clinical presentations. The “classical CD type” presents with mostly gastrointestinal symptoms such as abdominal pain, distension, chronic diarrhea, or failure to thrive. The “non-classic CD type” is characterized by fewer or no gastrointestinal symptoms and presents with extra-intestinal manifestations, such as neurologic, dermatologic, hematologic, endocrinologic, reproductive, renal, psychiatric, skeletal, and liver involvement (Celiloğlu, Karabiber, & Selimoğlu, 2011). The “asymptomatic or silent CD type” can present with no clinical symptoms and only positive serology (Bai et al., 2013). ...
Neuropsychiatric Symptoms in CD
Research on neuropsychiatric symptoms in patients with CD report age-related differences. In adult patients with CD, ataxia, epilepsy, peripheral neuropathy, inflammatory myopathies, myelopathies, headache, gluten encephalopathy, white matter abnormalities, anxiety disorders, depressive and mood disorders, ADHD, autism spectrum disorders, and schizophrenia have been reported (Jackson, Eaton, Cascella, Fasano, & Kelly, 2012). In children with CD, however, the risk of developing neuropsychiatric disturbances is only 2.6% (compared with 26% in adults; Ruggieri et al., 2008). This discrepancy may be due to shorter disease duration in children, earlier elimination of gluten from the diet, stricter adherence to a diet, or a different susceptibility to immune-mediated disorders (Lionetti et al., 2010; Ruggieri et al., 2008).
Discussion
ADHD-Like Behavior and CD
Based on this review, there is no conclusive evidence for a relationship between ADHD and CD. However, attention difficulties, distractibility, chronic fatigue, and headache have been observed in patients with CD, especially prior to treatment or when noncompliant to GFD (Terrone et al., 2013). Newly diagnosed children with CD often complained of “aches and pains,” “easily tired,” “easily distracted,” and “trouble concentrating.” After 1 year of GFD treatment, scores on these items were reduced and remained low in GFD-compliant children (Terrone et al., 2013). Also in newly diagnosed adults with CD, a significant improvement in cognitive functioning, particularly verbal fluency, attention, and motor function, is noted after a 12-month adherence to GFD (Lichtwark et al., 2014). Thus, it is possible that in untreated patients with CD, neurologic symptoms such as chronic fatigue, inattention, pain, and headache could predispose patients to ADHD-like behavior (mainly symptoms of inattentive type), which may be alleviated after GFD treatment.
Possible Mechanisms
Possible mechanisms underpinning the relation between attention/learning problems and CD point to accumulative effects of multiple effects, including both nutritional and immunologic/inflammatory factors. However, more indirect factors, related to nonspecific effects of chronic disease, cannot be ruled out (Zelnik et al., 2004). With respect to nutritional factors, micronutrient deficiencies and anemia are frequently seen in untreated patients with CD (Kupper, 2005; Wierdsma, van Bokhorst-de van der Schueren, Berkenpas, Mulder, & van Bodegraven, 2013). These factors may also play a role in causing ADHD-like behavior. However, when studying iron and zinc deficiencies in patients with ADHD, results remained inconclusive and needed further elaboration (for a review, see Millichap & Yee, 2012). There is emerging evidence that immunological mechanisms may contribute to ADHD development and manifestation (Verlaet, Noriega, Hermans, & Savelkoul, 2014). CD may induce an immune dysregulation in the gut, leading to chronic inflammation, which on its turn may be the cause for developing ADHD-like symptoms (Esparham, Evans, Wagner, & Drisko, 2014). Studies on the brain level point to the possible implication of serotonergic dysfunction in developing neuropsychiatric disorders in CD. More specifically, these studies refer to an impaired availability of tryptophan and decreased serotonin and dopamine metabolite concentrations (Hernanz & Polanco, 1991; Jackson et al., 2012; Pynnönen et al., 2005). Neuroimaging studies show structural and functional brain deficits in adult patients with CD. Structural deficits include bilateral decrease in cortical gray matter and caudate nuclei volumes (Bilgic et al., 2013), bilateral decrease in cerebellar gray matter, and smaller volume in multiple cortical regions (Currie et al., 2012). Functional deficits include a hypoperfusion of cerebral regions, primarily in the frontal cortex in untreated adult patients with CD, but not in treated patients (Addolorato et al., 2004; Usai et al., 2004). Such brain abnormalities may induce problems in high-cognitive functions such as attention span. Further research is however needed to confirm this hypothesis. To our knowledge, there are no studies on structural and functional brain deficits in pediatric patients with CD. A final hypothesis relates to increased oxidative stress that has been described in both ADHD (Lopresti, 2015) and CD (Stojiljković et al., 2009). Therefore, oxidative stress may represent a possible mediator in the development of ADHDlike behavior in CD patients. However, it remains uncertain whether oxidative stress itself contributes to the development or exacerbation of ADHD symptoms or whether it is the result of environmental factors (Lopresti, 2015). Further empirical studies are needed to understand the mechanisms underlying the potential association between ADHD, ADHD-like behavior, and CD.
Clinical Implications
Up till now, there is no conclusive evidence for a relationship between ADHD and CD. Therefore, it is not advised to perform routine screening of CD when assessing ADHD (and vice versa) or to implement GFD as a standard treatment in ADHD. Nevertheless, the possibility of untreated CD predisposing to ADHD-like behavior should be kept in mind. Therefore, it is recommended for clinicians to assess a broad range of physical symptoms, in addition to typical neuropsychiatric symptoms, when evaluating patients with ADHD.
Best regards. --BallenaBlanca (talk) 22:28, 14 April 2016 (UTC)

References

  1. ^ Cite error: The named reference JacksonEaton2012 was invoked but never defined (see the help page).
  2. ^ Chen; et al. (11 Feb 2013), "Comorbidity of allergic and autoimmune disease among patients with ADHD: a nationwide population-based study", J Atten Disord, PMID 23400216, The diseases significantly associated with patients with ADHD compared with the control group were the following: allergic diseases (asthma 25% vs. 18%, allergic rhinitis 41% vs. 30%, atopic dermatitis 18% vs. 13%, and urticaria 8% vs. 6%), autoimmune diseases (ankylosing spondylitis 0.1% vs. 0%, odds ratio [OR] 2.78; ulcerative colitis 0.2% vs. 0.1%, OR 2.31; autoimmune thyroid disease 2.1% vs. 0.8%, OR 2.53); and psychiatric disorders (depressive disorders 5.5% vs. 0.5%; anxiety disorders 15% vs. 0.4%). In contrast, Crohn's disease, celiac disease, and type 1 diabetes mellitus did not show any significant correlations with ADHD. {{citation}}: Explicit use of et al. in: |last= (help)
  3. ^ DeNisco; et al. (2005), "Evaluation and treatment of pediatric ADHD", Nurse Practitioner, 30 (8): 14-17, PMID 16094198, Attention deficit hyperactivity disorder is a heterogeneous behavioral disorder with several possible etiologies. Environmental and central nervous system insult, such as head trauma, exposure to lead, cigarette exposure,and low-birth weight (less than 1,000 grams) are thought to be a possible cause... Some common problems in the pediatric population that can cause ADHD-like symptoms include anemia, lead toxicity, thyroid problems, learning disabilities, uncorrected hearing or vision problems, substance abuse, depression, anxiety, bipolar disorder, and anxiety disorders. The target symptoms for each patient should be carefully documented for proper diagnosis and treatment. {{citation}}: Explicit use of et al. in: |last= (help)
  4. ^ Gillberg; et al. (2004), "Co-existing disorders in ADHD – implications for diagnosis and intervention", Eur Child Adolesc Psychiatry, 13 (Suppl 1): I80-92, PMID 15322959 {{citation}}: Explicit use of et al. in: |last= (help)
  5. ^ Breggin (1999), "Psychostimulants in the treatment of children diagnosed with ADHD: Risks and mechanism of action" (PDF), International Journal of Risk & Safety in Medicine, 12: 3–35
  6. ^ Hsueh-Yu Li (July 2006), "Impact of Adenotonsillectomy on Behavior in Children With Sleep-Disordered Breathing", Laryngoscope, 116, doi:10.1097/01.mlg.0000217542.84013.b5, PMID 16826049
  7. ^ Mazza (March 2014), "Distracted at School: Aprosexia, ADHD and Adenoids in American Culture", The Journal of American Culture, 37 (1), doi:10.1111/jacc.12103
  8. ^ Silva; et al. (2014), "Children diagnosed with attention deficit disorder and their hospitalisations: population data linkage study", Eur Child Adolesc Psychiatry, 23: 1043–1050, doi:10.1007/s00787-014-0545-8, PMID 24770488 {{citation}}: Explicit use of et al. in: |last= (help)
  9. ^ Ertürk, E; Wouters, S; Imeraj, L; Lampo, A (29 January 2016). "Association of ADHD and Celiac Disease: What Is the Evidence? A Systematic Review of the Literature". Journal of attention disorders (Review). PMID 26825336.

Source for gluten free diet not reliable

In the section on managing ADHD symptoms with diet, a literature review by Ertürk et al. (2016) is used to support this statement: "A 2016 review states that evidence does not support a clear link between celiac disease and ADHD, and that routine screening for celiac disease in people with ADHD and the use of a gluten-free diet are discouraged. However, untreated celiac disease, which often present with mild or even absent gastrointestinal complaints, could predispose to ADHD symptoms, especially those of inattentive type, which may be improved with a gluten-free diet."[1] Now that I've had a chance to thoroughly read the paper, I don't think it's a reliable source for this statement. My issue is with the second sentence, because it was easy to find alternate sources to the support the first sentence alone, like Sethi and Hughes (2015).[2] My issue with Ertürk et al.'s paper is that they contradict themselves in several locations and their conclusions are not supported by actual findings. Only 3 of the 8 studies they found a positive correlation between ADHD and celiacs and only 2 of those studies (both with the same lead author - Niederhofer) "showed" a decrease in ADHD-like symptoms after starting a GFD. All 3 were "low quality" with "very poor internal validity and small sample sizes" according to Sethi and Hughes.[2]

Quotes from sources
Ertürk et al. (2016)[1]

For context, in Feb 2016, Ertürk et al. did a lit review of all of the trials ever published on ADHD and celiacs and they found 8 that discussed a possible association between CD and ADHD:

  • Lahat et al. (2000) • Zelnik et al. (2004) • Pynnönen et al. (2004) • Niederhofer and Pittschieler (2006) • Ruggieri et al. (2008) • Niederhofer (2011) • Güngör et al. (2013) • Dazy et al. (2013)

After reviewing those 8 studies, these were their findings:

  • p2: Only one study considered ADHD as a possible onset manifestation of CD. However, no improvement was seen after starting a GFD treatment (Diaconu, Burlea, Grigore, Anton, & Trandafir, 2013)
  • 3-4: Only three out of eight studies reported a positive correlation between ADHD and CD: Two studies found an overall higher prevalence of ADHD in patients with CD (Niederhofer & Pittschieler, 2006; Zelnik et al., 2004), and one study reported an over representation of CD in patients with ADHD (Niederhofer, 2011). However, these studies show methodological limitations. The first study of Niederhofer (Niederhofer & Pittschieler, 2006) reported on ADHD symptoms rather than including a formal diagnosis of ADHD. In the other study (Niederhofer, 2011), only CD antibody serology was used to diagnose CD, without a confirmatory biopsy. In both studies, there was no control group (Niederhofer, 2011). The study of Zelnik et al. (2004) screened for combined ADHD and LD in patients with CD, without making a distinction between the presence of ADHD versus learning disorders in CD patients.

*Note Ertürk et al. didn't even mention if the 3 studies that showed a positive correlation between ADHD and celiacs found that GFD improved symptoms. In fact, Zelnik et al. explicitly found the opposite. According to other reliable sources, there's so much bias in the Niederhofer studies that they don't count.[2]

Yet, somehow Ertürk et al. came to the conclusion that:

  • p4: Newly diagnosed children with CD often complained of “aches and pains,” “easily tired,” “easily distracted,” and “trouble concentrating.” After 1 year of GFD treatment, scores on these items were reduced and remained low in GFD-compliant children (Terrone et al., 2013). Also in newly diagnosed adults with CD, a significant improvement in cognitive functioning, particularly verbal fluency, attention, and motor function, is noted after a 12-month adherence to GFD (Lichtwark et al., 2014). Thus, it is possible that in untreated patients with CD, neurologic symptoms such as chronic fatigue, inattention, pain, and headache could predispose patients to ADHD-like behavior (mainly symptoms of inattentive type), which may be alleviated after GFD treatment.

*Note that neither of the 2 studies cited in the conclusion were one of the 8 analyzed for the lit review. And if you look at those two studies, they don't support this statement. Lichtwak et al. (2014)[3] weren't explicitly measuring ADHD or inattention symptoms, Lichtwak and all of the co-authors noted massive conflicts of interest, and their study was heavily criticized for bias and poor design by Lebwohl et al. (2014) for additional reasons.[4] Terrone et al. (2013)[5] also weren't testing for tru ADHD, just "inattention" in combination with other mental health issues like depression, anxiety, oppositional behavior, etc., and they were really vague about what inattention symptoms were reported and didn't show the before and after data. There's a reason they weren't included in Erturk or Sethi and Hughes lit reviews, so it's pretty shady for Erturk to turn around and act like those studies support their hypothesis when the actual studies they analyzed didn't.

Sethi and Hughes (2015)[2] also did a lit review of the published studies on celiacs and ADHD. They found 8 studies (with only one difference from Erturk - Chen et al. instead of Pynnönen et al.):

  • Lahat et al. (2000) • Zelnik et al. (2004) • Niederhofer and Pittschieler (2006) • Ruggieri et al. (2008) • Niederhofer (2011) • Güngör et al. (2013) • Dazy et al. (2013) • Chen et al. (2013)

This is what Sethi and Hughes found:

Overall, based on the currently available low quality evidence, clinicians should not be routinely screening ADHD patients for celiac disease in the absence of additional symptoms (i.e. weight loss, diarrhea, bloating, arthralgias, dermatitis herpetiformis etc.). Additionally, a gluten-free diet should not be a routine recommendation for those patients diagnosed with ADHD, unless there is a concurrent biopsy-proven diagnosis of celiac disease. For several parents, even if serological tests for celiac disease are negative, they may insist on trying their child on an empiric trial of a gluten-free diet. In the absence of objective findings of celiac disease or gluten sensitivity, clinicians should advise against such practices and inform parents of the potential harms of a gluten-free diet. First, a gluten-free diet can be a significant financial burden for a family. Second, starting a child on a gluten-free diet can potentially adversely impact a child’s ability to participate in social activities such as school pizza lunches or birthday parties. And third, a gluten-free diet that is started empirically without first consulting with a dietician carries the risk of long-term nutritional deficiencies.

With regards to the primary aim of this study, five out of six observational studies found no association between celiac disease and ADHD. The study by Zelnick et al., was the only study to find a potential association, however, this study had a high risk of reporting bias and detection bias. Both of the controlled trials by Niederhofer found that consumption of a gluten-free diet resulted in a statistically significant decrease in Hypescheme scores. These studies, however, also suffered from very poor internal validity and small sample sizes. Overall, based on the currently available low quality evidence, clinicians should not be routinely screening ADHD patients for celiac disease in the absence of additional symptoms, or unless belonging to a high risk group.

In the context of a trial, testing ADHD patients for celiac disease—using an objective blood test— is less vulnerable to detection bias as compared with testing celiac disease patients for ADHD... With regards to whether or not a gluten-free diet can help minimize symptoms of ADHD, there is a need for higher quality evidence that involves both blinding and a placebo controlled arm.

More importantly, beginning a gluten-free diet with out concrete biological markers for celiacs is contraindicated, so there's absolutely no reason we should be suggesting it might help ADHD symptoms. That suggestions should only come from their doctor after definitive diagnosis of celiacs.

  • According to the U.S. National Library of Medicine (2014): "You should NOT begin the gluten-free diet before you are diagnosed. Starting the diet will affect testing for the disease."[6]
  • Also according to Sethi and Hughes (2015): "For several parents, even if serological tests for celiac disease are negative, they may insist on trying their child on an empiric trial of a gluten-free diet. In the absence of objective findings of celiac disease or gluten sensitivity, clinicians should advise against such practices and inform parents of the potential harms of a gluten-free diet. First, a gluten-free diet can be a significant financial burden for a family. Second, starting a child on a gluten-free diet can potentially adversely impact a child’s ability to participate in social activities such as school pizza lunches or birthday parties. And third, a gluten-free diet that is started empirically without first consulting with a dietician carries the risk of long-term nutritional deficiencies."[2]

I propose this change: "A 2015 review states that evidence does not support a clear link between celiac disease and ADHD, and that routine screening for celiac disease in people with ADHD and the use of a gluten-free diet are discouraged."[2] Another alternative would be not mentioning celiacs at all, which is my #1 preference. PermStrump(talk) 03:54, 15 April 2016 (UTC)

Permstrump said "After reviewing those 8 studies, these were their findings: p2: Only one study considered ADHD as a possible onset manifestation of CD. However, no improvement was seen after starting a GFD treatment (Diaconu, Burlea, Grigore, Anton, & Trandafir, 2013)" This study is not included among the 8 of analysis (the reason is not specified).
Permstrump said: "*Note Ertürk et al. didn't even mention if the 3 studies that showed a positive correlation between ADHD and celiacs found that GFD improved symptoms. In fact, Zelnik et al. explicitly found the opposite. According to other reliable sources, there's so much bias in the Niederhofer studies that they don't count.[2]" Sethi and Hughes (2015)[2] is not a reliable source WP:MEDRS. Journal of Family Medicine & Community Health belongs to SciMedCentral publisher and SciMedCentral is included in Beall's List of predators journals]. So we let it out. The 3 studies that showed a positive correlation are:
  • Niederhofer & Pittschieler, 2006, (PMID 17085630) CONCLUSION: The data indicate that ADHD-like symptomatology is markedly overrepresented among untreated CD patients and that a gluten-free diet may improve symptoms significantly within a short period of time. The results of this study also suggest that CD should be included in the list of diseases associated with ADHD-like symptomatology.''
  • Zelnik et al.,2004 (PMID 15173490) in effect, states that in their study Therapeutic benefit, with gluten-free diet, was demonstrated only in patients with transient infantile hypotonia and migraine headache. but also "We conclude that the spectrum of neurologic disorders in patients with CD is wider than previously appreciated and includes, in addition to previously known entities such as cerebellar ataxia, epilepsy, or neuromuscular diseases, milder and more common problems such as migraine headache and learning disabilities, including ADHD."
  • Niederhofer, 2011 (PMID 21977364) "CONCLUSIONS: Celiac disease is markedly overrepresented among patients presenting with ADHD. A gluten-free diet significantly improved ADHD symptoms in patients with celiac disease in this study. The results further suggest that celiac disease should be included in the ADHD symptom checklist."
  • And if we look at the Table 1 of the reliable systematic review,[1] we see that only the two studies of Niederhofer evaluate ADHD prior to diagnosis and analyze results after GFD. Inclusion criteria of Zelnik study is CD on GFD. Really, of 8 studies included on this systematic review, only the two ones of Niederhofer apply the inclusion criteria previous to CD diagnosis. Thus, this conclusion "untreated celiac disease could predispose to ADHD symptoms, which may be improved with a gluten-free diet" are perfectly supported. In addition, they mention two other studies with the same conclusions. However, because of methodological limitations of all analayzed studies, they state "Up till now, there is no conclusive evidence for a relationship between ADHD and CD. Therefore, it is not advised to perform routine screening of CD when assessing ADHD (and vice versa) or to implement GFD as a standard treatment in ADHD.", which is also reflected on ADHD page.
Permstrump said: "More importantly, beginning a gluten-free diet with out concrete biological markers for celiacs is contraindicated, so there's absolutely no reason we should be suggesting it might help ADHD symptoms. " Nobody is recommending to start a gluten-free diet without a diagnosis of CD. "Untreated CD" means both CD diagnosed patients with lack of compliance with the diet and undiagnosed patients, prior to CD diagnosis.
And above all, Wikipedia is not a primary source, not an original research WP:NOR, we have to include conclusions of verifiable secondary sources and this source [1] is a systematic review, published on Journal of Attention Disorders, with a current impact factor of 3.78. The effort of Permstrump reviewing this source is appreciated, but we must not forget that it is a peer-reviewed journal, the criteria for accepting and publishing articles are very strict (most are rejected) and that this review has already been rigorously evaluated by specialists. Therefore, the conclusions are supported and accepted. So I disagree removing the last sentence. We must reflect the conclusions with neutrallity, and not just what we like to say, per WP:NPOV.
Best regards. --BallenaBlanca (talk) 07:36, 15 April 2016 (UTC)
6 out of 8 of the studies Ertürk et al. looked at did not support their hypothesis that GFD improves ADHD-like symptoms. The only 2 studies that supported it were both by the same person (Niederhofer). And we've decided to give equal weight to what Ertürk said about Niederhofer as we are to the other 6 authors. Equal weight is not NPOV (see WP:BALANCE). BallenaBlanca said, "Nobody is recommending to start a gluten-free diet without a diagnosis of CD. "Untreated CD" means by both CD diagnosed patients with lack of compliance with the diet and undiagnosed patients prior to CD diagnosis." That's what the article currently sounds like it's saying. PermStrump(talk) 07:55, 15 April 2016 (UTC)
You are confusing the results. If we analyze ADHD in CD treated patients, and there is no association, it doesn't mean that GFD doesn't improve ADHD symptoms, just the opposite, because the possible preventing role of the diet (In children with CD, however, the risk of developing neuropsychiatric disturbances is only 2.6% (compared with 26% in adults; Ruggieri et al., 2008). This discrepancy may be due to shorter disease duration in children, earlier elimination of gluten from the diet, stricter adherence to a diet, or a different susceptibility to immune-mediated disorders (Lionetti et al., 2010; Ruggieri et al., 2008).)[7] In this review of 8 studies, 3 studies analyze treated CD people (CD on GFD), 3 studies analyze prevalence of celiac antibodies in people with ADHD, and 2 studies analyze people prior to CD diagnosis and after GFD (and found an improvement with a GFD, similar to other two studies not included among these 8 ones). Author's conclusions are the mentioned above and in the ADHD page.
Similar to your reasoning, we could insist on making the conclusion that gluten-free diet may prevent ADHD symptoms in CD people and include it (which moreover is reflected in the paper, so yes we could write it...).
We are Wikipedia editors and this systematic review is written, and already reviewed, by specialists (peer-reviewed). We must reflect the conclusions, that only are equal weight if we mention all of conclusions, and not only a part, because of the different methodologies of the studies analyzed.
Best regards. --BallenaBlanca (talk) 09:03, 15 April 2016 (UTC)
As wikipedia editors, when there's ONE review saying saying ONE other researcher made a certain finding that no one else has made, we can and should conclude that it's WP:UNDUE to include. No, we could not argue that a gluten-free diet may prevent ADHD symptoms because literally none of the studies said that. Moreover, Erturk et al. don't even say in the "clinical implications" section that GFD may improve symptoms, it's only mentioned earlier in the paper. At the end they conclude, "Up till now, there is no conclusive evidence for a relationship between ADHD and CD. Therefore, it is not advised to perform routine screening of CD when assessing ADHD (and vice versa) or to implement GFD as a standard treatment in ADHD. Nevertheless, the possibility of untreated CD predisposing to ADHD-like behavior should be kept in mind. Therefore, it is recommended for clinicians to assess a broad range of physical symptoms, in addition to typical neuropsychiatric symptoms, when evaluating patients with ADHD." This ADHD article is hyperfocusing on 1-2 sentences from Erturk et al.'s paper that do not accurately reflect the entirety of the paper and its overall conclusions. It sounds very much like we're telling people if their stomach is mildly upset and they get distracted easily, they should try eating a gluten free diet, which (a) isn't what any the studies found and (b) is the opposite of the medical recommendation. PermStrump(talk) 12:33, 15 April 2016 (UTC)
"No, we could not argue that a gluten-free diet may prevent ADHD symptoms because literally none of the studies said that." Non literally, but the authors of systematic review say "In children with CD, however, the risk of developing neuropsychiatric disturbances is only 2.6% (compared with 26% in adults; Ruggieri et al., 2008). This discrepancy may be due to shorter disease duration in children, earlier elimination of gluten from the diet, stricter adherence to a diet, or a different susceptibility to immune-mediated disorders", and ADHD is included among neuropsychiatric disturbances.
"It sounds very much like we're telling people if their stomach is mildly upset and they get distracted easily, they should try eating a gluten free diet" Well, now I understand your concerns. Let's specify, to avoid confusion, adding "which may be improved after diagnosis and treatment of celiac disease with a gluten-free diet" [4]. I think now it is quite clear. What do you think?
Best regards. --BallenaBlanca (talk) 15:07, 15 April 2016 (UTC)
Oh! While I was writing this, Doc James made another edition. [5] I agree with the two options. --BallenaBlanca (talk) 15:14, 15 April 2016 (UTC)
Which two options are you referring to? Doc James (talk · contribs · email) 18:40, 15 April 2016 (UTC)
[6] (mine) and [7] (yours). I prefer the second one (your latest edit): brief and clear. Best regards. --BallenaBlanca (talk) 18:53, 15 April 2016 (UTC)
Doc James, it seems that we can not be so brief, because of concerns of other users Permstrump[8] and Garzfoth [9] To avoid confussions, it seems that is better to expand the text. I will try.
Let me now if you agree. Best regards. --BallenaBlanca (talk) 12:46, 16 April 2016 (UTC)

References

  1. ^ a b c d Ertürk, E; Wouters, S; Imeraj, L; Lampo, A (29 January 2016). "Association of ADHD and Celiac Disease: What Is the Evidence? A Systematic Review of the Literature". Journal of attention disorders (Review). PMID 26825336.
  2. ^ a b c d e f g h Sethi, A; Hughes, P (2015), "Celiac Disease and Attention Deficit Hyperactivity Disorder: A Systematic Review of the Literature" (PDF), Journal of Family Medicine & Community Health, 2 (8): 1069, ISSN 2379-0547
  3. ^ Lichtwark; et al. (2014), "Cognitive impairment in coeliac disease improves on a gluten-free diet and correlates with histological and serological indices of disease severity", Alimentary Pharmacology & Therapeutics, 40: 160-170, doi:10.1111/apt.12809 {{citation}}: Explicit use of et al. in: |last= (help)
  4. ^ Lebwohl, "Editorial: 'brain fog' and coeliac disease – evidence for its existence", Aliment Pharmacol Ther 2014; 40: 562-568 doi:10.1111/apt.12852, A serious issue, related to the small sample size, is the relative lack of variability in clinical, serological and histological outcomes. Every one of these subjects (100%) was found to have excellent adherence to the gluten-free diet, and nine of 10 had Marsh 0 or 1 findings on follow-up biopsy at 52 weeks, rates of healing far greater than typically seen among groups of patients with CD. It is therefore difficult to know whether improvements in these cognitive tests reflect the gluten-free diet as nearly everyone healed, and there was not a control arm. Supporting the notion that this is a selected population was the exclusion of more than 30% of the enrolled participants (5/16). It is premature to conclude that these results characterise the precise cognitive deficit in CD, as the statistical testing in this study did not account for multiple comparisons and there was not a specific pre-specified outcome.
  5. ^ Terrone; et al. (2013), "The Pediatric Symptom Checklist as screening tool for neurological and psychosocial problems in a paediatric cohort of patients with coeliac disease", Acta Paediatrica, 102: e325-e328, doi:10.1111/apa.12239 {{citation}}: Explicit use of et al. in: |last= (help)
  6. ^ U.S. National Library of Medicine (21 Feb 2014), "Celiac disease - sprue", MedlinePlus
  7. ^ Cite error: The named reference Erturk was invoked but never defined (see the help page).

It seems it has been an error

In this edit, Jytdog said “use most recent review”, and he removed the conclusions of 2013 source, but also removed the most recent (of 2014).

I will rescue 2014 conclusions from the text worded by Doc James in this review [10] to adjust and let the most recent review about elimination diets (which they are not synonymous of gluten-free diet, they are a broader term) as Jytdog propose. Nevertheless, it seems that is better not to remove the conclusions of the other review of 2013, to refflect the controversies and give the reader all views and what has been written on the subject.

Let's see what Doc James and other users think.

Best regards. --BallenaBlanca (talk) 12:20, 16 April 2016 (UTC)

This article is not the place to discuss the intricacies of celiac disease. Therefore removed "Its diagnosis requires consider the broad range of physical symptoms of this disease, which can present with mild or absent gastrointestinal complaints and a wide range of non-gastrointestinal symptoms which can affect several organs of the body." This belongs on the celiacs article IMO. (see PMID 26825336) Doc James (talk · contribs · email) 17:47, 16 April 2016 (UTC)
I think the above comment is Doc James based on the edit history, FYI, for the lazy. Elimination diet is not exactly synonymous with gluten and includes a wide range of other foods that more commonly cause GI upset (e.g., milk, eggs). I was coincidentally removing the Nigg et al. (2014) statement at the same time as Jytdog last night and we had an edit conflict. I'm not positive, but I assume we had the same thought process, which was that at the end of the day, Nigg and Sonuga-Barke (2013) essentially said the same thing, which was that any benefits from elimination diets were in studies that selected specifically for kids with ADHD and food sensitivities. I also preferred to cite Sonuga-Barke because Nigg combined all elimination diets in their review, where as Sonuga-Barke looked at the different kinds separately, so citing Sonuga-Barke allows us to be more specific about which types of diets have shown more benefit. The quote chosen for the Nigg citation is taken out of context. In the "Key Points" section at the very front of the article, Nigg et al. say, "A consensus has emerged among most reviewers that an elimination diet produces a small aggregate effect but may have greater benefit among some children. Very few studies enable proper evaluation of the likelihood of response in children with ADHD who are not already preselected based on prior diet response." This is how the article currently presents those 2 sources after BallenaBlanca's recent revert of Jytdog's edits ([157]=Sonuga-Barke et al. 2013; [90]=Nigg et al. 2014):
Tentative evidence supports free fatty acid supplementation and reduced exposure to food coloring.[157] However, these benefits may be limited to children with food sensitivities or those who are simultaneously being treated with ADHD medications.[157] A 2014 review states that an elimination diet could be an effective treatment in a small number of children with ADHD.[90] A 2013 review however did not support an elimination diet.[157]
In the context of what both Sonuga-Barke and Nigg actually said, this is redundant, somewhat incoherent, and a distortion of Nigg et al. (2014). PermStrump(talk) 16:20, 16 April 2016 (UTC)
Permstrump, perhaps you didn't see that this (green) text that you attribute to me is not my wording, but Doc James wording [11]. Compare them and you will notice: This is an old revision of this page, as edited by Doc James (talk | contribs) at 13:46, 16 April 2016 (→‎Diet: adjusted).
Also, I have not reverted Joytdog, I think I have explained it well enough [12]. It was an interpretion error about the meaning of elimination diets and I tried to correct it, respecting the observations of Jytdog, altough I believed that was necessary to add the controversies and also the conclusions of 2013 source, as in fact Doc James did [13].
Please, I ask you be careful with these details, to avoid misinterpretations. I'm trying to reach an agreement among all.
Best regards. --BallenaBlanca (talk) 17:44, 16 April 2016 (UTC)
Corrected some wording. We do not need to lead each sentence with the author. Doc James (talk · contribs · email) 17:47, 16 April 2016 (UTC)
  • I've removed "However, untreated celiac disease could predispose to ADHD-like symptoms that may see some improvement with treatment with a gluten-free diet". This is WP:UNDUE - it is a) obvious that treating anyone who has an undiagnosed condition makes them better; b) as the previous sentence just said, there is no call to screen everyone with ADHD for coeliac but this sentence implies that we should do. Reading the content as it stood this stood out like a sore thumb. Jytdog (talk) 20:11, 16 April 2016 (UTC)
The way Doc James fixed it makes it's clear which information came from which study without needing their names. I didn't particularly care about having their names in there; I was just trying to clarify the original wording and that was the best I came up with. The current version is my favorite so far. PermStrump(talk) 20:43, 16 April 2016 (UTC)

Jytdog, you said that you have removed "However, untreated celiac disease could predispose to ADHD-like symptoms that may see some improvement with treatment with a gluten-free diet" because of:

b) as the previous sentence just said, there is no call to screen everyone with ADHD for coeliac but this sentence implies that we should do.” Includin the sentence that you have deleted is not WP:UNDUE, on the contrary saying “A 2016 review did not support a clear link between celiac disease and ADHD, and stated that routine screening for celiac disease in people with ADHD and the use of a gluten-free diet as standard ADHD treatment are discouraged.[158]” and hiding “untreated celiac disease could predispose to ADHD-like symptoms that may see some improvement with treatment with a gluten-free diet"” may be cherry picking or quote mining: you are ignoring the rest of the article, ignoring “those that moderate the original quote” (and you have also deleted previous conversations of this talk page, in which I showed the context of conclusions). I write again:

Ertürk et al. say:

Clinical Implications. Up till now, there is no conclusive evidence for a relationship between ADHD and CD. Therefore, it is not advised to perform routine screening of CD when assessing ADHD (and vice versa) or to implement GFD as a standard treatment in ADHD. Nevertheless, the possibility of untreated CD predisposing to ADHD-like behavior should be kept in mind. Therefore, it is recommended for clinicians to assess a broad range of physical symptoms, in addition to typical neuropsychiatric symptoms, when evaluating patients with ADHD.”

"Untreated, CD has a wide range of clinical presentations. The “classical CD type” presents with mostly gastrointestinal symptoms such as abdominal pain, distension, chronic diarrhea, or failure to thrive. The “non-classic CD type” is characterized by fewer or no gastrointestinal symptoms and presents with extra-intestinal manifestations, such as neurologic, dermatologic, hematologic, endocrinologic, reproductive, renal, psychiatric, skeletal, and liver involvement (Celiloğlu, Karabiber, & Selimoğlu, 2011). The “asymptomatic or silent CD type” can present with no clinical symptoms and only positive serology (Bai et al., 2013)."

“In children with CD, however, the risk of developing neuropsychiatric disturbances is only 2.6% (compared with 26% in adults; Ruggieri et al., 2008). This discrepancy may be due to shorter disease duration in children, earlier elimination of gluten from the diet, stricter adherence to a diet, or a different susceptibility to immune-mediated disorders”

“Based on this review, there is no conclusive evidence for a relationship between ADHD and CD. However, attention difficulties, distractibility, chronic fatigue, and headache have been observed in patients with CD, especially prior to treatment or when noncompliant to GFD … Thus, it is posible that in untreated patients with CD, neurologic symptoms such as chronic fatigue, inattention, pain, and headache could predispose patients to ADHD-like behavior (mainly symptoms of inattentive type), which may be alleviated after GFD treatment.”

"Possible Mechanisms"

“Possible mechanisms underpinning the relation between attention/learning problems and CD point to accumulative effects of multiple effects, including both nutritional and immunologic/inflammatory factors. However, more indirect factors, related to nonspecific effects of chronic disease, cannot be ruled out (Zelnik et al., 2004). With respect to nutritional factors, micronutrient deficiencies and anemia are frequently seen in untreated patients with CD (Kupper, 2005; Wierdsma, van Bokhorst-de van der Schueren, Berkenpas, Mulder, & van Bodegraven, 2013). These factors may also play a role in causing ADHD-like behavior. However, when studying iron and zinc deficiencies in patients with ADHD, results remained inconclusive and needed further elaboration (for a review, see Millichap & Yee, 2012). There is emerging evidence that immunological mechanisms may contribute to ADHD development and manifestation (Verlaet, Noriega, Hermans, & Savelkoul, 2014). CD may induce an immune dysregulation in the gut, leading to chronic inflammation, which on its turn may be the cause for developing ADHD-like symptoms (Esparham, Evans, Wagner, & Drisko, 2014). Studies on the brain level point to the possible implication of serotonergic dysfunction in developing neuropsychiatric disorders in CD. More specifically, these studies refer to an impaired availability of tryptophan and decreased serotonin and dopamine metabolite concentrations (Hernanz & Polanco, 1991; Jackson et al., 2012; Pynnönen et al., 2005). Neuroimaging studies show structural and functional brain deficits in adult patients with CD. Structural deficits include bilateral decrease in cortical gray matter and caudate nuclei volumes (Bilgic et al., 2013), bilateral decrease in cerebellar gray matter, and smaller volume in multiple cortical regions (Currie et al., 2012). Functional deficits include a hypoperfusion of cerebral regions, primarily in the frontal cortex in untreated adult patients with CD, but not in treated patients (Addolorato et al., 2004; Usai et al., 2004). Such brain abnormalities may induce problems in high-cognitive functions such as attention span. Further research is however needed to confirm this hypothesis. To our knowledge, there are no studies on structural and functional brain deficits in pediatric patients with CD. A final hypothesis relates to increased oxidative stress that has been described in both ADHD (Lopresti, 2015) and CD (Stojiljković et al., 2009). Therefore, oxidative stress may represent a possible mediator in the development of ADHDlike behavior in CD patients. However, it remains uncertain whether oxidative stress itself contributes to the development or exacerbation of ADHD symptoms or whether it is the result of environmental factors (Lopresti, 2015). Further empirical studies are needed to understand the mechanisms underlying the potential association between ADHD, ADHD-like behavior, and CD.”

a) obvious that treating anyone who has an undiagnosed condition makes them better; This is an ambiguous, simplistic and non specific reasoning. We are talking about ADHD, you must focus on ADHD. If we give treatment and cure sore throat, sinusitis, flu... in a person with ADHD, he/she will obviously feel better, but that will not take away the symptoms of ADHD. ADHD symptoms will only improve if we treat a medical condition which may cause in some people ADHD symptoms, as hyperthyroidism, sleep apnea, drug interactions, etc. And as we see above, Ertürk et al. after review the literature state that several studies show that ADHD symptoms in some people with ADHD and CD improve with a gluten-free diet (which is not the same as “makes them better”) and list the current hypothesis for this causative effect.

Also, if you are so kind, I'd like you to explain me what is the criteria that you apply to "remove excess quotation" (one quotation that talks about eliminations diets, and other one with the conclusions of the systematic review about ADHD on CD people, and the effect of gluten-free diet in undiagnosed CD people with ADHD, extracted because this is a non free-access paper) and " remove quotation clutter from ref. makes editing way harder than it needs to be)" (removing again the quotation talking about the conclusions of the systematic review about ADHD on CD people, and the effect of gluten-free diet in undiagnosed CD people with ADHD), and you consider, however, that these others 13 quotations can remain:

  • 17. (231 characters, talking about epidemiology and underdiagnosis)
  • 23. (655 characters, talking about pharmacological interventions)
  • 90. (258 characters, talking about elimination diets)
  • 97. (1,505 characters, talking about psychostimulants)
  • 98. (919 characters, talking about treatment with 5HT)
  • 110. (617 characters, talking about pharmacotherapy and interventions to improve motivational processes)
  • 134. (750 characters, talking about exercise interventions)
  • 135. (1,224 characters, talking about exercise interventions)
  • 145. (379 characters, saying that changes and alterations in limbic regions are more pronounced in non-treated populations)
  • 146. (726 characters, talking about amphetamine psychosis and findings from one trial which indicate that the use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis)
  • 147. (522 characters, talking about side effects of stimulants)
  • 151. (574 characters, talking about treatment with stimulants, amphetamines and methylphenidate, and school failure in untreated children)
  • 157. (244 characters, talking about free fatty acid supplementation and artificial food color exclusions)

Best regards. --BallenaBlanca (talk) 06:32, 17 April 2016 (UTC)

It is not a question of character count. It is that a) there is no current recommendation to test all people with ADHD for coeliac; b) the obvious fact that a person with any untreated disease improves if you treat it. And the only reason we are having this discussion is because you won't listen to every other person in this discussion. You are not collaborating you are driving your POV down on throats. Stop it already. Jytdog (talk) 06:48, 17 April 2016 (UTC)
No problem, Jytdog. I will stop edit on ADHD page for the moment, I will continue listenning other users and I will continue collaborating.
Perhaps, the reason why you think I am no listening and collaborating is that you have not noticed that you have archived previous conversations (16 april), conversations that are not closed WP:TALK Wikipedia:Talk page guidelines#Closing discussions, this is the continuation. Perhaps I may have been wrong with the hierarchy of this section when I created it and wrote ==, instead of ===
If you delete my contributions, in which I was clearly listening, collaborating and trying to reach a consensus, and in which other users as Doc James agreed with the inclusion of the reference to gluten-free diet (not my point of view), other users who read it now will be making a wrong idea. The information again remains hidden. I disagree with archive them, you didn't ask us if you can archive them. WP:TALK
Thus, I will rescue the active conversation ("If content is archived prematurely, such as when the discussion is still relevant to current work or discussion of a subject was not concluded, restore the content to the talk page from the archive."WP:ARCHIVENOTDELETE) and fix layout/hierarchy errors.
Best regards. --BallenaBlanca (talk) 10:39, 17 April 2016 (UTC)
What I archived were WP:TEXTWALL from you - unreadable walls of text that were yet more examples of you overwhelming the conversation in your efforts to push and push and push. They are not examples of collaboration. Really - no one agrees with what you want here. Jytdog (talk) 10:46, 17 April 2016 (UTC)
Resolved, I agree. [14] --BallenaBlanca (talk) 18:17, 18 April 2016 (UTC)

Reviews

Some of these sources were reviews. This edit also changed 75% from genetics to 5%?[15] Doc James (talk · contribs · email) 18:03, 17 April 2016 (UTC)

nice catch on that 15x change! yikes. Jytdog (talk) 08:47, 18 April 2016 (UTC)
Oops! Sorry about that. I just meant to delete the random characters before the 7 and didn't notice that I nicked the 7. I'll write more about why I removed some of the other stuff. Some of the things I had more of a reason than what I wrote in the edit summary (like the DSM IV thing, but I don't remember off the top of my head). I have to go back and look to see what they were. PermStrump(talk) 15:08, 18 April 2016 (UTC)
Starting with 1 paragraph about evolutionary psychology behind ADHD, here's a link to the changes and I'm looking at the 1st chunk added back in under line 94:
  • As ADHD is common, natural selection likely favored the traits, at least individually, and they may have provided a survival advantage.[1] For example, some women may be more attracted to males who are risk takers, increasing the frequency of genes that predispose to ADHD in the gene pool.[2] As it is more common in children of anxious or stressed mothers, some argue that ADHD is an adaptation that helps children face a stressful or dangerous environment with, for example, increased impulsivity and exploratory behavior.[3]
The first 2 sources disappear from the search results in my employer’s database (a university library) when I filter for peer reviewed articles. The description of both journals says that they are peer reviewed, but I guess not 100% of the content is peer reviewed. For example, the description for Revista Neurologica says, “Key Features” are peer reviewed and that “Other Features” include: book reviews and “Reviews included (any)”, so presumably the “other features” aren’t peer reviewed. The paper appeared in a supplement issue of that journal, so my guess is that the supplement wasn’t peer reviewed. It has happened before where some articles in the same journal were labeled peer reviewed but others weren't, so somehow the database seems to know that. I can’t read the Spanish one, but I couldn’t verify the content from the 2nd source regardless of its peer review status. As for the 3rd source, this isn’t an accurate interpretation of what the author was trying to convey. It reflects one sentence out of 5 paragraphs on the potential evolutionary theories behind ADHD and this point wasn’t the takeaway message that I got from it. The author was basically describing other authors’ untested speculations without validating one over another or coming to any final conclusions, so I felt choosing any of the 5 theories was kind of cherry picking b/c they were all different and untested anyway. More to come... PermStrump(talk) 17:22, 18 April 2016 (UTC)
I have provisionally withdrawn this sentence added on 17 April 2016: "These findings did not apply to any food coloring that is approved the the U.S. FDA".[4] [16] Permstrump, I can be wrong, but I did not find these conclusions in the given source. Could you explain us, please? Best regards. --BallenaBlanca (talk) 18:18, 18 April 2016 (UTC)
BallenaBlanca: It's in Nigg et al. 2012, which is cited in the next sentence, so I didn't think I needed to copy it again 2 sentence in a row, but I could see how that was confusing. It's also in Galanter 2013 (PMID 23450282), Arnold et al. 2012, and Rojas 2005 (PMID 15977318). I'm fine with the sentence the way it is now. It used to say something like, "the UK has put policies in place, but the US hasn't," (paraphrased), which was really misleading, but as long as it just says, "the UK put policies in place," then I don't know how important it is to go into the details in this article about why the US hasn't. PermStrump(talk) 05:28, 19 April 2016 (UTC)
Doc James: Do you still oppose removing that paragraph given my reasons above? I have more to say about the other things I had removed, but I'm waiting, because other things are unrelated and it would be too many different directions at one time. PermStrump(talk) 03:59, 20 April 2016 (UTC)
This edit [17] also removed these 6 reviews (I updated the sources type):[5][6][7][8][9][10]
Also, this sentence:[18] "Exposure to drugs, alcohol, or nicotine during pregnancy are associated with a range of disorders, including ADHD, but it’s not clear if they cause these conditions."[11] is not supported by the source, which does not mention drugs, alcohol nor nicotine. And publisher are the Centers for Disease Control and Prevention and not National Center on Birth Defects and Developmental Disabilities (the latest is mentioned as source used by CDC, among others).
In addition, I'm not sure about the accuracy of this sentence:[19] "According to the U.S. CDC, environmental exposures have been linked to increased ADHD symptoms, but the evidence has been inconsistent".[11]" If we look at the source, we see: It is not known what causes ADHD. ADHD is often seen in families, and genes appear to play a role, but other factors may contribute or make symptoms worse. For example, some environmental exposures have been linked to increased ADHD symptoms, but the evidence has been inconsistent. And if we click on the link (Facts About ADHD), we can read:
In addition to genetics, scientists are studying other possible causes and risk factors including:
  • Brain injury
  • Environmental exposures (e.g., lead)
  • Alcohol and tobacco use during pregnancy
  • Premature delivery
  • Low birth weight
Research does not support the popularly held views that ADHD is caused by eating too much sugar, watching too much television, parenting, or social and environmental factors such as poverty or family chaos. Of course, many things, including these, might make symptoms worse, especially in certain people. But the evidence is not strong enough to conclude that they are the main causes of ADHD.
Best regards. --BallenaBlanca (talk) 09:07, 20 April 2016 (UTC)

Looking at the sources:

  • This is listed as a review [20]
  • This is also a review [21]
  • As is this [22]

Doc James (talk · contribs · email) 14:08, 20 April 2016 (UTC)


Garzfoth you have reverted/modified this edit [23] of Doc James (who has reviewed this issue several times) and contradicted his decision about the inclusion of information about untreated celiac disease in Diet section, with which other users and me have agree (if you look above, you will see). [24] [25]
Well, I respected your decission of including it in differential diagnosis section [26], and I completed it with non-celiac gluten sensitivity (NCGS), following your same line.
Where is the problem? Why did you revert my edit [27] saying "Your source fails WP:MEDRS, has various issues, and nowhere could I find the source ref for the ADHD claim!! WTF? (TW))" How can you say that this secondary peer reviewed source PMID 23567359, published on The American Journal of Gastroenterology (current impact factor of 10.755) is not a reliable source and "nowhere could I find the source ref for the ADHD claim"? Well, if you are looking for ADHD on the source, you will really not find it, but if you search "attention-deficit/hyperactivity disorder" you will find it. Fortunately, it is a free access source: (quote literally) NCGS can be characterized by gastrointestinal symptoms, such as diarrhea, abdominal discomfort, or pain, and bloating and flatulence, or extraintestinal manifestations, such as headache, lethargy, attention-deficit/hyperactivity disorder, ataxia, or recurrent oral ulceration, which improve or disappear after gluten withdrawal in patients in whom celiac disease and wheat allergy have been ruled out.
I would like that you explain me why you follow different criteria and remove this secondary source, but you restore informations about drugs used to treat neuropsychiatric disorder based solely on a primary source, with this explanation "The use of a primary source for receptor/binding affinities is justified in WP:MEDRS. (TW)" [28] [29] [30] [31] Perhaps I'm wrong, but can not find the justification of this in WP:MEDRS. Would you be kind enough to show me the part of the text of WP:MEDRS to which you refer?
Best regards. --BallenaBlanca (talk) 23:46, 23 April 2016 (UTC)
Let's get this issue straightened out, shall we?
  • Doc James' edit - you are abusing the appeal to authority here, my edit is superior, you are the only one who's POV-pushing here.
  • Reverting your edit - I read the source article, and noticed that it cites another article as a source for those symptoms (and I searched for the word "attention", "ADHD", and "ADD" in all documents). I read the cited article, and noticed that it cites yet another article as a source for those symptoms. I read the cited article (this is now three articles deep), and found no mention whatsoever of NCGS causing those symptoms - in fact, I could not find any discussion of the subject at all in the article. At that point, it was quite clear that your source not only fails WP:MEDRS, but also WP:RS as well, and it is completely unacceptable to use this as a source to back your claim.
  • On the subject of receptor/binding affinities, please see https://en.wikipedia.org/wiki/Wikipedia_talk:WikiProject_Medicine/Archive_76#Is_in_vitro_content_.22factual.22.3F for a clearer explanation from some of Wikipedia's major medical/pharmacology editors.
I am now reverting your edit again due to this very clear violation of Wikipedia policy, and I hope you now understand why receptor/binding affinity tables are handled differently from other medical content (and thus why I reverted your reversions in those articles). Garzfoth (talk) 01:01, 24 April 2016 (UTC)
I have no strong feeling either way
  • The "American Journal of Gastroenterology" has a high impact factor at more than 10
  • The review only mentioned NCGS and ADHD in passing in a list of other possible symptoms
It should at least go in the NCGS article.
Doc James (talk · contribs · email) 07:54, 24 April 2016 (UTC)
unreadable and almost all OFFTOPIC; please feel free to restate concisely, focused on article content
The following discussion has been closed. Please do not modify it.
Doc James, you say that it should "at least" go in the NCGS article; therefore, this implies that could also go here, right? And that the reference is perfectly valid and match with WP:MEDRS, right? It has already been rigorously peer reviewed and verified by specialists in the subject, before its publication. Simple Wikipedia editors are not more qualified and this is not our attribution...
Garzfoth, you are accusing me, I remember you the Wikipedia policies WP:ACCUSE. And yes, I requested for an administrator mediation, I feel attacked, it is a perfectly valid conduct WP:CONDUCTDISPUTE. I am not "abusing the appeal to authority", I'm trying to reach agreements and I trust the impartiality of Doc James. This reversion yours of a previous edit by Doc James is not "superior" and, since you mention it, adding untreated celiac disease on Differential Diagnosis section is not incompatible with reflecting in Management section a proven reality in celiac people with ADHD: they improve ADHD symptoms with a GFD. I could not even mention the reasons why ADHD improves in CD people with a GFD (very interesting possible mechanisms). On the CD page we can not extend these explanations because CD page would be too long (there are many related diseases and is a very complex disease). In this specific ADHD page you oppose to even the mere mention of the effects of gluten-free diet (people have the right to know that ADHD caused by CD is not a irreversible damage). Where we can explain it, then? Why are you so afraid to mention the words "gluten-free diet", especially considering that refer only to a minority of people, which we state very clear? Doc James, I think we should re-think this Garzfoth's edit.
Garzfoth, it is very curious that you are now accusing me of a "very clear violation of Wikipedia policy" (!?) because of I used a secondary peer-reviewed source PubMed indexed, with an impact factor greater than 10, to support the simple mention of NCGS into an already present list of diseases to do a differential diagnosis, and you say that I am "POV-pushing", while you are very interested in updating information about drugs. Let's see some of your recent edits [32]: Psychiatric medication, Escitalopram, Citalopram, Paroxetine, Fluoxetine, Sertraline, ‎Fluvoxamine, Controlled Drugs and Substances Act, Methylphenidate, Duloxetine, Controlled Substances Act, Phenylpropanolamine, Ergotamine, Ergometrine, Acetic anhydride, Salvinorin A, Pyrovalerone, Zolpidem, Trenbolone, Tibolone, Stanozolol, Dehydroepiandrosterone, Oxymetholone, Oxandrolone, Norethandrolone, Norboletone, ‎Nandrolone, Mibolerone, Metenolone, Metandienone, Mesterolone, Furazabol, ‎Fluoxymesterone, Ethylestrenol, Drostanolone, Clostebol, Boldenone, Mefenorex, Fenproporex, Fencamfamine, Cathine, Tetrazepam, Pinazepam, Oxazolam, Medazepam, Ketazolam, Haloxazolam, Ethyl, loflazepate, Cloxazolam, Camazepam, Brotizolam, Methyprylon, Mazindol, Ethinamate, Ethchlorvynol, Clotiazepam, Glutethimide, Nalbuphine, Butorphanol, Pipradrol, Phendimetrazine, Amfepramone, Chlorphentermine, Sodium, thiopental, Thiamylal, Thialbarbital, Vinylbital, Vinbarbital, Talbutal, Sigmodal, Secobarbital, Heptobarbital, Probarbital, Phenobarbital, Pentobarbital, Propallylonal, Metharbital, ‎Methylphenobarbital, Hexobarbital, Hexethal, Heptabarb, Cyclopentobarbital, Cyclobarbital, Butobarbital, Butallylonal, Butalbital, Butabarbital, Barbital, Aprobarbital, Alphenal, Trifluoromethylphenylpiperazine, Zipeprol, Lefetamine, ‎Alpha-Ethyltryptamine, Methcathinone, Rolicyclidine, Phencyclamine, Tenocyclidine, Harmaline, Harmaline, Diethyltryptamine, Mecloqualone, Parahexyl, Nabilone, Cannabinol, Para-Ethoxyamphetamine, Benzphetamine, Para-Methoxyamphetamine, 2,5-Dimethoxy-4-methylamphetamine, Etilamfetamine, Tilidine, Sufentanil, Remifentanil, Α-Methylfentanyl, Ohmefentanyl, Fentanyl, Carfentanil, Alfentanil, Piritramide, Bezitramide, Clonitazene, Propiram, Phenampromide, ‎Diampromide, Pentazocine, Metazocine, Phenazocine, Racemorphan, Methorphan, Phenomorphan, Norlevorphanol, Levophenacylmorphan, Levomethorphan, Drotebanol, ‎Racemoramide, Levomoramide, Dextromoramide, Ethylmethylthiambutene, Dimethylthiambutene, Diethylthiambutene, Dextropropoxyphene, Dioxaphetyl butyrate, ‎Dimenoxadol, Noracymethadol, Dimepheptanol, Betamethadol, ‎Betacetylmethadol, Alphamethadol, Alphacetylmethadol, Acetylmethadol, Phenadoxone, Norpipanone, Isomethadone, Proheptazine, ‎Trimeperidine, Piminodine, Phenoperidine, Norpethidine, Ketobemidone, Hydroxypethidine, Furethidine, Etoxeridine, Difenoxin, Diphenoxylate, Anileridine, Meprodine, Allylprodine, Cyprenorphine, Nalmefene, Naloxone, Naltrexone, Noscapine, Ecgonine, Noscapine, Naltrexone, Naloxone, Nalmefene, Cyprenorphine, Apomorphine, Thebacon, Pholcodine, Norcodeine, Nicomorphine, Nicocodeine, Nalorphine, Myrophine, Methyldihydromorphine, Methyldesorphine, Hydromorphone, Hydromorphinol, Etorphine, Ethylmorphine, Dihydromorphine, Dihydrocodeine, Codoxime, Benzylmorphine, Acetyldihydrocodeine, Acetorphine, Thebaine, ‎Pseudoephedrine, Phenylpropanolamine, Adderall, Amphetamine, Dextroamphetamine, Levoamphetamine, etc......
Best regards. --BallenaBlanca (talk) 11:09, 24 April 2016 (UTC)
In reply to Doc James:
  • Please read the chain of cited articles, impact factor is irrelevant when a source is fraudulently claiming something that is not supported by its references.
In reply to BallenaBlanca:
  • Please read the chain of cited articles, impact factor is irrelevant when a source is fraudulently claiming something that is not supported by its references. The source is not valid for your use in any way, it can be used to support different claims, but not this particular one.
  • Please demonstrate where I am accusing you of anything beyond the use of a logical fallacy. I assumed that your use of this source was in good faith and that you did not notice the issue - which is completely fair. However, I cannot continue to assume good faith if you ignore the above bullet point, and especially if you are attempting to turn this into an issue of user conduct on my part. There are a number of editors who are very frustrated with your behavior with regards to certain subjects and on talk page conversations in general, I am not alone in my frustration with your behavior, and good faith can only stretch so far before this turns into a more formal issue.
  • "and, since you mention it, adding untreated celiac disease on Differential Diagnosis section is not incompatible with reflecting in Management section a proven reality in celiac people with ADHD: they improve ADHD symptoms with a GFD" - this is not supported by PMID 26825336, which states "there is no conclusive evidence for a relationship between ADHD and CD", and "it is not advised to perform routine screening of CD when assessing ADHD (and vice versa) or to implement GFD as a standard treatment in ADHD". CD patients should be diagnosed appropriately and treated according to their diagnosis irregardless of if they have ADHD or not, as with any of the other conditions listed as possible "mimics" of ADHD.
  • "Garzfoth, it is very curious that you are now accusing me of a "very clear violation of Wikipedia policy" (!?) because of I used a secondary peer-reviewed source PubMed indexed, with an impact factor greater than 10, to support the simple mention of NCGS into an already present list of diseases to do a differential diagnosis" - You're clearly WP:NOTGETTINGIT.
  • "and you say that I am "POV-pushing", while you are very interested in updating information about drugs. Let's see some of your recent edits" - Oh my god, you just exposed my interest in pharmacology! How horrific! Anyways, I am listed as a member of WP:PHARM, my interest in this is no big secret. Here's my top edits in the wiki namespace: https://tools.wmflabs.org/xtools/topedits/?lang=en&wiki=wikipedia&user=Garzfoth&namespace=0. I've invested a huge amount of time into ensuring that Wikipedia's medical and pharmacology articles are as accurate and complete as possible (as well as neutral, readable, sourced well, etc), but I do edit a few other subjects as you can see in that list or just my list of contribs (with the same goals in mind), and if you look through my edits, you'll see that I wander around on different tangents from time to time. Anyways, my point is, this is not evidence of POV-pushing, this is an attempt to smear my name by poisoning the well with vague implied negative allegations about my interest in pharmacology. Not cool at all. @Jytdog:, would you mind stepping in here again to comment on these issues (both the POV and sourcing ones)? Thanks. Garzfoth (talk) 18:45, 24 April 2016 (UTC)

I apologize for my previous message, Garzfoth. It was inappropriate nor are ways to argue.

I've gotten the full texts and I read the chain of cited articles. Now I understand what you meant, I had not understood well it before, sorry. I agree.

Well, I will accept your edit, it's clear that the issue was where to include "untreated celiac disease" and that we all accept to include it into Differential diagnosis section. I will add a quotation, because it is not a free access text, and thus avoid future problems or doubts when other editors review the page, and for my part, we can leave this issue closed.

Best regards. --BallenaBlanca (talk) 04:33, 26 April 2016 (UTC)


References

  1. ^ Cardo E, Nevot A, Redondo M; et al. (March 2010). "Trastorno por déficit de atención/hiperactividad: ¿un patrón evolutivo?". Rev Neurol (in Spanish). 50 Suppl 3: S143–7. PMID 20200842. {{cite journal}}: Unknown parameter |trans_title= ignored (|trans-title= suggested) (help)CS1 maint: multiple names: authors list (link)
  2. ^ Cite error: The named reference pmid=16849269 was invoked but never defined (see the help page).
  3. ^ Glover V (April 2011). "Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective". J Child Psychol Psychiatry. 52 (4): 356–67. doi:10.1111/j.1469-7610.2011.02371.x. PMID 21250994.
  4. ^ FDA (March 2011), Background Document for the Food Advisory Committee: Certified Color Additives in Food and Possible Association with Attention Deficit Hyperactivity Disorder in Children (PDF), U.S. Food and Drug Administration
  5. ^ Burger PH, Goecke TW, Fasching PA, Moll G, Heinrich H, Beckmann MW, Kornhuber J (September 2011). "[How does maternal alcohol consumption during pregnancy affect the development of attention deficit/hyperactivity syndrome in the child]". Fortschr Neurol Psychiatr (Review) (in German). 79 (9): 500–506. doi:10.1055/s-0031-1273360. PMID 21739408.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Abbott LC, Winzer-Serhan UH (April 2012). "Smoking during pregnancy: lessons learned from epidemiological studies and experimental studies using animal models". Crit. Rev. Toxicol. (Review). 42 (4): 279–303. doi:10.3109/10408444.2012.658506. PMID 22394313.
  7. ^ Eubig PA, Aguiar A, Schantz SL (December 2010). "Lead and PCBs as risk factors for attention deficit/hyperactivity disorder". Environ. Health Perspect. (Review. Research Support, N.I.H., Extramural. Research Support, U.S. Gov't, Non-P.H.S.). 118 (12): 1654–1667. doi:10.1289/ehp.0901852. PMC 3002184. PMID 20829149.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ de Cock M, Maas YG, van de Bor M (August 2012). "Does perinatal exposure to endocrine disruptors induce autism spectrum and attention deficit hyperactivity disorders? Review". Acta Paediatr. (Review. Research Support, Non-U.S. Gov't). 101 (8): 811–818. doi:10.1111/j.1651-2227.2012.02693.x. PMID 22458970.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: year (link)
  9. ^ Thapar, A.; Cooper, M.; Jefferies, R.; Stergiakouli, E. (March 2012). "What causes attention deficit hyperactivity disorder?". Arch Dis Child (Review. Research Support, Non-U.S. Gov't). 97 (3): 260–5. doi:10.1136/archdischild-2011-300482. PMID 21903599.
  10. ^ Millichap JG (February 2008). "Etiologic classification of attention-deficit/hyperactivity disorder". Pediatrics (Review). 121 (2): e358–65. doi:10.1542/peds.2007-1332. PMID 18245408.
  11. ^ a b CDC (16 Mar 2016), Attention-Deficit / Hyperactivity Disorder (ADHD), National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, retrieved 17 Apr 2016

DSM4

Just because we have the DSM5 does not mean every bit of research based on the DSM4 is all of a sudden obsolete. Doc James (talk · contribs · email) 17:51, 17 April 2016 (UTC)

Well sure, but to be clear: There is no such thing as "research based on the DSM4". Research involves a hypothesis, premise, or merely a fact finding mission. While the terms used in the associating white papers may be DSM4 centric, the DSM itself is simply the diagnostic criteria, and does not render any research per se valid or invalid. You can use the vetted results of any research whatsoever to determine (or not) causal relationships, and with those relationships you can describe them in DSM5 or see if they fit any longer within DSM5 at all without worrying that the research is now somehow on shaky ground. For example, if research was centric to Asperger, it doesn't mean that because the term is no longer used in 5 that the research itself is without merit. It simply means that Asperger no longer falls strictly within the ASD "spectrum" as before, not that whatever research done with patients presenting with Asperger somehow ceases to apply. How could it?Tgm1024 (talk) 23:38, 1 May 2016 (UTC)

Merge

Merge https://en.wikipedia.org/wiki/Hyperkinetic_disorder into ADHD, it's listed as a synonym and the ICD 10 code is F90 which is the same ICD 10 code listed on the ADHD page. — Preceding unsigned comment added by Throwawaysomyipdoesntshowup (talkcontribs) 14:56, 3 July 2016 (UTC)

Genetics

Currently, this is how the last half of the section on genetic causes reads:

Several authors have hypothesized that evolution may have played a role in the prevalence of ADHD, particularly hyperactive and impulsive traits in males.[74] Jonathan Williams and Eric Taylor (2006) hypothesized that some women may be more attracted to males who are risk takers, increasing the frequency of genes that predispose to hyperactivity and impulsivity in the gene pool.[75] According to psychobiologist Vivette Glover, some authors have claimed that these traits may be an adaptation that helped males face stressful or dangerous environment with, for example, increased impulsivity and exploratory behavior.[74][75] Others have argued that in certain situations, ADHD traits may have been beneficial to society as a whole even while being harmful to the individual.[74][75][76] According to Esther Cardo and colleagues (2010), the high prevalence and heterogeneity of ADHD may have increased reproductive fitness and benefited society by adding diversity to the gene pool despite being detrimental to the individual.[76] Walter Adriani and colleagues (2012) hypothesized that in certain environments, some ADHD traits may have offered personal advantages to individuals, such as quicker response to predators or superior hunting skills.[77]

People with Down syndrome are more likely to have ADHD.[78]

The sentence about Down syndrome seems really out of place, but I'm not sure where it fits better or if it's worth keeping and I'd be interested in hearing other opinions. IMO the amount of space given to evopsych hypotheses that are unlikely to be tested is WP:UNDUE. I suggest reducing the text to:

Several authors have hypothesized that evolution may have played a role in the prevalence of ADHD, particularly hyperactive and impulsive traits in males.[74] Jonathan Williams and Eric Taylor (2006) hypothesized that some women may be more attracted to males who are risk takers, increasing the frequency of genes that predispose to hyperactivity and impulsivity in the gene pool.[75] According to psychobiologist Vivette Glover, some authors have claimed that these traits may be an adaptation that helped males face stressful or dangerous environment with, for example, increased impulsivity and exploratory behavior.[74][75] Others have argued that in certain situations, ADHD traits may have been beneficial to society as a whole even while being harmful to the individual.[74][75][76] According to Esther Cardo and colleagues (2010), the high prevalence and heterogeneity of ADHD may have increased reproductive fitness and benefited society by adding diversity to the gene pool despite being detrimental to the individual.[76] Walter Adriani and colleagues (2012) hypothesized that in certain environments, some ADHD traits may have offered personal advantages to individuals, such as quicker response to predators or superior hunting skills.[77]

My reasoning is that reference [74] (PMID 21250994) is a review and the hypotheses that I didn't strike out were mentioned in the review, whereas the others come from primary sources. Thoughts? PermStrump(talk) 22:33, 24 July 2016 (UTC)

Content

No idea why this ref about COPD was added "Switzerland strongly limits the authorised medications,[1]"? Doc James (talk · contribs · email) 01:45, 28 July 2016 (UTC)

why the revert on cause of ADHD?

Garzfoth Hello. You reverted here. [33] Could you please explain then in what cases the cause is known and where in that source it states that?Charlotte135 (talk) 00:56, 26 July 2016 (UTC)

I assume the revert was based upon the second sentence under ADHD#Cause. Seppi333 (Insert ) 11:13, 27 July 2016 (UTC)
Hello Seppi333. Yes, I had seen this. However the vast majority of sources state "unknown" and "interaction between nature/nurture." Therefore I'm still inclined to take such a big statement out of the article, based on a single source, or include but make it clear this is only a minority/fringe view in the literature.Charlotte135 (talk) 12:55, 27 July 2016 (UTC)
The revert was based on sentence 2, the known connection with genetics, and the extensive number of sources I've read on this subject that disagree with such a simplistic explanation of ADHD's causes (scientific studies for the most part, as well as textbooks, major reports, etc). Sorry about the delay in responding. Garzfoth (talk) 13:10, 27 July 2016 (UTC)
We cannot say genetics is the single cause without mentioning the interaction with the environment. The exact cause is still unknown in major reliable sources. If other sources are not presented, I might go with what I said above. Maybe Doc James has an opinion on the wording here.Charlotte135 (talk) 23:12, 27 July 2016 (UTC)
Most source refer to genetics as a factor, so to say the cause is totally unknown doesn't feel like an accurate reflection of the sources. Would this be an acceptable compromise?

Current: "Despite being the most commonly studied and diagnosed mental disorder in children and adolescents, the cause is unknown in the majority of cases."
Compromise: "Despite being the most commonly studied and diagnosed mental disorder in children and adolescents, the immediate cause is unknown."

PermStrump(talk) 03:17, 28 July 2016 (UTC)
Hi Permstrump. Yes, that works for me. Thanks for suggesting the compromise.Charlotte135 (talk) 05:33, 28 July 2016 (UTC)