In this abstract methylphenidate, like opioids, reduced BDNF the memory chemical which was already lower in the evening in ADHD children.
I propose that this decline reduces the effectiveness of stimulant therapy AND combined treatment with stimulant and lifestyle and supplements to increase BDNF would be superior. Lower levels of BDNF were seen in comorbid hyperactivity and conduct disorders. Could these commodities too inattention reduce with elevated BDNF?
It may be that the BDNF gene is epigenically turned down. If so then melatonin, vitamin D, hydrogen rich water and sulforaphane could reverse the turned off gene and increase BDNF production.
With regard to the paradox of no effect on depression, stimulants in addition to exercise are treatments for depressant. This treatment may be a cover up like prednisone in rheumatoid joint destruction relieving only symptoms.
BDNF concentrations and daily fluctuations differ among ADHD children and respond differently to methylphenidate with no relationship with depressive symptomatology
Abstract
Rationale
Brain-derived neurotrophic factor (BDNF) enhances the growth and maintenance of several monoamine neuronal systems, serves as a neurotransmitter modulator and participates in the mechanisms of neuronal plasticity. Therefore, BDNF is a good candidate for interventions in the pathogenesis and/or treatment response of attention deficit hyperactivity disorder (ADHD).
Objective
We quantified the basal concentration and daily fluctuation of serum BDNF, as well as changes after methylphenidate treatment.
Method
A total of 148 children, 4–5 years old, were classified into groups as follows: ADHD group (n = 107, DSM-IV-TR criteria) and a control group (CG, n = 41). Blood samples were drawn at 2000 and 0900 hours from both groups, and after 4.63 ± 2.3 months of treatment, blood was drawn only from the ADHD group for BDNF measurements. Factorial analysis was performed (Stata software, version 12.0).
Results
Morning BDNF (36.36 ± 11.62 ng/ml) in the CG was very similar to that in the predominantly inattentive children (PAD), although the evening concentration in the CG was higher (CG 31.78 ± 11.92 vs PAD 26.41 ± 11.55 ng/ml). The hyperactive–impulsive group, including patients with comorbid conduct disorder (PHI/CD), had lower concentrations. Methylphenidate (MPH) did not modify the concentration or the absence of daily BDNF fluctuations in the PHI/CD children; however, MPH induced a significant decrease in BDNF in PAD and basal day/night fluctuations disappeared in this ADHD subtype. This profile was not altered by the presence of depressive symptoms.
Conclusions
Our data support a reduction in BDNF in untreated ADHD due to the lower concentrations in PHI/CD children, which is similar to other psychopathologic and cognitive disorders. MPH decreased BDNF only in the PAD group, which might indicate that BDNF is not directly implicated in the methylphenidate-induced amelioration of the neuropsychological and organic immaturity of ADHD patients.
Joseph Thomas (Tony) Liverman, Jr.
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