Biochemical Studies on Autism

Yuwiler, Arthur; Geller, Edward; Ritvo, Eva C.

doi:10.1007/978-1-4757-0797-7_25

Cited by 7 publications

(4 citation statements)

References 114 publications

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“…The observation of normal or lowered urinary 5-HT suggests plasma free 5-HT levels are not elevated and, therefore, that the platelets of autistic subjects are not exposed to higher levels of 5-HT in vivo. To an even greater degree than has been suggested previously (Yuwiler, Geller & Ritvo, 1985), issues involving the platelet and its handling of 5-HT bear careful reappraisal.…”

Section: Discussionmentioning

confidence: 99%

Whole Blood Serotonin in Autistic and Normal Subjects

Anderson

Freedman

Cohen

et al. 1987

Child Psychology Psychiatry

289

113

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Whole blood serotonin and tryptophan were measured in 87 normal subjects and in 40 autistic subjects. Whole blood serotonin concentrations (mean +/- SE) were significantly higher in drug-free (N = 21) autistics (205 +/- 16 ng/ml) than in normals (136 +/- 5.4 ng/ml). The Gaussian distribution of serotonin levels in the unmedicated autistic group suggests the elevation was not due to a subgroup of autistic subjects. Autistics medicated with anticonvulsants or neuroleptics had significantly lower serotonin levels than did drug-free autistic subjects. Whole blood tryptophan levels and platelet counts were similar in the autistic and normal groups. The possible causes of the hyperserotonemia of autism are discussed.

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Section: Discussionmentioning

confidence: 99%

Whole Blood Serotonin in Autistic and Normal Subjects

Anderson

Freedman

Cohen

et al. 1987

Child Psychology Psychiatry

289

113

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“…However, the small number of monkeys precluded assessing a possible association between baseline physiological measures and the magnitude of fenfluramine's behavioral effects. Humans also exhibit intraindividual stability and show between individual differences in these measures (Hanley et al 1977;Yuwiler et al 1985). Large scale clinical or animal studies may determine whether either of these measures can be used to predict the magnitude, latency, or persistence of the effects of fenfluramine.…”

Section: Discussionmentioning

confidence: 99%

“…The temporal relationship between fenfluramine-induced changes in behavior and alteration in blood and brain serotonin is also unclear (Steranka and Sanders-Bush 1979;Yuwiler et al 1985). Upon initiation of fenfluramine treatment, behavior changes in autistic children occur concomitantly with declines in blood serotonin.…”

mentioning

confidence: 99%

Effects of chronic fenfluramine on blood serotonin, cerebrospinal fluid metabolites, and behavior in monkeys

et al. 1986

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The effects of long term (70 days) fenfluramine treatment on selected physiological and behavioral measures were examined in four adult male vervet monkeys (Cercopithecus aethiops sabaeus). Relative to pretreatment baseline values, whole blood serotonin (WBS) and cerebrospinal fluid 5-hydroxyindole acetic acid (5-HIAA) were reduced, cerebrospinal fluid homovanillic acid (HVA) was unaltered, and aggressive and locomotor behavior were increased. Both physiological and behavioral effects were reversible: all measures returned to baseline values in the 35 day post-treatment period, with WBS resuming pretreatment values more rapidly than CSF 5-HIAA. At the relatively low doses (1-4 mg/kg/day) employed in the present study fenfluramine produced behavioral effects similar to those resulting from PCPA and opposite to those following tryptophan administration. Thus the behavioral effects of long-term fenfluramine may involve reductions in serotonergic transmission.

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“…Platelet 5-HT uptake consists of a brief, rapid uptake phase in the first 2 minutes followed by a slower phase (Stahl and Meltzer, 1978). By measuring uptake for 30-90 minutes, active uptake, passive diffusion, release, and degradation are all contributing to "uptake" (Yuwiler et al, 1985).…”

Section: Bloodmentioning

confidence: 99%

Autism: Review of neurochemical investigation

Cook

1990

Synapse

171

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The neurochemistry of autism, the most well-validated childhood neuropsychiatric disorder, has been studied extensively over the past three decades. Autism is of interest neurochemically because it represents a relatively homogeneous disorder with a triad of social, communicative, and intellectual developmental disturbance. Because a sufficient animal model has been lacking and relatively few diagnosed people with autism have died, most investigation has been of peripheral fluids and tissues. The most consistent finding has been that over 25% of autistic children and adolescents are hyperserotonemic. However, after 29 years of investigation, the mechanism of hyperserotonemia has not been determined. Hyperserotonemia has been found to be familial. Elevated plasma norepinephrine has also been a replicated finding. Cerebrospinal fluid (CSF) opiate activity has been found to be elevated in two studies. Plasma cyclic adenosine monophosphate (cAMP) has been found to be elevated in autistic children. A high rate of nonsuppression after dexamethasone and blunted or delayed growth hormone response to L-dopa have been found. Abnormal cell-mediated immunity has been replicated consistently in autism. Although several pharmacological trials have been conducted and shown promise in initial open trials, only "typical" antipsychotic drugs have shown replicable chronic ameliorating effects in double-blind trials. However, chronic neurotoxicity (tardive dyskinesia) has also been revealed. Findings of morphological changes in the cerebellum have been replicated. Findings in need of replication include diminished platelet function, increased baseline CSF homovanillic acid, decreased nerve cell adhesion molecule serum fragment, blunted prolactin response to fenfluramine, amelioration of symptoms by naltrexone and bromocriptine, reduced electroretinographic (ERG) b-wave amplitude, and morphological changes in the hippocampus, amygdala, and septal nuclei. In addition to refining and replicating past findings, future directions that may be fruitful include investigation of neurochemical aspects of platelet function, of interactions between monoaminergic systems, of phosphatidylinositides, and of pharmacological response to "atypical" antipsychotic agents and relatively selective serotonin receptor subtype agonists or antagonists.

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Biochemical Studies on Autism

Cited by 7 publications

References 114 publications

Whole Blood Serotonin in Autistic and Normal Subjects

Whole Blood Serotonin in Autistic and Normal Subjects

Effects of chronic fenfluramine on blood serotonin, cerebrospinal fluid metabolites, and behavior in monkeys

Autism: Review of neurochemical investigation

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