The role of mercury in the pathogenesis of autism.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
T Binstock
Publications and source records attributed to T Binstock.
Intra-monocyte pathogens delineate autism subgroups.
Immune panels of many autism-spectrum children reveal signs of atypical infections and shifted cell counts. In conjunction with trait-related cerebral hypometabolism and hypoperfusion, these findings suggest a hypothesis: Several autism-spectrum subgroups derive from intra-monocyte pathogens such as measles virus, cytomegalovirus, human herpesvirus 6, and Yersinia enterocolitica. Furthermore, with much inter-child variation, their effects manifest as diminished hematopoiesis, impaired peripheral immunity, and altered blood-brain barrier function often accompanied by demyelination. In some such children, one or more of these pathogens persists as a chronic-active, seemingly subclinical infection etiologically significant to the child's autistic traits. Within these subgroups, immune impairments and atypical infections may be treatable.
Autistic Disorder↗
Autism: a novel form of mercury poisoning.
Autism is a syndrome characterized by impairments in social relatedness and communication, repetitive behaviors, abnormal movements, and sensory dysfunction. Recent epidemiological studies suggest that autism may affect 1 in 150 US children. Exposure to mercury can cause immune, sensory, neurological, motor, and behavioral dysfunctions similar to traits defining or associated with autism, and the similarities extend to neuroanatomy, neurotransmitters, and biochemistry. Thimerosal, a preservative added to many vaccines, has become a major source of mercury in children who, within their first two years, may have received a quantity of mercury that exceeds safety guidelines. A review of medical literature and US government data suggests that: (i) many cases of idiopathic autism are induced by early mercury exposure from thimerosal; (ii) this type of autism represents an unrecognized mercurial syndrome; and (iii) genetic and non-genetic factors establish a predisposition whereby thimerosal's adverse effects occur only in some children.
Autistic Disorder↗
An immune hypothesis of sexual orientation.
Sexual orientation is encoded within immune-cell subsets (ICS) of mucosal and epithelial tissues. Gender orientation may be encoded within other ICS. Many immune cells: recognize and react to H-Y and H-X antigens; and enact these perceptions and reactions in accord with the perceiver's and the perceived's MHC haplotype, XX or XY status, and immune-self recognition. Non-heterosexual orientations derive from excessive cross-priming, accompanied by clonal deletions, clonal expansions, anergy and tolerance. For at least some tissues, cross-priming sufficient to induce altered orientations may occur during critical periods of immunological development and can occur during fetal and infant development via maternal-fetal transfusion, placental pathology, and impaired maternal nutrient-status or via excessive peripheral apoptosis during postnatal illness. Mast cell interactions with neurons illustrate how mucosal perceptions can be transduced into neuronal signals that modulate CNS events. This hypothesis is testable by mixed-lymphocyte reactions in appropriate cell subsets. Dendritic-cell immunizations are a potential therapy.
Clonal Anergy↗
Anterior insular cortex: linking intestinal pathology and brain function in autism-spectrum subgroups.
Autism includes deficits in communications skills and is associated with intestinal pathology. Numerous parents and some physicians report that an autistic child's attention and language improve in response to treatments which eliminate certain dietary antigens and/or which improve intestinal health. For at least some autism-spectrum children, the link between intestinal pathology, attention, and language may derive from shared neuroanatomic pathways within the anterior insular cortex (aIC); from a neurotrophic virus such as herpes simplex (HSV) migrating within afferents to the insular cortex; and/or from synaptic exhaustion in the aIC as induced by chronically inappropriate neuronal activity in the enteric nervous system and/or its vagal efferents.
Autistic Disorder↗
From fertilization to adult sexual behavior.
Research has established the broad mammalian developmental plan that genes on the sex chromosomes influence gonad development which determines gonadal hormone production (or its absence) leading to modification of the genitalia and simultaneously biasing the nervous system to organize adult sexual behavior. This might be considered the "gonad to hormones to behavior" model. It is clear, however, that although this model generally works well it is incomplete. The model does not account for behavioral influences attributed to the environment or to genetic but nongonadal or hormonal factors. In this essay we probe those areas of sexual development that are neither differentiated by hormones nor activated by them. The concept of the environment used for our discussion is very broad; it incorporates considerations of both the molar and the molecular levels. The general sense of the word "environment" as something exterior to the person is retained, even if that something influences intraperson processes. In addition, we focus directly on molecular events themselves. Here the "environment" involved can be that within a DNA segment. We also expand the notion of "biologically based sex differences." Although many, and perhaps most, important sex differences arise from gonadal and hormonal development, also important are sex differences which are neither gonadal nor hormonal. All these factors affect the internal workings of the individual and intervene in structuring how the social environment might or might not modify sexual behavior. This discourse calls attention to features that are central to the so-called nature-nurture discussion.
Fertilization↗