Here is some text - I don't take it as textbook:
Post# of 65629
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Posted On: 03/21/2019 12:05:32 PM
Here is some text - I don't take it as textbook:
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( Looks to me like our toxic environment is at fault )
That would include things like diet coke, MSG, food chemicals.
Causes
It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism's characteristic triad of symptoms.[61] However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.[61][62]
Three diagrams of chromosome pairs A, B that are nearly identical. 1: B is missing a segment of A. 2: B has two adjacent copies of a segment of A. 3: B's copy of A's segment is in reverse order.
Deletion (1), duplication (2) and inversion (3) are all chromosome abnormalities that have been implicated in autism.[63]
Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations with major effects, or by rare multigene interactions of common genetic variants.[64][65] Complexity arises due to interactions among multiple genes, the environment, and epigenetic factors which do not change DNA sequencing but are heritable and influence gene expression.[31] Many genes have been associated with autism through sequencing the genomes of affected individuals and their parents.[66] Studies of twins suggest that heritability is 0.7 for autism and as high as 0.9 for ASD, and siblings of those with autism are about 25 times more likely to be autistic than the general population.[51] However, most of the mutations that increase autism risk have not been identified. Typically, autism cannot be traced to a Mendelian (single-gene) mutation or to a single chromosome abnormality, and none of the genetic syndromes associated with ASDs have been shown to selectively cause ASD.[64] Numerous candidate genes have been located, with only small effects attributable to any particular gene.[64] Most loci individually explain less than 1% of cases of autism.[67] The large number of autistic individuals with unaffected family members may result from spontaneous structural variation — such as deletions, duplications or inversions in genetic material during meiosis.[68][69] Hence, a substantial fraction of autism cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.[63] Autism may be underdiagnosed in women and girls due to an assumption that it is primarily a male condition.[70]
Maternal nutrition and inflammation during preconception and pregnancy influences fetal neurodevelopment. Intrauterine growth restriction is associated with ASD, in both term and preterm infants.[16] Maternal inflammatory and autoimmune diseases may damage fetal tissues, aggravating a genetic problem or damaging the nervous system.[17]
Exposure to air pollution during pregnancy, especially heavy metals and particulates, may increase the risk of autism.[71] Environmental factors that have been claimed without evidence to contribute to or exacerbate autism include certain foods, infectious diseases, solvents, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines,[24] and prenatal stress. Some such as the MMR vaccine have been completely disproven.[72][73][74]
Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. This has led to unsupported theories blaming vaccine "overload", a vaccine preservative, or the MMR vaccine for causing autism.[75] The latter theory was supported by a litigation-funded study that has since been shown to have been "an elaborate fraud".[76] Although these theories lack convincing scientific evidence and are biologically implausible,[75] parental concern about a potential vaccine link with autism has led to lower rates of childhood immunizations, outbreaks of previously controlled childhood diseases in some countries, and the preventable deaths of several children.[77][78]
Mechanism
Autism's symptoms result from maturation-related changes in various systems of the brain. How autism occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors.[79] The behaviors appear to have multiple pathophysiologies.[33]
There is evidence that gut–brain axis abnormalities may be involved.[60][80][59] A 2015 review proposed that immune dysregulation, gastrointestinal inflammation, malfunction of the autonomic nervous system, gut flora alterations, and food metabolites may cause brain neuroinflammation and dysfunction.[60] A 2016 review concludes that enteric nervous system abnormalities might play a role in neurological disorders such as autism. Neural connections and the immune system are a pathway that may allow diseases originated in the intestine to spread to the brain.[80]
Several lines of evidence point to synaptic dysfunction as a cause of autism.[19] Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion.[81] Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes.[82] All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, there is strong evidence that autism arises very early in development.[83]
< >
( Looks to me like our toxic environment is at fault )
That would include things like diet coke, MSG, food chemicals.
Causes
It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism's characteristic triad of symptoms.[61] However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.[61][62]
Three diagrams of chromosome pairs A, B that are nearly identical. 1: B is missing a segment of A. 2: B has two adjacent copies of a segment of A. 3: B's copy of A's segment is in reverse order.
Deletion (1), duplication (2) and inversion (3) are all chromosome abnormalities that have been implicated in autism.[63]
Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations with major effects, or by rare multigene interactions of common genetic variants.[64][65] Complexity arises due to interactions among multiple genes, the environment, and epigenetic factors which do not change DNA sequencing but are heritable and influence gene expression.[31] Many genes have been associated with autism through sequencing the genomes of affected individuals and their parents.[66] Studies of twins suggest that heritability is 0.7 for autism and as high as 0.9 for ASD, and siblings of those with autism are about 25 times more likely to be autistic than the general population.[51] However, most of the mutations that increase autism risk have not been identified. Typically, autism cannot be traced to a Mendelian (single-gene) mutation or to a single chromosome abnormality, and none of the genetic syndromes associated with ASDs have been shown to selectively cause ASD.[64] Numerous candidate genes have been located, with only small effects attributable to any particular gene.[64] Most loci individually explain less than 1% of cases of autism.[67] The large number of autistic individuals with unaffected family members may result from spontaneous structural variation — such as deletions, duplications or inversions in genetic material during meiosis.[68][69] Hence, a substantial fraction of autism cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.[63] Autism may be underdiagnosed in women and girls due to an assumption that it is primarily a male condition.[70]
Maternal nutrition and inflammation during preconception and pregnancy influences fetal neurodevelopment. Intrauterine growth restriction is associated with ASD, in both term and preterm infants.[16] Maternal inflammatory and autoimmune diseases may damage fetal tissues, aggravating a genetic problem or damaging the nervous system.[17]
Exposure to air pollution during pregnancy, especially heavy metals and particulates, may increase the risk of autism.[71] Environmental factors that have been claimed without evidence to contribute to or exacerbate autism include certain foods, infectious diseases, solvents, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines,[24] and prenatal stress. Some such as the MMR vaccine have been completely disproven.[72][73][74]
Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. This has led to unsupported theories blaming vaccine "overload", a vaccine preservative, or the MMR vaccine for causing autism.[75] The latter theory was supported by a litigation-funded study that has since been shown to have been "an elaborate fraud".[76] Although these theories lack convincing scientific evidence and are biologically implausible,[75] parental concern about a potential vaccine link with autism has led to lower rates of childhood immunizations, outbreaks of previously controlled childhood diseases in some countries, and the preventable deaths of several children.[77][78]
Mechanism
Autism's symptoms result from maturation-related changes in various systems of the brain. How autism occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors.[79] The behaviors appear to have multiple pathophysiologies.[33]
There is evidence that gut–brain axis abnormalities may be involved.[60][80][59] A 2015 review proposed that immune dysregulation, gastrointestinal inflammation, malfunction of the autonomic nervous system, gut flora alterations, and food metabolites may cause brain neuroinflammation and dysfunction.[60] A 2016 review concludes that enteric nervous system abnormalities might play a role in neurological disorders such as autism. Neural connections and the immune system are a pathway that may allow diseases originated in the intestine to spread to the brain.[80]
Several lines of evidence point to synaptic dysfunction as a cause of autism.[19] Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion.[81] Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes.[82] All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, there is strong evidence that autism arises very early in development.[83]
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