Wednesday, July 30, 2008

Autism is not a mental illness (according to Dear Abby)

DEAR ABBY: I just finished reading your June 9 column and am shocked at what I read. Your response regarding autism was way off base. You said, "Autism is a mental health disorder ... some people consider ... to be shameful."
Autism is a neurological disorder, NOT a mental health disorder......

DEAR MELISSA: My thanks to you -- and the many other readers -- who wrote to correct me..... autism is often considered a mental health disorder because it affects behavior, cognitive ability and social skills. However, it is genetically predetermined -- biologically based.
Experts clearly agree that autism is a neurologically based condition. The current criteria used to diagnose autism are contained in the Diagnostic and Statistical Manual of Mental Disorders, a publication of the American Psychiatric Association. However, this does not mean that autism is a "mental illness." Autism is most accurately described as a "neurodevelopmental disorder."

Most psychiatric conditions have at least some biological basis. Schizophrenia can also be considered a "neurodevelopmental disorder," though it has a later onset than autism. There is no clear dividing line between what is considered a neurological brain disease and what is considered a mental illness.





7 comments:

concerned heart said...

Yes, schizophrenia and autism are not really different except in degree in many cases. Schizophrenia Risk and the Paternal Germ Line
By Dolores Malaspina



Paternal age at conception is a robust risk factor for schizophrenia. Possible mechanisms include de novo point mutations or defective epigenetic regulation of paternal genes. The predisposing genetic events appear to occur probabilistically (stochastically) in proportion to advancing paternal age, but might also be induced by toxic exposures, nutritional deficiencies, suboptimal DNA repair enzymes, or other factors that influence the fidelity of genetic information in the constantly replicating male germ line. We propose that de novo genetic alterations in the paternal germ line cause an independent and common variant of schizophrenia.

Seminal findings
We initially examined the relationship between paternal age and the risk for schizophrenia because it is well established that paternal age is the major source of de novo mutations in the human population, and most schizophrenia cases have no family history of psychosis. In 2001, we demonstrated a monotonic increase in the risk of schizophrenia as paternal age advanced in the rich database of the Jerusalem Perinatal Cohort. Compared with the offspring of fathers aged 20-24 years, in well-controlled analyses, each decade of paternal age multiplied the risk for schizophrenia by 1.4 (95 percent confidence interval: 1.2-1.7), so that the relative risk (RR) for offspring of fathers aged 45+ was 3.0 (1.6-5.5), with 1/46 of these offspring developing schizophrenia. There were no comparable maternal age effects (Malaspina et al., 2001).

Epidemiological evidence
This finding has now been replicated in numerous cohorts from diverse populations (Sipos et al., 2004; El-Saadi et al., 2004; Zammit et al., 2003; Byrne et al., 2003; Dalman and Allenbeck, 2002; Brown et al., 2002; Tsuchiya et al., 2005). By and large, each study shows a tripling of the risk for schizophrenia for the offspring of the oldest group of fathers, in comparison to the risk in a reference group of younger fathers. There is also a "dosage effect" of increasing paternal age; risk is roughly doubled for the offspring of men in their forties and is tripled for paternal age >50 years. These studies are methodologically sound, and most of them have employed prospective exposure data and validated psychiatric diagnoses. Together they demonstrate that the paternal age effect is not explained by other factors, including family history, maternal age, parental education and social ability, family social integration, social class, birth order, birth weight, and birth complications. Furthermore, the paternal age effect is specific for schizophrenia versus other adult onset psychiatric disorders. This is not the case for any other known schizophrenia risk factor, including many of the putative susceptibility genes (Craddock et al., 2006).

There have been no failures to replicate the paternal age effect, nor its approximate magnitude, in any adequately powered study. The data support the hypothesis that paternal age increases schizophrenia risk through a de novo genetic mechanism. The remarkable uniformity of the results across different cultures lends further coherence to the conclusion that this robust relationship is likely to reflect an innate human biological phenomenon that progresses over aging in the male germ line, which is independent of regional environmental, infectious, or other routes.

Indeed, the consistency of these data is unparalleled in schizophrenia research, with the exception of the increase in risk to the relatives of schizophrenia probands (i.e., 10 percent for a sibling). Yet, while having an affected first-degree relative confers a relatively higher risk for illness than having a father >50 years (~10 percent versus ~2 percent), paternal age explains a far greater portion of the population attributable risk for schizophrenia. This is because a family history is infrequent among schizophrenia cases, whereas paternal age explained 26.6 percent of the schizophrenia cases in our Jerusalem cohort. If we had only considered the risk in the cases with paternal age >30 years, our risk would be equivalent to that reported by Sipos et al. (2004) in the Swedish study (15.5 percent). When paternal ages >25 years are considered, the calculated risk is much higher. Although the increment in risk for fathers age 26 through 30 years is small (~14 percent), this group is very large, which accounts for the magnitude of their contribution to the overall risk. The actual percentage of cases with paternal germ line-derived schizophrenia in a given population will depend on the demographics of paternal childbearing age, among other factors. With an upswing in paternal age, these cases would be expected to become more prevalent.

Biological plausibility
We used several approaches to examine the biological plausibility of paternal age as a risk factor for schizophrenia. First, we established a translational animal model using inbred mice. Previously it had been reported that the offspring of aged male rodents had less spontaneous activity and worse learning capacity than those of mature rodents, despite having no noticeable physical anomalies (Auroux et al., 1983). Our model carefully compared behavioral performance between the progeny of 18-24-month-old sires with that of 4-month-old sires. We replicated Auroux's findings, demonstrating significantly decreased learning in an active avoidance test, less exploration in the open field, and a number of other behavioral decrements in the offspring of older sires (Bradley-Moore et al., 2002).

Next, we examined if parental age was related to intelligence in healthy adolescents. We reasoned that if de novo genetic changes can cause schizophrenia, there might be effects of later paternal age on cognitive function, since cognitive problems are intertwined with core aspects of schizophrenia. For this study, we cross-linked data from the Jerusalem birth cohort with the neuropsychological data from the Israeli draft board (Malaspina et al., 2005a). We found that maternal and paternal age had independent effects on IQ scores, each accounting for ~2 percent of the total variance. Older paternal age was exclusively associated with a decrement in nonverbal (performance) intelligence IQ, without effects on verbal ability, suggestive of a specific effect on cognitive processing. In controlled analyses, maternal age showed an inverted U-shaped association with both verbal and performance IQ, suggestive of a generalized effect.

Finally, we examined if paternal age was related to the risk for autism in our cohort. We found very strong effects of advancing paternal age on the risk for autism and related pervasive developmental disorders (Reichenberg et al., in press). Compared to the offspring of fathers aged 30 years or younger, the risk was tripled for offspring of fathers in their forties and was increased fivefold when paternal age was >50 years. Together, these studies provide strong and convergent support for the hypothesis that later paternal age can influence neural functioning. The translational animal model offers the opportunity to identify candidate genes and epigenetic mechanisms that may explain the association of cognitive functioning with advancing paternal age.

A variant of schizophrenia
A persistent question is whether the association of paternal age and schizophrenia could be explained by psychiatric problems in the parents that could both hinder their childbearing and be inherited by their offspring. If this were so, then cases with affected parents would have older paternal ages. This has not been demonstrated. To the contrary, we found that paternal age was 4.7 years older for sporadic than familial cases from our research unit at New York State Psychiatric Institute (Malaspina et al., 2002). In addition, epidemiological studies show that advancing paternal age is unrelated to the risk for familial schizophrenia (Byrne et al., 2003; Sipos et al., 2004). For example, Sipos found that each subsequent decade of paternal age increased the RR for sporadic schizophrenia by 1.60 (1.32 to 1.92), with no significant effect for familial cases (RR = 0.91, 0.44 to 1.89). The effect of late paternal age in sporadic cases was impressive. The offspring of the oldest fathers had a 5.85-fold risk for sporadic schizophrenia (Sipos et al., 2004); relative risks over 5.0 are very likely to reflect a true causal relationship (Breslow and Day, 1980).

Michael Rack, MD said...

concerned heart:
thanks for the updated on increased paternal age as a risk factor for schizophrenia.

You sure have a lot of blogs!

Alex said...

Autism is not a mental illness. i accept this sentence. My two cousin brothers are affected by autism.

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Anonymous said...

Autism is one of what I believe are a number of what are called passive developmental disorders- and autism is the most common. Autism is a disability caused by a brain development disorder of unknown cause, yet some suspect the cause is some sort of neurological dysfunction. Usually, symptoms of the disease present themselves before the toddler reaches the age of three. Before Autism was more understood, others labeled them as childhood schizophrenia or as having a psychosis or mental retardation.
Out of 16 related characteristics, eight must be present to be considered autistic, according to others. As with all passive developmental disorders, the person expresses language, social, and behavioral difficulties. Treatment includes what are called psychotropic medications that delay the progression of the disorder, as well as relieve some of the symptoms of one who is autistic. Behavioral therapy is common as a treatment regimen as well. Boys get Autism much more than girls.
Then there is the controversy between many who claim that thimerosal- a preservative containing mercury, which is a neurotoxin that was used in vaccines until 2001, was the catalyst for autism in children. Over 5000 lawsuits have been filed because of this belief, and some have been successful for the plaintiff. Yet most agree the correlation between thimersal and autism is void of scientific merit. Furthermore, the cases of autism have not decreased since the preservative was discontinued in 2001.
Aside from Autism, the other four passive developmental disorders are known as autism spectrum disorders.
Asperger’s Syndrome is more common than autism, and the symptoms are milder, as there is minimal delay in language abilities, if at all. What is expressed with Asperger’s syndrome is mild autistic symptoms. In time, the patient may express atypical personality disorders, though. While intelligence is within normal limits with the Asperger’s patient, social interactions and abilities preset difficulty for such a patient. As with Autism, medications and behavioral therapy are treatment regimens with one with this syndrome
Rett’s Syndrome or disorder presents with not only atypical behavior, but also suffers from restricted physical growth and movement. There is cognitive and social impairment as well. The disorder affects mostly girls, and the cause is due to a gene mutation.
Chldhood Disintegrative disorder is rare, and is 10 times less common than autism. The disorder has a late onset with mild autistic symptoms. The disorder affects mostly boys, and regression is sudden and possible with this disorder. Skills lost with this disorder may be language, social, self-care, as well as play or motor skills. Decreased function or impairment with this disorder may include social skills and behavioral flaws. Central Nervous System pathology is a suspected cause of this disorder.
Finally, there are passive development disorders that are not otherwise specified. This may include atypical autism, for example. Yet as with the rest of types of these disorders, the symptoms vary in their intensity, and the range of abilities of these developmental disorders vary widely as well. Medicinal treatment along with cognitive and behavioral therapy prove to be most beneficial for all the different types of Passive Development Disorders that unfortunately exist for unknown reasons,

Dan Abshear

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Erik said...

So, I do not really consider it may have effect.
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