**4. Immigrant status and ethnicity**

*Immigrant* describes mothers who give birth while residing in a country which is not their own country of birth. *Ethnic* describes mothers who belong to a minority racial group in their country of residence which may or may not be their country of birth. To some extent, the groups of immigrant and ethnic mothers overlap. When examining social forces in relation to ASD and ID, it is important to take into account the often complex process associated with making a diagnosis of ASD.

#### **4.1. Immigrant status**

#### *4.1.1. Immigrant mothers and autism*

In all of the eight studies of immigrant mothers of children and ASD, [17, 22, 30, 57, 62, 75-77] the research concluded that immigrant mothers were more likely to have a child with ASD and particularly ASD with ID. [17, 22] In relation to immigrant mothers from Asia one of these studies was conducted by an Australian research group from New South Wales and used birth records and active surveillance to ascertain children with ASD. The group found that immi‐ grant mothers born in South-East or North-East Asia were more likely to have a child with ASD than other immigrant mothers. [57] A Western Australian study, using linked population data, also found that immigrant mothers from South-East or North-East Asia were at increased risk of having a child with ASD with ID. [17] A similar situation was described in Sweden where immigrant mothers from East Asia were more than three times as likely to have a child with ASD. [76]

of typically developing children. However, an additional association exists with older mothers

An under-ascertainment of ASD due to social factors and, to a lesser extent an over-ascertain‐ ment of ID could be contributing to the socioeconomic effects seen with ASD and ID. For instance, in terms of the severity of ASD, researchers in California, with birth cohorts from 1992 to 2000, divided the children with ASD into two groups of equal size where the less severe group comprised children in the top 50% of cases according to level of functioning and the most severe group was the lower 50%. [41] They found that the children from the less severe group were more often found in neighbourhoods which housed wealthier and more educated individuals. Conversely, the same researchers reported that where low SES was measured by a Medi-Cal payment for the birth, the ratio of more severe to less severe cases was always greater than one. The researchers' interpretation was that the most difficult to diagnose cases of ASD, that is the less severely affected, were under-ascertained in lower SES populations. [41] The association of high SES with ASD also might be compounded by some of the characteristics known to be related to mothers of children with ASD. Older women with the support of a partner and with fewer children would seem more likely to achieve a more complex diagnosis requiring more assessments for their child than younger single mothers. Socio-demographic associations with ASD in most Western countries do not appear to operate as strongly and might even be absent in some Northern European countries. This might be due to a different social welfare structure in this region and specifically related to the universal screening for developmental disability. In addition to these and other social factors which could bias

being also more likely to have a child with severe ID.

396 Recent Advances in Autism Spectrum Disorders - Volume I

ascertainment, biological factors may be operating with older parents.

*Immigrant* describes mothers who give birth while residing in a country which is not their own country of birth. *Ethnic* describes mothers who belong to a minority racial group in their country of residence which may or may not be their country of birth. To some extent, the groups of immigrant and ethnic mothers overlap. When examining social forces in relation to ASD and ID, it is important to take into account the often complex process associated with making

In all of the eight studies of immigrant mothers of children and ASD, [17, 22, 30, 57, 62, 75-77] the research concluded that immigrant mothers were more likely to have a child with ASD and particularly ASD with ID. [17, 22] In relation to immigrant mothers from Asia one of these studies was conducted by an Australian research group from New South Wales and used birth records and active surveillance to ascertain children with ASD. The group found that immi‐ grant mothers born in South-East or North-East Asia were more likely to have a child with

**4. Immigrant status and ethnicity**

a diagnosis of ASD.

**4.1. Immigrant status**

*4.1.1. Immigrant mothers and autism*

Black immigrant mothers and immigrant mothers from developing countries were also found to be more likely to have a child with ASD compared to other immigrant mothers. One study from the UK [75] and another from Sweden [76] reported that black immigrant mothers [75] and immigrant mothers from sub-Saharan Africa [76] were much more likely to have a child with ASD compared to non-immigrant mothers. Further, a small Swedish case-control study compared the prevalence of autistic disorder and pervasive development disorder not otherwise specified (PDDNOS) in black African children with at least one parent born in Somali to the prevalence in children without a Somali background. [77] The researchers reported that these 17 black mothers were from three to four times more likely to have a child with ASD compared to the mothers without a Somali background. [77]

There is evidence that 'the intensity of the mother's skin colour' is related to her risk of having a child with ASD. A Swedish study compared the risk of ASD in the children of immigrants from each of North, East and other parts of Africa. [22] The mothers from North Africa were predominantly Moroccan and hence were probably fairer than the other two groups of mothers. For example, the East African group was predominantly from Somalia and Ethiopia while the ethnicity of the group from other parts of Africa was not described. The risk of ASD in the North African group was elevated (1.5) but not significantly higher than that of nonimmigrant parents. On the other hand, the risk in the East African mothers and mothers from other parts of Africa of having a child with ASD was 1.9 and 3.5. [22]

Immigrant mothers from distant countries and those who emigrated during pregnancy were more likely to have a child with ASD than other immigrant mothers. For instance, researchers from the UK and Denmark found that immigrant mothers born outside of Europe were more likely to have a child with ASD. [62, 75] Similarly, a Swedish study found that immigrant mothers who were not from either of the US or Europe were nearly three times as likely to have a child with ASD compared to mothers from Nordic countries. [30] Another Swedish study ascertained that immigrant mothers who emigrated during pregnancy were even more likely to have a child with ASD than mothers who emigrated at other times. [22]

There is evidence that immigrant mothers are at different risks of ASD without ID and ASD with ID. Two Swedish studies found that immigrant mothers, excepting those from neigh‐ bouring Northern Europe, were less likely to have a child with ASD without ID [22] and Asperger syndrome [76] compared to non-immigrant mothers. One of these studies, along with an Australian study, reported that immigrant mothers were more likely to have a child with ASD with ID. [17, 22] In addition, the Swedish study found that the African immigrant mothers were more likely to have a child with ASD with ID compared to non-immigrant mothers. [22] Similar results were found in a small Swedish case-control study, where all seventeen of the Somali children with autism presented with ASD with ID. [77]

Another group of researchers reported that certain immigrant mothers were less likely to have a child with ASD than non-immigrant mothers. The US study conducted a national telephone survey which chose respondents who resided with their biological child and the child's other parent. [78] These researchers reported that non-immigrant Hispanic children had about twice the prevalence of ASD of immigrant Hispanic children. [78] These results were at variance to those in the previous studies of immigrant mothers. The lower likelihood of ASD in immigrant Hispanics compared to non-immigrant Hispanics could be explained by the relative ease of access of Mexican Hispanics to the US. With many countries, immigrants must meet stringent criteria prior to entry and some of these relate to the health of their offspring, their age, wealth, education and occupation. However, Mexican Hispanics would be less likely to experience the same stress, climatic change and exposure to new infections as most other immigrants groups. Moreover, immigrant parents from some of the other studies have usually relocated from more distant locations. For example, one reported findings which related to immigrants from Somali to Sweden, [77] another to non-European immigrants to Britain [75] and another to immigrants to the isolated continent of Australia. [57]

*4.1.2. Immigrant mothers and intellectual disability*

**4.2. Ethnicity**

mothers [17, 29]

Compared to ASD, there was a reverse scenario identified with ID. Overall, immigrant mothers were 20-50% less likely to have a child with mild or moderate ID than non-immigrant mothers. [17, 20, 21] In Australia, Asian immigrant mothers were less likely to have a child with mild or moderate ID than non-immigrant mothers. [17, 20] As with ASD, the reversal with mild or moderate ID might be due to their higher SES compared to other immigrant groups. [81-83]

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

399

Differing results were found with the association of ID in the children of Mexican immigrants in a similar manner to the unexpected lower likelihood of Hispanic immigrant mothers having a child with ASD. A study of children with severe or profound ID, and born in California, found that immigrant mothers from Mexico, who would have been likely to be Hispanic, were nearly twice as likely to have a child with severe or profound ID compared to parents born in the US. [52] The idiosyncrasies associated with this immigrant group, compared to those immigrants from more distant locations, might explain this finding. They are likely to be less empowered than their non-immigrant counterparts and, as mentioned previously, their immigration was likely to be less regulated. Hence, from a socio-demographic viewpoint, they

In many studies, immigrant status and ethnicity were not differentiated. Therefore, within the ethnic group of mothers, there would have been mothers who, due to their country of birth, were both ethnic and immigrant. A recurrent trend of the research is that mothers from minority ethnic groups were less likely to have a child with ASD and more likely to have a

Epidemiologists have found that mothers from ethnic minorities and particularly Aboriginal mothers were less likely to have a child with ASD. For example, in the US, the Hispanic mothers were less likely to have a child with ASD compared to non-Hispanic mothers. [23, 59, 84] In New York, the prevalence in Latinos was around half that in non-Latinos. [40] Some of these mothers from minority ethnic groups would have also been immigrant and, as reported, immigrant mothers usually have higher rates of ASD. This means that mothers from ethnic minority groups and who are native to their country might be expected to have the lowest likelihood of a child with ASD. This is the case in both Australia and Canada, where Aboriginal mothers had about half the odds of having a child with ASD compared to non-Aboriginal

Compared to ASD, there was a reverse situation with ID since overall mothers from ethnic minority groups were more likely to have a child with ID. Asian mothers giving birth in California were 40% more likely to have a child with severe or profound ID although this result was not significant. [21] Hispanic mothers were more likely to have a child with either mild or moderate ID or severe or profound ID than Caucasian mothers. Again, in each of the ID groups, the results narrowly failed to achieve significance. [21] By comparison, Australian Aboriginal mothers were more than three times more likely to have a child with mild or moderate ID and were 60% more likely to have a child with severe or profound ID. [17, 20]

are more likely to present with low SES which is a risk factor for ID.

child with ID than mothers who were not from minority ethnic groups.

Overall, immigrant mothers and particularly black or Asian immigrant mothers, mothers from distant, developing countries and those who travelled while pregnant were at a higher risk of having a child with ASD. The mothers at highest risk of a child with ASD were from groups who would be expected to experience the most stress. For example, those relocating from a developing country and those pregnant at the time might be expected to experience higher stress than mothers who are relocating from a developed country or are not pregnant. This stress, along with the environmental changes associated with immigration, may have specific and negative effects on the developing fetal central nervous system. [22]

The risk of immigrant mothers having a child with ASD might be further exacerbated by an increased exposure to novel viruses [75] and intrauterine infections. [57] Other hypotheses to explain this association relate to low vitamin D levels [75, 79] and these have been further fuelled by animal studies. One study of rat pups with gross vitamin D deficiencies reported that they had structural brain abnormalities which were similar to those in children with ASD. [80] Furthermore, ASD was particularly common in black or Asian immigrant women and darker women more often have a vitamin D deficiency. [80] Generally, immigrant mothers are more likely to have a child with ASD with ID and less likely to have a child with ASD without ID. This may indicate different aetiologies for these subgroups.

Along with these biologically–based hypotheses, social factors may affect the likelihood of an immigrant mother having a child diagnosed with one of ASD, ASD with ID or ASD without ID. For instance, a diagnosis of ASD without ID would be particularly difficult where the child's parents were in an unfamiliar country, with a different language and where unusual behaviours might be explained by cultural differences. [22] In Australia, excluding the relatively small group of refugees, and in the US, Asian immigrants and their children are more often of a higher SES than other immigrant mothers. [81, 82] This might explain why the association with ASD was greater in this group than in other immigrant groups.

#### *4.1.2. Immigrant mothers and intellectual disability*

Compared to ASD, there was a reverse scenario identified with ID. Overall, immigrant mothers were 20-50% less likely to have a child with mild or moderate ID than non-immigrant mothers. [17, 20, 21] In Australia, Asian immigrant mothers were less likely to have a child with mild or moderate ID than non-immigrant mothers. [17, 20] As with ASD, the reversal with mild or moderate ID might be due to their higher SES compared to other immigrant groups. [81-83]

Differing results were found with the association of ID in the children of Mexican immigrants in a similar manner to the unexpected lower likelihood of Hispanic immigrant mothers having a child with ASD. A study of children with severe or profound ID, and born in California, found that immigrant mothers from Mexico, who would have been likely to be Hispanic, were nearly twice as likely to have a child with severe or profound ID compared to parents born in the US. [52] The idiosyncrasies associated with this immigrant group, compared to those immigrants from more distant locations, might explain this finding. They are likely to be less empowered than their non-immigrant counterparts and, as mentioned previously, their immigration was likely to be less regulated. Hence, from a socio-demographic viewpoint, they are more likely to present with low SES which is a risk factor for ID.

#### **4.2. Ethnicity**

Another group of researchers reported that certain immigrant mothers were less likely to have a child with ASD than non-immigrant mothers. The US study conducted a national telephone survey which chose respondents who resided with their biological child and the child's other parent. [78] These researchers reported that non-immigrant Hispanic children had about twice the prevalence of ASD of immigrant Hispanic children. [78] These results were at variance to those in the previous studies of immigrant mothers. The lower likelihood of ASD in immigrant Hispanics compared to non-immigrant Hispanics could be explained by the relative ease of access of Mexican Hispanics to the US. With many countries, immigrants must meet stringent criteria prior to entry and some of these relate to the health of their offspring, their age, wealth, education and occupation. However, Mexican Hispanics would be less likely to experience the same stress, climatic change and exposure to new infections as most other immigrants groups. Moreover, immigrant parents from some of the other studies have usually relocated from more distant locations. For example, one reported findings which related to immigrants from Somali to Sweden, [77] another to non-European immigrants to Britain [75] and another to immigrants

Overall, immigrant mothers and particularly black or Asian immigrant mothers, mothers from distant, developing countries and those who travelled while pregnant were at a higher risk of having a child with ASD. The mothers at highest risk of a child with ASD were from groups who would be expected to experience the most stress. For example, those relocating from a developing country and those pregnant at the time might be expected to experience higher stress than mothers who are relocating from a developed country or are not pregnant. This stress, along with the environmental changes associated with immigration, may have specific

The risk of immigrant mothers having a child with ASD might be further exacerbated by an increased exposure to novel viruses [75] and intrauterine infections. [57] Other hypotheses to explain this association relate to low vitamin D levels [75, 79] and these have been further fuelled by animal studies. One study of rat pups with gross vitamin D deficiencies reported that they had structural brain abnormalities which were similar to those in children with ASD. [80] Furthermore, ASD was particularly common in black or Asian immigrant women and darker women more often have a vitamin D deficiency. [80] Generally, immigrant mothers are more likely to have a child with ASD with ID and less likely to have a child with ASD without

Along with these biologically–based hypotheses, social factors may affect the likelihood of an immigrant mother having a child diagnosed with one of ASD, ASD with ID or ASD without ID. For instance, a diagnosis of ASD without ID would be particularly difficult where the child's parents were in an unfamiliar country, with a different language and where unusual behaviours might be explained by cultural differences. [22] In Australia, excluding the relatively small group of refugees, and in the US, Asian immigrants and their children are more often of a higher SES than other immigrant mothers. [81, 82] This might explain why the association with ASD was greater in this group than in other

and negative effects on the developing fetal central nervous system. [22]

ID. This may indicate different aetiologies for these subgroups.

immigrant groups.

to the isolated continent of Australia. [57]

398 Recent Advances in Autism Spectrum Disorders - Volume I

In many studies, immigrant status and ethnicity were not differentiated. Therefore, within the ethnic group of mothers, there would have been mothers who, due to their country of birth, were both ethnic and immigrant. A recurrent trend of the research is that mothers from minority ethnic groups were less likely to have a child with ASD and more likely to have a child with ID than mothers who were not from minority ethnic groups.

Epidemiologists have found that mothers from ethnic minorities and particularly Aboriginal mothers were less likely to have a child with ASD. For example, in the US, the Hispanic mothers were less likely to have a child with ASD compared to non-Hispanic mothers. [23, 59, 84] In New York, the prevalence in Latinos was around half that in non-Latinos. [40] Some of these mothers from minority ethnic groups would have also been immigrant and, as reported, immigrant mothers usually have higher rates of ASD. This means that mothers from ethnic minority groups and who are native to their country might be expected to have the lowest likelihood of a child with ASD. This is the case in both Australia and Canada, where Aboriginal mothers had about half the odds of having a child with ASD compared to non-Aboriginal mothers [17, 29]

Compared to ASD, there was a reverse situation with ID since overall mothers from ethnic minority groups were more likely to have a child with ID. Asian mothers giving birth in California were 40% more likely to have a child with severe or profound ID although this result was not significant. [21] Hispanic mothers were more likely to have a child with either mild or moderate ID or severe or profound ID than Caucasian mothers. Again, in each of the ID groups, the results narrowly failed to achieve significance. [21] By comparison, Australian Aboriginal mothers were more than three times more likely to have a child with mild or moderate ID and were 60% more likely to have a child with severe or profound ID. [17, 20]

The higher rates of ID and the lower rates of ASD found in most ethnic minority and particu‐ larly indigenous communities may relate to the differing gene frequencies of these groups from the general population. However, differences could be exacerbated by environmental factors such as maternal alcohol consumption [85] without this being specifically identified as an aetiological factor. [86] Another consideration could be that marginalized groups are less empowered than others to pursue a diagnosis of ASD in contrast to a diagnosis of ID and that the infrastructures established for diagnostic assessment do not meet their needs. This second factor may also account for the lower prevalence of ASD and higher prevalence of ID with respect to the Australian Aboriginal community. [87]

64, 89] or personality [62, 89, 90] disorder than mothers of typically developing children. Further, parents of a child with ASD were more likely to have increased rates of disorders which were related to affective disorder, [42] obsessive compulsive disorder, [27] anxiety, [27] paranoia, [27] and somatization [27] than the parents of typically developing children. One of these studies was conducted by a Californian team and recruited 269 parents of children with ASD via an existing university research program and control parents of typically developing children who were students (or their contacts) at the university. Self-reported mental health measures were obtained via questionnaire. [27] Other reported associations with parents of a child with ASD were increased rates of schizophrenia, [42, 89, 91] psychosis [42] and depres‐ sion, [27, 64, 89] compared to the parents of typically developing children. Mothers of a child with ASD were more likely to have had pregnancies complicated by depression [92, 93] than mothers of typically developing children. Another research group explored mental health by comparing the rates of mental disorders in parents of people with ASD to those in parents of people with Down syndrome. [94] Parents of a child with ASD were more likely to have had

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

401

Studies have most commonly investigated the mental health of mothers of children with disabilities rather than the developmental outcomes in children born to mothers with mental health diagnoses. In one case-control study, the latter approach was employed and linked data from population-based registries was used to compare the likelihood of ASD with ID or ID in the children of more than 3 000 mothers with schizophrenia, bipolar disorder or unipolar major depression to the likelihood of these disorders in control mothers. Of these, around 1 300 mothers had bipolar disorder and these were assessed as nearly ten times more likely to have a child with ASD with ID than mothers without these disorders. [95] However, there were only four children with a mother with pre-existing bipolar disorder so these large odds are associated with particularly wide confidence intervals and only just reached significance. The same study found that children of mothers with either schizophrenia, unipolar major depression or bipolar disorder or a combination of these disorders were about three times as likely to have a child with ID as mothers without these disorders. [95] Furthermore, mothers with ID themselves were more likely to have a child with ID compared to mothers with no

Personality traits have been more often identified in the parents of children with ASD. For instance, parents of children with ASD were more likely to manifest a range of subtle autisticlike characteristics than parents of typically developing children. These characteristics have been grouped together as the Broad Autism Phenotype and include social cognition deficits, such as reasoning about the emotions of others, [96] autistic-like traits, [97] and impaired

A questionnaire entitled the Autism Spectrum Quotient (AQ) [100] was designed to assess the Broad Autism Phenotype in the five domains of social skills, communication, attention to detail, attention switching and imagination. [101] Researchers from the UK conducted a casecontrol study comprising parents of children with and without ASD from more than 1 500

an anxiety disorder than the parents of children with Down syndrome.

history of psychiatric disorder or ID. [95]

aspects of executive function. [98, 99]

**5.2. Personality traits**

In two Californian studies, contrasting findings were found for the previously described associations of ethnicity with ASD. Firstly, a cohort study found that Hispanic mothers were no less likely to have a child with ASD with ID than white mothers. [52] The same study also reported that Californian black mothers were more than five times as likely to have a child with ASD with ID as white mothers. [52] Furthermore, Californian Asian mothers were almost four times as likely to have a child with ASD with ID as white mothers. [52] Again, this may be a reflection of the higher proportion of immigrants in these groups. A second explanation in relation to the Asian mothers could be the fact that Asian mothers in US tend to have a higher SES than most other ethnic mothers. The second of the two Californian studies reported that Asian mothers giving birth in California were 30% less likely to have a child with mild or moderate ID*.* [21] This may also be a reflection of their higher SES.

#### **4.3. Summary**

Generally, immigrant mothers, and especially black and Asian immigrant mothers, were more likely to have a child with ASD compared to non-immigrant mothers. Furthermore, immigrant mothers were more likely to have a child with ASD with ID and less likely to have a child with ASD without ID compared to non-immigrant mothers. Immigrant mothers from distant or developing countries and mothers who emigrated when they were pregnant were even more likely to have a child with ASD. By contrast, in the US, Hispanic immigrant mothers were less likely to have a child with ASD than non-immigrant Hispanic mothers. Furthermore, nonimmigrant mothers and particularly Aboriginal mothers were more likely to have a child with ID and especially mild or moderate ID than mothers who were not ethnic.

### **5. Health and associated characteristics**

#### **5.1. Mental health**

The *World Health Organisation* describes mental health as a state of mental well-being. [88] This state of well-being can be enhanced by the prevention of mental disorders and the treatment and rehabilitation of those with mental disorders. Compromised mental health has been reported in the mothers of children with ASD and to a lesser extent in the mothers of children with ID compared to mothers of children without these disorders. For example, researchers found that mothers of a child with ASD were more likely to have a pre-existing psychiatric [62, 64, 89] or personality [62, 89, 90] disorder than mothers of typically developing children. Further, parents of a child with ASD were more likely to have increased rates of disorders which were related to affective disorder, [42] obsessive compulsive disorder, [27] anxiety, [27] paranoia, [27] and somatization [27] than the parents of typically developing children. One of these studies was conducted by a Californian team and recruited 269 parents of children with ASD via an existing university research program and control parents of typically developing children who were students (or their contacts) at the university. Self-reported mental health measures were obtained via questionnaire. [27] Other reported associations with parents of a child with ASD were increased rates of schizophrenia, [42, 89, 91] psychosis [42] and depres‐ sion, [27, 64, 89] compared to the parents of typically developing children. Mothers of a child with ASD were more likely to have had pregnancies complicated by depression [92, 93] than mothers of typically developing children. Another research group explored mental health by comparing the rates of mental disorders in parents of people with ASD to those in parents of people with Down syndrome. [94] Parents of a child with ASD were more likely to have had an anxiety disorder than the parents of children with Down syndrome.

Studies have most commonly investigated the mental health of mothers of children with disabilities rather than the developmental outcomes in children born to mothers with mental health diagnoses. In one case-control study, the latter approach was employed and linked data from population-based registries was used to compare the likelihood of ASD with ID or ID in the children of more than 3 000 mothers with schizophrenia, bipolar disorder or unipolar major depression to the likelihood of these disorders in control mothers. Of these, around 1 300 mothers had bipolar disorder and these were assessed as nearly ten times more likely to have a child with ASD with ID than mothers without these disorders. [95] However, there were only four children with a mother with pre-existing bipolar disorder so these large odds are associated with particularly wide confidence intervals and only just reached significance.

The same study found that children of mothers with either schizophrenia, unipolar major depression or bipolar disorder or a combination of these disorders were about three times as likely to have a child with ID as mothers without these disorders. [95] Furthermore, mothers with ID themselves were more likely to have a child with ID compared to mothers with no history of psychiatric disorder or ID. [95]

#### **5.2. Personality traits**

The higher rates of ID and the lower rates of ASD found in most ethnic minority and particu‐ larly indigenous communities may relate to the differing gene frequencies of these groups from the general population. However, differences could be exacerbated by environmental factors such as maternal alcohol consumption [85] without this being specifically identified as an aetiological factor. [86] Another consideration could be that marginalized groups are less empowered than others to pursue a diagnosis of ASD in contrast to a diagnosis of ID and that the infrastructures established for diagnostic assessment do not meet their needs. This second factor may also account for the lower prevalence of ASD and higher prevalence of ID with

In two Californian studies, contrasting findings were found for the previously described associations of ethnicity with ASD. Firstly, a cohort study found that Hispanic mothers were no less likely to have a child with ASD with ID than white mothers. [52] The same study also reported that Californian black mothers were more than five times as likely to have a child with ASD with ID as white mothers. [52] Furthermore, Californian Asian mothers were almost four times as likely to have a child with ASD with ID as white mothers. [52] Again, this may be a reflection of the higher proportion of immigrants in these groups. A second explanation in relation to the Asian mothers could be the fact that Asian mothers in US tend to have a higher SES than most other ethnic mothers. The second of the two Californian studies reported that Asian mothers giving birth in California were 30% less likely to have a child with mild or

Generally, immigrant mothers, and especially black and Asian immigrant mothers, were more likely to have a child with ASD compared to non-immigrant mothers. Furthermore, immigrant mothers were more likely to have a child with ASD with ID and less likely to have a child with ASD without ID compared to non-immigrant mothers. Immigrant mothers from distant or developing countries and mothers who emigrated when they were pregnant were even more likely to have a child with ASD. By contrast, in the US, Hispanic immigrant mothers were less likely to have a child with ASD than non-immigrant Hispanic mothers. Furthermore, nonimmigrant mothers and particularly Aboriginal mothers were more likely to have a child with

The *World Health Organisation* describes mental health as a state of mental well-being. [88] This state of well-being can be enhanced by the prevention of mental disorders and the treatment and rehabilitation of those with mental disorders. Compromised mental health has been reported in the mothers of children with ASD and to a lesser extent in the mothers of children with ID compared to mothers of children without these disorders. For example, researchers found that mothers of a child with ASD were more likely to have a pre-existing psychiatric [62,

respect to the Australian Aboriginal community. [87]

400 Recent Advances in Autism Spectrum Disorders - Volume I

moderate ID*.* [21] This may also be a reflection of their higher SES.

ID and especially mild or moderate ID than mothers who were not ethnic.

**5. Health and associated characteristics**

**4.3. Summary**

**5.1. Mental health**

Personality traits have been more often identified in the parents of children with ASD. For instance, parents of children with ASD were more likely to manifest a range of subtle autisticlike characteristics than parents of typically developing children. These characteristics have been grouped together as the Broad Autism Phenotype and include social cognition deficits, such as reasoning about the emotions of others, [96] autistic-like traits, [97] and impaired aspects of executive function. [98, 99]

A questionnaire entitled the Autism Spectrum Quotient (AQ) [100] was designed to assess the Broad Autism Phenotype in the five domains of social skills, communication, attention to detail, attention switching and imagination. [101] Researchers from the UK conducted a casecontrol study comprising parents of children with and without ASD from more than 1 500 families. Parents of children with ASD were more likely to exhibit autistic-like traits in all domains except that of attention to detail [102] than parents of typically developing children. Furthermore, these researchers and others found that a Broad Autism Phenotype occurred more commonly in parents of children with simplex ASD [97, 102] (where only one family member has ASD) and multiplex ASD [100, 103] (where more than one family member has ASD) than in parents of typically developing children. A dose-response effect was also described with parents in multiplex ASD families expressing a Broad Autism Phenotype significantly more often than parents in simplex ASD families. [32]

**5.4. Health behaviours**

other forms of ASD.

to discern an association between smoking and ID.

Smoking during pregnancy has been associated with both ASD and ID in the offspring. In one study, mothers who smoked during pregnancy were reported to be more likely to have a child with ASD than mothers who did not smoke. [30] In 2011, a Swedish nested case-control study using medical registry data, found that mothers who smoked during early pregnancy were 70% less likely to have a child with ASD but almost twice as likely to have a child with Asperger syndrome. [76] This raises the possibility that Asperger syndrome has a distinct aetiology from

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

403

On the other hand, differing results were found in a US population-based, case-cohort study which explored the association of mothers who smoked during pregnancy and ASD. [105] Data from more than 6 000 000 mothers and their children were adjusted for potential confounders such as maternal age, education, and marital status. The definition of smoking during pregnancy was not described in the paper, so presumably this encompasses all mothers who had admitted to smoking one or more cigarettes during their pregnancy. The researchers reported that mothers who smoked during pregnancy were no more likely to have a child with ASD than mothers who did not smoke. Two large recently published cohort studies published in 2010 and 2011 also found no association between mothers who smoked during pregnancy and ASD. [29, 106] However, the first study examined only associations between maternal smoking and ASD generally [29] Hence, any associations between the relatively small group of mothers of children with Asperger syndrome may have been lost in the broader analysis. In addition, smoking was defined as *any smoking during pregnancy* which may have lessened the likelihood of an association with ASD. These were different outcomes to the second study, where mothers of children with ASD with ID and ASD without ID were considered separately and mothers who smoked ten or more cigarettes a day were a distinct group from the less intense smokers. [106] The first research group suggested that associations found with other studies were attributable to a confounding by maternal socio-demographic characteristics. [29] The findings of associations between smoking during pregnancy and ID are also limited. A population study in the US ascertained that mothers who smoked 20 or more cigarettes a day were more likely to have a male child, but not a female child, with ID than mothers who did not smoke during pregnancy. [107] A large Finnish cohort study found that mothers who smoked after 2 months of pregnancy were no more likely to have a child with ID than mothers who did not smoke after this time. [46] This definition of smoking is broader than that of the first study so the likelihood of identifying an association between maternal smoking and ID may be reduced. Further, smoking during the first two months of pregnancy or gender of the fetus was not considered for inclusion in the model. An alternative study, with a more stringent definition of maternal smoking and which addressed these omissions, would be more likely

Mothers who consume excessive alcohol during pregnancy were assessed as more likely to have a child with ID (but not ASD). This cause of ID is termed fetal alcohol syndrome (FAS) or fetal alcohol spectrum disorder (FASD). Fetal alcohol syndrome is at the most severe end of the spectrum and is diagnosed by characteristic facial features, brain dysmorphology, intellectual and other disabilities. [108] The milder diagnosis of FASD [109] does not require

Some factors associated with maternal mental health may have a deleterious effect on the fetus and increase the likelihood of a child developing ASD or ID. For example, mothers with schizophrenia may remain on antipsychotic drugs during their pregnancies and these drugs, perhaps along with lower levels of maternal self-care (such as diet and medical care) and genetic factors related to the disease may adversely affect the development in the fetus. The milder autistic features in the parents of children with ASD might also be attributable to genetic factors associated with ASD. [33] In their affected children, these factors, along with additional genetic factors from the other parent, may sometimes produce the clinical phenotype of ASD.

#### **5.3. Physical characteristics**

Here are a group of diverse findings pertaining to the physical attributes of the mothers of interest. One study identified that mothers of children with ASD were significantly taller, particularly those of children with ASD without ID compared to the mothers of typically developing children. [17] This study population comprised more than 300 000 mothers and the mean heights of mothers of children with ASD with ID and mothers of children with ASD without ID were 164.3 and 164.9 cm. These means were significantly higher than the mean of the mothers of typically developing children (163.4cm). Another study found that mothers of children with ASD were both taller and heavier than mothers of typically developing children. [93] Similarly, a Canadian population study found that among non-smoking women, taller and heavier women were more likely to have a child with ASD compared to the mothers of typically developing children. [29]

Compared to the mothers of children with ASD, differing associations between maternal height and the mothers of children with ID were identified. Using population data, researchers identified that shorter women and those of medium height were more likely to have a child with mild or moderate ID than other mothers. [20] Further, the shortest group of women were more likely to have a child with severe or profound ID than other women. [20] Others found that mothers of children with mild or moderate ID, with a mean height of 162.1 cm were significantly shorter then than the mothers of typically developing children whose mean was 164.3 cm. However, the mothers of children with severe or profound ID were not significantly shorter than the mothers of typically developing children. [17] However, associations have also been described between SES and height, [104] and so the observed height differences between the mothers of children with ASD and ID may be a reflection of the different mean SES of these groups.

#### **5.4. Health behaviours**

families. Parents of children with ASD were more likely to exhibit autistic-like traits in all domains except that of attention to detail [102] than parents of typically developing children. Furthermore, these researchers and others found that a Broad Autism Phenotype occurred more commonly in parents of children with simplex ASD [97, 102] (where only one family member has ASD) and multiplex ASD [100, 103] (where more than one family member has ASD) than in parents of typically developing children. A dose-response effect was also described with parents in multiplex ASD families expressing a Broad Autism Phenotype

Some factors associated with maternal mental health may have a deleterious effect on the fetus and increase the likelihood of a child developing ASD or ID. For example, mothers with schizophrenia may remain on antipsychotic drugs during their pregnancies and these drugs, perhaps along with lower levels of maternal self-care (such as diet and medical care) and genetic factors related to the disease may adversely affect the development in the fetus. The milder autistic features in the parents of children with ASD might also be attributable to genetic factors associated with ASD. [33] In their affected children, these factors, along with additional genetic factors from the other parent, may sometimes produce the clinical phenotype of ASD.

Here are a group of diverse findings pertaining to the physical attributes of the mothers of interest. One study identified that mothers of children with ASD were significantly taller, particularly those of children with ASD without ID compared to the mothers of typically developing children. [17] This study population comprised more than 300 000 mothers and the mean heights of mothers of children with ASD with ID and mothers of children with ASD without ID were 164.3 and 164.9 cm. These means were significantly higher than the mean of the mothers of typically developing children (163.4cm). Another study found that mothers of children with ASD were both taller and heavier than mothers of typically developing children. [93] Similarly, a Canadian population study found that among non-smoking women, taller and heavier women were more likely to have a child with ASD compared to the mothers of

Compared to the mothers of children with ASD, differing associations between maternal height and the mothers of children with ID were identified. Using population data, researchers identified that shorter women and those of medium height were more likely to have a child with mild or moderate ID than other mothers. [20] Further, the shortest group of women were more likely to have a child with severe or profound ID than other women. [20] Others found that mothers of children with mild or moderate ID, with a mean height of 162.1 cm were significantly shorter then than the mothers of typically developing children whose mean was 164.3 cm. However, the mothers of children with severe or profound ID were not significantly shorter than the mothers of typically developing children. [17] However, associations have also been described between SES and height, [104] and so the observed height differences between the mothers of children with ASD and ID may be a reflection of the different mean

significantly more often than parents in simplex ASD families. [32]

**5.3. Physical characteristics**

402 Recent Advances in Autism Spectrum Disorders - Volume I

typically developing children. [29]

SES of these groups.

Smoking during pregnancy has been associated with both ASD and ID in the offspring. In one study, mothers who smoked during pregnancy were reported to be more likely to have a child with ASD than mothers who did not smoke. [30] In 2011, a Swedish nested case-control study using medical registry data, found that mothers who smoked during early pregnancy were 70% less likely to have a child with ASD but almost twice as likely to have a child with Asperger syndrome. [76] This raises the possibility that Asperger syndrome has a distinct aetiology from other forms of ASD.

On the other hand, differing results were found in a US population-based, case-cohort study which explored the association of mothers who smoked during pregnancy and ASD. [105] Data from more than 6 000 000 mothers and their children were adjusted for potential confounders such as maternal age, education, and marital status. The definition of smoking during pregnancy was not described in the paper, so presumably this encompasses all mothers who had admitted to smoking one or more cigarettes during their pregnancy. The researchers reported that mothers who smoked during pregnancy were no more likely to have a child with ASD than mothers who did not smoke. Two large recently published cohort studies published in 2010 and 2011 also found no association between mothers who smoked during pregnancy and ASD. [29, 106] However, the first study examined only associations between maternal smoking and ASD generally [29] Hence, any associations between the relatively small group of mothers of children with Asperger syndrome may have been lost in the broader analysis. In addition, smoking was defined as *any smoking during pregnancy* which may have lessened the likelihood of an association with ASD. These were different outcomes to the second study, where mothers of children with ASD with ID and ASD without ID were considered separately and mothers who smoked ten or more cigarettes a day were a distinct group from the less intense smokers. [106] The first research group suggested that associations found with other studies were attributable to a confounding by maternal socio-demographic characteristics. [29]

The findings of associations between smoking during pregnancy and ID are also limited. A population study in the US ascertained that mothers who smoked 20 or more cigarettes a day were more likely to have a male child, but not a female child, with ID than mothers who did not smoke during pregnancy. [107] A large Finnish cohort study found that mothers who smoked after 2 months of pregnancy were no more likely to have a child with ID than mothers who did not smoke after this time. [46] This definition of smoking is broader than that of the first study so the likelihood of identifying an association between maternal smoking and ID may be reduced. Further, smoking during the first two months of pregnancy or gender of the fetus was not considered for inclusion in the model. An alternative study, with a more stringent definition of maternal smoking and which addressed these omissions, would be more likely to discern an association between smoking and ID.

Mothers who consume excessive alcohol during pregnancy were assessed as more likely to have a child with ID (but not ASD). This cause of ID is termed fetal alcohol syndrome (FAS) or fetal alcohol spectrum disorder (FASD). Fetal alcohol syndrome is at the most severe end of the spectrum and is diagnosed by characteristic facial features, brain dysmorphology, intellectual and other disabilities. [108] The milder diagnosis of FASD [109] does not require the presence of all of the characteristic physical features required for FAS. [110] Studies from Sweden and the US attributed between 2-10% of mild or moderate ID to FAS or FASD. [111, 112] While the US study considered that a further 3% of severe or profound ID was caused by FAS or FASD. [112]

1985-6 and included around 250 mothers of children with ID in each of the cohorts. [46] In both cohorts, mothers with obesity prior to their pregnancies were more likely to have a child with ID than women without pre-pregnancy obesity. However, the association of ID with pre-pregnancy obesity was an increasing risk reflected in the greater odds in the latter cohort(2.4) compared with the original cohort(1.8). [46] Another of the research groups reported that women with an early age of menarche were more likely to have a child with ASD than other women. [120] Early menarche, along with pre-pregnancy obesity, could indicate the possibility of maternal hormonal involvement in the risk of ASD and ID. [120] Then again, the relationship with ID may be resulting from confounding by the association between socioeconomic disadvantage and obesity in highly developed countries. [121] In the light of the increasing prevalence of obesity in these countries, these

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

405

associations with ASD and ID are an important future research direction. [122]

disorders. [125]

Women with an auto-immune disorder or anomalies of the immune system were more likely to have a child with ASD and/or ID than women who did not. [25, 26, 123] Furthermore, the majority of associations in this area were with ASD rather than ID. For example, in a casecontrol study using linked data with more than 1 200 cases, mothers with an auto-immune disorder were 60% more likely to have a child with ASD than mothers without an auto-immune disorder. [26] These findings were supported by a small case-control study of 61 mothers of children with ASD. [123] Other studies have found that women with a particular auto-immune disease were more likely to have a child with ASD than women who did not have the disease. For instance, a case-control study with 407 cases found that women with psoriasis were more likely to have a child with ASD than mothers without this disorder. [124] Another research group used linked population data with more than 3 000 mothers of a child with ASD and nearly 700 000 control mothers. They reported that women with rheumatoid arthritis or celiac disease were more likely to have a child with ASD than mothers who did not have one of these

One study found that women with pre-existing diabetes were more likely to have a child with ASD than women without pre-existing diabetes [29] However, a study used linked data from the national birth and inpatient registries and reported that women with preexisting diabetes were no more likely to have a child with ASD than other mothers. [30] In relation to ID, a group of US researchers investigated a possible association with diabetes by comparing more than 160 000 mother-child dyads. The researchers identified that mothers with pre-existing diabetes were more than 10% more likely to have a child with ID. [126] Diabetes during pregnancy was also associated with both ASD and ID. For instance, two studies found that mothers with diabetes during pregnancy were more likely to have a child with ASD [25] and ASD with ID [127] than mothers without the disor‐ der. The first of these was a Canadian population study which included nearly 800 cases of ASD and more than 66 000 births. Mothers who developed gestational diabetes were associated with a 76% increased risk of ASD compared to women who did not develop the condition. [25] The second was an Australian population study which found that mothers who had diabetes during pregnancy were nearly three times as likely to have a child with ASD with ID than mothers without diabetes. [127] More attenuated results were

In a Western Australian record linkage study heavy prenatal alcohol exposure was found to be an important cause, accounting for 2.5% of non-genetic intellectual disability. [85] Underascertainment, particularly of FASD, may result from non-disclosure of alcohol consumption during pregnancy due to the associated stigma. [113] In addition, perhaps due to inadequate training, [114] clinicians may lack awareness and confidence in making this diagnosis. [113] Also, clinicians may be concerned at the psychological effect on the mother of a FASD diagnosis and may not pursue this in situations where it is not conclusive or they feel it would not be beneficial to the mother or child.

Large cohort studies and linked data have provided researchers with the opportunity to study whole populations of mothers and their children with and without ASD and/or ID. Data can also be adjusted for a range of possible confounders such as SES and age. This enables the identification of new risk factors for ASD and/or ID and the elimination of others. For example, the association of smoking during pregnancy with ASD and/or ID in the offspring has weakened in the most recent studies using linked population data. Persisting associations are an increased risk of Asperger syndrome or PDD-NOS in mothers who smoked during pregnancy and an increased risk of ID in the male children of mothers who smoked heavily during pregnancy. Maternal alcohol consumption during pregnancy remains a risk factor for ID.

The remaining associations of maternal smoking with ASD and ID in the offspring could result from the effect of this exposure on overall fetal development and particularly growth restric‐ tion, [115, 116] preterm birth [115] and low birth-weight [117] Moreover, sub-optimal fetal growth has been associated with mild or moderate ID in Caucasian children. [118] The association of maternal alcohol consumption with ID might be due the multiple effects of alcohol on the fetus and placenta. [119] For example, alcohol can induce oxidative stress in placental villous tissue. Other demonstrated effects are an increase in neural tube defects and increased heart rate and cortisol levels in the exposed infant.

#### **5.5. Physical health**

The research literature has provided evidence that maternal physical health, both prior to and during pregnancy is related to the likelihood of a mother having a child with ASD and/or ID. Various pre-existing conditions in the mother and related or unrelated complications of her pregnancy increase the likelihood of a mother having a child with ASD and/or ID compared to mothers who do not have the condition.

Pre-pregnancy obesity is an example of a condition which increases the likelihood of a woman having a child with ASD and/or ID. Obese women were more likely to have a child with ASD, [24, 54, 120] or ID [24, 46] than women who were not obese. One of these studies was a Finnish study which used linked data from the birth cohorts of 1966 and 1985-6 and included around 250 mothers of children with ID in each of the cohorts. [46] In both cohorts, mothers with obesity prior to their pregnancies were more likely to have a child with ID than women without pre-pregnancy obesity. However, the association of ID with pre-pregnancy obesity was an increasing risk reflected in the greater odds in the latter cohort(2.4) compared with the original cohort(1.8). [46] Another of the research groups reported that women with an early age of menarche were more likely to have a child with ASD than other women. [120] Early menarche, along with pre-pregnancy obesity, could indicate the possibility of maternal hormonal involvement in the risk of ASD and ID. [120] Then again, the relationship with ID may be resulting from confounding by the association between socioeconomic disadvantage and obesity in highly developed countries. [121] In the light of the increasing prevalence of obesity in these countries, these associations with ASD and ID are an important future research direction. [122]

the presence of all of the characteristic physical features required for FAS. [110] Studies from Sweden and the US attributed between 2-10% of mild or moderate ID to FAS or FASD. [111, 112] While the US study considered that a further 3% of severe or profound ID was caused by

In a Western Australian record linkage study heavy prenatal alcohol exposure was found to be an important cause, accounting for 2.5% of non-genetic intellectual disability. [85] Underascertainment, particularly of FASD, may result from non-disclosure of alcohol consumption during pregnancy due to the associated stigma. [113] In addition, perhaps due to inadequate training, [114] clinicians may lack awareness and confidence in making this diagnosis. [113] Also, clinicians may be concerned at the psychological effect on the mother of a FASD diagnosis and may not pursue this in situations where it is not conclusive or they feel it would not be

Large cohort studies and linked data have provided researchers with the opportunity to study whole populations of mothers and their children with and without ASD and/or ID. Data can also be adjusted for a range of possible confounders such as SES and age. This enables the identification of new risk factors for ASD and/or ID and the elimination of others. For example, the association of smoking during pregnancy with ASD and/or ID in the offspring has weakened in the most recent studies using linked population data. Persisting associations are an increased risk of Asperger syndrome or PDD-NOS in mothers who smoked during pregnancy and an increased risk of ID in the male children of mothers who smoked heavily during pregnancy. Maternal alcohol consumption during pregnancy

The remaining associations of maternal smoking with ASD and ID in the offspring could result from the effect of this exposure on overall fetal development and particularly growth restric‐ tion, [115, 116] preterm birth [115] and low birth-weight [117] Moreover, sub-optimal fetal growth has been associated with mild or moderate ID in Caucasian children. [118] The association of maternal alcohol consumption with ID might be due the multiple effects of alcohol on the fetus and placenta. [119] For example, alcohol can induce oxidative stress in placental villous tissue. Other demonstrated effects are an increase in neural tube defects and

The research literature has provided evidence that maternal physical health, both prior to and during pregnancy is related to the likelihood of a mother having a child with ASD and/or ID. Various pre-existing conditions in the mother and related or unrelated complications of her pregnancy increase the likelihood of a mother having a child with ASD and/or ID compared

Pre-pregnancy obesity is an example of a condition which increases the likelihood of a woman having a child with ASD and/or ID. Obese women were more likely to have a child with ASD, [24, 54, 120] or ID [24, 46] than women who were not obese. One of these studies was a Finnish study which used linked data from the birth cohorts of 1966 and

increased heart rate and cortisol levels in the exposed infant.

to mothers who do not have the condition.

FAS or FASD. [112]

beneficial to the mother or child.

404 Recent Advances in Autism Spectrum Disorders - Volume I

remains a risk factor for ID.

**5.5. Physical health**

Women with an auto-immune disorder or anomalies of the immune system were more likely to have a child with ASD and/or ID than women who did not. [25, 26, 123] Furthermore, the majority of associations in this area were with ASD rather than ID. For example, in a casecontrol study using linked data with more than 1 200 cases, mothers with an auto-immune disorder were 60% more likely to have a child with ASD than mothers without an auto-immune disorder. [26] These findings were supported by a small case-control study of 61 mothers of children with ASD. [123] Other studies have found that women with a particular auto-immune disease were more likely to have a child with ASD than women who did not have the disease. For instance, a case-control study with 407 cases found that women with psoriasis were more likely to have a child with ASD than mothers without this disorder. [124] Another research group used linked population data with more than 3 000 mothers of a child with ASD and nearly 700 000 control mothers. They reported that women with rheumatoid arthritis or celiac disease were more likely to have a child with ASD than mothers who did not have one of these disorders. [125]

One study found that women with pre-existing diabetes were more likely to have a child with ASD than women without pre-existing diabetes [29] However, a study used linked data from the national birth and inpatient registries and reported that women with preexisting diabetes were no more likely to have a child with ASD than other mothers. [30] In relation to ID, a group of US researchers investigated a possible association with diabetes by comparing more than 160 000 mother-child dyads. The researchers identified that mothers with pre-existing diabetes were more than 10% more likely to have a child with ID. [126] Diabetes during pregnancy was also associated with both ASD and ID. For instance, two studies found that mothers with diabetes during pregnancy were more likely to have a child with ASD [25] and ASD with ID [127] than mothers without the disor‐ der. The first of these was a Canadian population study which included nearly 800 cases of ASD and more than 66 000 births. Mothers who developed gestational diabetes were associated with a 76% increased risk of ASD compared to women who did not develop the condition. [25] The second was an Australian population study which found that mothers who had diabetes during pregnancy were nearly three times as likely to have a child with ASD with ID than mothers without diabetes. [127] More attenuated results were

ascertained by Californian researchers who conducted a case-control study and com‐ pared the mothers of more than 500 children with ASD, 172 mothers of children with developmental disabilities other than ASD to typically developing children. [24] They found that mothers with gestational diabetes were more likely (but not significantly more likely) to have a child with ASD than mothers without the disorder. The lack of signifi‐ cance may be due to the reduced power of this smaller study. Two studies identified an association between gestational diabetes and ID or a condition similar to ID. [24, 127] One was a large retrospective cohort study using linked registry data. Here the researchers found that mothers with diabetes during pregnancy were nearly 70% more likely to have a child with mild or moderate ID [127] compared to mothers without this disorder. The other research group found that mothers with diabetes during pregnancy were nearly two and a half times more likely to have a child with a developmental disability other than ASD than mothers without diabetes during pregnancy. [24]

during pregnancy were 60% more likely to have a child with ASD than other mothers. In contrast, a large cohort study of more than 650 000 nurses found that mothers with hyperten‐ sion during pregnancy were no more likely to have a child with ASD than mothers without with hypertension during pregnancy. [25] Possibly, these nurses, with their increased medical knowledge, sought treatment before their blood pressure reached a level which would have

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

407

Hypertension and oedema are two common symptoms of pre-eclampsia or toxaemia [132] which is a condition occurring in about 8% of first pregnancies. [133] Women who experience this condition, along with those who suffer oedema, were more likely to have a child with ASD and/or ID. Three groups of researchers found that women with pre-eclampsia [25, 29, 134] and those suffering oedema [92] during their pregnancies were more likely to have a child with ASD than women without these conditions during their pregnancies. In contrast, a much smaller case-control study, found that woman with pre-eclampsia had reduced (though not significantly so) likelihood of a child with ASD. [60] Pre-eclampsia was also associated with ID. [135] This association was found by researchers in a population-based, retrospective cohort study in South Carolina. Here, women who suffered pre-eclampsia were nearly 60% more

Associations of maternal epilepsy have been demonstrated with both ASD and ID. Women who experienced epilepsy during pregnancy were more likely to have a child with ASD with ID [127] or mild or moderate ID. [127] These Australian researchers conducted a retrospective cohort study of nearly 3 000 mothers of children with ASD and/or ID of unknown cause and around 237 000 mothers of typically developing children using linked population data from medical registries. They established that mothers with epilepsy during pregnancy were more than four and a half times as likely to have a child with ASD with ID [127] and more than three and a half times as likely to have a child with mild or moderate ID compared to mothers without epilepsy during their pregnancies. [127] A case-control study in US had only 61 control mothers of a child with ASD. [123] Here, mothers who had experienced seizure prior to their pregnancies were nearly six times as likely to have a child with ASD. However, possibly due

In addition to epilepsy, mothers who experienced a range of other conditions during pregnancy were found to be more likely to have a child with ASD than other mothers. Overall, health issues during pregnancy were associated with a higher risk of ASD. Researchers reported that women who had allergies, [124] asthma, [124] bleeding, [30] or high body temperature [93] during their pregnancies were more likely to have a child with ASD than women who had not experienced these conditions during their pregnancies. Asthma during pregnancy was also associated with ID, with pregnant women with asthma being more likely to have a child with mild or moderate

Other conditions during pregnancy have been associated with ID. For instance, an Australian populationstudyfoundthatwomenwhohadrenalorurinaryconditionsduringpregnancywere more than twice as likely to have a child with mild or moderate ID as women without these conditions during pregnancy. [127] Furthermore, women who suffered anaemia during their pregnancies were more than five times as likely to have a child with severe or profound ID than

to the small size of the study, results did not reach significance.

ID than mothers without this condition during pregnancy. [127]

been damaging to the unborn child.

likely to have a child with ID.

Further, differences have been identified relating to the immunological status of mothers of children with ASD prior to their pregnancies. An independent case-control study identified fetal brain antibodies in mothers of children with ASD but not in controls mothers. [128] This study found that mothers of children with ASD were significantly more likely to have an auto-antibody reactivity pattern for human fetal brain proteins than mothers of typically developing children.

Cytokines are regulators of immune response and maternal immune dysfunction has been associated with the neurological development of the fetus. [129] A case-control study identified that mothers of children with ASD and/or ID were more likely to have aberrant cytokine profiles compared to the mothers of typically developing children. [130] In this study, the concentration of serum cytokines at mid-pregnancy in the mothers of children with ASD with ID, developmental disabilities other than ASD and typically developing children were compared. Mothers of a child with ASD with ID were more likely to have higher concentrations of three particular cytokines than mothers of a typically developing child. In addition, mothers of a child with a developmental disability other than ASD were more likely to have higher concentrations of a different set of three different cytokines (to the ASD group) than mothers of typically developing children. [130]

Auto-immune diseases and other immune dysfunction might impinge on the immature nervous system of the developing fetus. This could have a deleterious effect on future cognitive function [131] and increase the likelihood of ASD and ID. [130]

Hypertension or high blood pressure is either a temporary or sustained elevation of the blood pressure in the arteries. [132] Moreover, the elevation is at a level where cardiovascular or other damage may occur. Hypertension during pregnancy was associated with an increased risk of ASD in the child. Three studies provided evidence that women who experienced hypertension during pregnancy were more likely to have a child with ASD [24, 30, 54] than women who had not suffered hypertension. In one of the studies, Swedish researchers conducted a nested, matched case-control study with data from over 400 children with ASD and over 2 000 controls. [30] Records of children's hospitalisation over 10 years were linked to birth records. The researchers concluded that mothers who suffered a hypertensive disease during pregnancy were 60% more likely to have a child with ASD than other mothers. In contrast, a large cohort study of more than 650 000 nurses found that mothers with hyperten‐ sion during pregnancy were no more likely to have a child with ASD than mothers without with hypertension during pregnancy. [25] Possibly, these nurses, with their increased medical knowledge, sought treatment before their blood pressure reached a level which would have been damaging to the unborn child.

ascertained by Californian researchers who conducted a case-control study and com‐ pared the mothers of more than 500 children with ASD, 172 mothers of children with developmental disabilities other than ASD to typically developing children. [24] They found that mothers with gestational diabetes were more likely (but not significantly more likely) to have a child with ASD than mothers without the disorder. The lack of signifi‐ cance may be due to the reduced power of this smaller study. Two studies identified an association between gestational diabetes and ID or a condition similar to ID. [24, 127] One was a large retrospective cohort study using linked registry data. Here the researchers found that mothers with diabetes during pregnancy were nearly 70% more likely to have a child with mild or moderate ID [127] compared to mothers without this disorder. The other research group found that mothers with diabetes during pregnancy were nearly two and a half times more likely to have a child with a developmental disability other than

Further, differences have been identified relating to the immunological status of mothers of children with ASD prior to their pregnancies. An independent case-control study identified fetal brain antibodies in mothers of children with ASD but not in controls mothers. [128] This study found that mothers of children with ASD were significantly more likely to have an auto-antibody reactivity pattern for human fetal brain proteins than

Cytokines are regulators of immune response and maternal immune dysfunction has been associated with the neurological development of the fetus. [129] A case-control study identified that mothers of children with ASD and/or ID were more likely to have aberrant cytokine profiles compared to the mothers of typically developing children. [130] In this study, the concentration of serum cytokines at mid-pregnancy in the mothers of children with ASD with ID, developmental disabilities other than ASD and typically developing children were compared. Mothers of a child with ASD with ID were more likely to have higher concentrations of three particular cytokines than mothers of a typically developing child. In addition, mothers of a child with a developmental disability other than ASD were more likely to have higher concentrations of a different set of three different cytokines (to the ASD group) than mothers

Auto-immune diseases and other immune dysfunction might impinge on the immature nervous system of the developing fetus. This could have a deleterious effect on future cognitive

Hypertension or high blood pressure is either a temporary or sustained elevation of the blood pressure in the arteries. [132] Moreover, the elevation is at a level where cardiovascular or other damage may occur. Hypertension during pregnancy was associated with an increased risk of ASD in the child. Three studies provided evidence that women who experienced hypertension during pregnancy were more likely to have a child with ASD [24, 30, 54] than women who had not suffered hypertension. In one of the studies, Swedish researchers conducted a nested, matched case-control study with data from over 400 children with ASD and over 2 000 controls. [30] Records of children's hospitalisation over 10 years were linked to birth records. The researchers concluded that mothers who suffered a hypertensive disease

ASD than mothers without diabetes during pregnancy. [24]

function [131] and increase the likelihood of ASD and ID. [130]

mothers of typically developing children.

406 Recent Advances in Autism Spectrum Disorders - Volume I

of typically developing children. [130]

Hypertension and oedema are two common symptoms of pre-eclampsia or toxaemia [132] which is a condition occurring in about 8% of first pregnancies. [133] Women who experience this condition, along with those who suffer oedema, were more likely to have a child with ASD and/or ID. Three groups of researchers found that women with pre-eclampsia [25, 29, 134] and those suffering oedema [92] during their pregnancies were more likely to have a child with ASD than women without these conditions during their pregnancies. In contrast, a much smaller case-control study, found that woman with pre-eclampsia had reduced (though not significantly so) likelihood of a child with ASD. [60] Pre-eclampsia was also associated with ID. [135] This association was found by researchers in a population-based, retrospective cohort study in South Carolina. Here, women who suffered pre-eclampsia were nearly 60% more likely to have a child with ID.

Associations of maternal epilepsy have been demonstrated with both ASD and ID. Women who experienced epilepsy during pregnancy were more likely to have a child with ASD with ID [127] or mild or moderate ID. [127] These Australian researchers conducted a retrospective cohort study of nearly 3 000 mothers of children with ASD and/or ID of unknown cause and around 237 000 mothers of typically developing children using linked population data from medical registries. They established that mothers with epilepsy during pregnancy were more than four and a half times as likely to have a child with ASD with ID [127] and more than three and a half times as likely to have a child with mild or moderate ID compared to mothers without epilepsy during their pregnancies. [127] A case-control study in US had only 61 control mothers of a child with ASD. [123] Here, mothers who had experienced seizure prior to their pregnancies were nearly six times as likely to have a child with ASD. However, possibly due to the small size of the study, results did not reach significance.

In addition to epilepsy, mothers who experienced a range of other conditions during pregnancy were found to be more likely to have a child with ASD than other mothers. Overall, health issues during pregnancy were associated with a higher risk of ASD. Researchers reported that women who had allergies, [124] asthma, [124] bleeding, [30] or high body temperature [93] during their pregnancies were more likely to have a child with ASD than women who had not experienced these conditions during their pregnancies. Asthma during pregnancy was also associated with ID, with pregnant women with asthma being more likely to have a child with mild or moderate ID than mothers without this condition during pregnancy. [127]

Other conditions during pregnancy have been associated with ID. For instance, an Australian populationstudyfoundthatwomenwhohadrenalorurinaryconditionsduringpregnancywere more than twice as likely to have a child with mild or moderate ID as women without these conditions during pregnancy. [127] Furthermore, women who suffered anaemia during their pregnancies were more than five times as likely to have a child with severe or profound ID than women without anaemia during pregnancy. [127] Two research groups ascertained that infectionsduringpregnancywereassociatedwithASD.Theyfoundthatwomenwhosepregnan‐ cies were complicated by urinary tract infection, [93] or any bacterial or viral infection [93, 136] were more likely to have a child with ASD than mothers who did not experience an infection.

the relationships with ASD and ID are most often reversed. High SES was most often associated

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

409

Different associations of marital status were found with each of ASD and ID. With ASD, the only two studies found in the area had opposing results. With all but one study, single mothers were at increased risk of unspecified ID and mild or moderate ID, compared to women who

In the majority of the studies, increased maternal age, along with increased paternal and parental age, were associated with ASD and ASD without ID. With ID, two associations emerged. Younger mothers had an increased risk of bearing a child with mild or moderate ID.

Lower parity had a consistent positive association with ASD in most studies. With mild or moderate ID and unspecified ID, the relationship was reversed and the association was with

In Table 3, the associations with immigrant status and ethnicity are summarized. Most often, immigrant mothers are more likely to have a child with ASD or ASD with ID than nonimmigrant mothers. On the other hand, ASD without ID was associated with non-immigrants, excepting those immigrants from nearby countries. The Mexican/Hispanic immigrant mothers in the US were a separate group since these mothers were less likely to have a child with ASD

With ethnicity, the associations differed from those with immigrant status, in spite of the overlap between the groups. Except for Asian and black mothers, mothers from ethnic minority groups were at a lower risk of children with ASD compared to Caucasian mothers. With the exception of Asianmothers,therelationshipwithIDwasreversedsincemothersfromethnicminoritygroups,

Table 4 shows the many associations of health and behavioural traits with ASD and highlights the quite small proportion common to both ASD and ID. With mental health, ten research groups reported associations with ASD. Contrastingly, only one study found an association with the mothers of children with ID. Autistic-like traits were associated only with the parents

As with other socio-demographic factors, ASD and ID had an overall reverse association with height. Taller and heavier women were more likely to have offspring with ASD and shorter women to have offspring with ID. The associations with maternal smoking during pregnancy were minimal. Excessive alcohol consumption during pregnancy was only associated with

Both ASD and ID had associations with immune function, though the association with ASD was broader. Both pre-existing diabetes and diabetes during pregnancy were associated with ASD and/or ID. Further, abnormal levels of cytokines during pregnancy were also associated with each of ASD and ID. Other associations were with only ASD and were auto-immune disorder generally, psoriasis, rheumatoid arthritis, celiac disease and maternal fetal brain

with the ASD groups of mothers and low SES, most often associated with ID.

But severe or profound ID was associated with increased maternal age.

than Mexican/Hispanic non-immigrant mothers.

greater parity. However, with severe or profound ID, there was no association.

and particularly Aboriginal mothers, were at an increased risk of a child with ID.

offspring with ID. Obesity though was associated with both ASD and ID.

were living with a partner.

of children with ASD.

antibodies.

Infections during pregnancy were also associated with ID. For example, one study reported that mothers who suffered trichomoniasis during pregnancy were more likely to have a child with ID than mothers without this condition during pregnancy. [137] A cohort study used Medicaid claims and linked infant records to investigate the association of treated and untreated urinary tract infections during pregnancy with later ID in the child. [138] The researchers reported that pregnant women with untreated urinary tract infections were 30% more likely to have a child with ID than pregnant women without these infections. Moreover, mothers with untreated urinary tract infections were 22% more likely to have a child with ID than mothers with antibiotic treated urinary tract infections. [138]

There is always a risk that the use of certain medications during pregnancy may have adverse effects on a developing fetus. This use is likely to be related to a woman's health and the decision to use a particular medication at this time must be difficult. Sometimes, medications initially considered safe have been later implicated to adversely affect the future health of the unborn child. For instance, six studies found that the children of mothers who used antidepressants, [64, 139] anti-convulsants, [140] psycho-active drugs, [64] prescribed medications [54, 93] and medications generally [141] had a higher risk of a child with ASD. One of these was a population-based case-control study in Stockholm. [64] Using registry data, the re‐ searchers assessed that mothers who took psycho-active drugs or anti-depressants during their pregnancies were more than four times as likely to have a child with ASD.

It is also possible that the increased use of prescribed medications in mothers of children with ASD may have resulted from a bias in data collection. In one of the studies which found an increased use of prescribed medications, case mothers were recruited via their response to an advertisement in a support agency newsletter or via their membership of a support agency. [93] Each of these methods might have resulted in a bias in the direction of a high SES. This, in turn, may have produced an increased use of prescribed medications in the case mothers. On the other hand, the study which found an increased use of medications generally was a population study using medical registries. [141] The reported associations are likely to be mediated by a complex interaction of factors. For instance, in addition to possible SES bias, there could be a genetic association such as the familial link of depressive disorders or epilepsy with ASD. Another possibility is an environmental effect which results from the physiological impact of maternal medication use on the uterine environment.

#### **5.6. Summary**

Before the birth of their affected children, certain socio-demographic, health and physical attributes differentiate mothers of children with ASD and/or ID from those of mothers in the general population. Further, these attributes often vary by the disability group of their child. In Tables 2 to 4, these differences are grouped into categories according to their associations with groups of mothers. An examination of Table 2 shows that with socio-demographic factors, the relationships with ASD and ID are most often reversed. High SES was most often associated with the ASD groups of mothers and low SES, most often associated with ID.

women without anaemia during pregnancy. [127] Two research groups ascertained that infectionsduringpregnancywereassociatedwithASD.Theyfoundthatwomenwhosepregnan‐ cies were complicated by urinary tract infection, [93] or any bacterial or viral infection [93, 136] were more likely to have a child with ASD than mothers who did not experience an infection. Infections during pregnancy were also associated with ID. For example, one study reported that mothers who suffered trichomoniasis during pregnancy were more likely to have a child with ID than mothers without this condition during pregnancy. [137] A cohort study used Medicaid claims and linked infant records to investigate the association of treated and untreated urinary tract infections during pregnancy with later ID in the child. [138] The researchers reported that pregnant women with untreated urinary tract infections were 30% more likely to have a child with ID than pregnant women without these infections. Moreover, mothers with untreated urinary tract infections were 22% more likely to have a child with ID

There is always a risk that the use of certain medications during pregnancy may have adverse effects on a developing fetus. This use is likely to be related to a woman's health and the decision to use a particular medication at this time must be difficult. Sometimes, medications initially considered safe have been later implicated to adversely affect the future health of the unborn child. For instance, six studies found that the children of mothers who used antidepressants, [64, 139] anti-convulsants, [140] psycho-active drugs, [64] prescribed medications [54, 93] and medications generally [141] had a higher risk of a child with ASD. One of these was a population-based case-control study in Stockholm. [64] Using registry data, the re‐ searchers assessed that mothers who took psycho-active drugs or anti-depressants during their

It is also possible that the increased use of prescribed medications in mothers of children with ASD may have resulted from a bias in data collection. In one of the studies which found an increased use of prescribed medications, case mothers were recruited via their response to an advertisement in a support agency newsletter or via their membership of a support agency. [93] Each of these methods might have resulted in a bias in the direction of a high SES. This, in turn, may have produced an increased use of prescribed medications in the case mothers. On the other hand, the study which found an increased use of medications generally was a population study using medical registries. [141] The reported associations are likely to be mediated by a complex interaction of factors. For instance, in addition to possible SES bias, there could be a genetic association such as the familial link of depressive disorders or epilepsy with ASD. Another possibility is an environmental effect which results from the physiological

Before the birth of their affected children, certain socio-demographic, health and physical attributes differentiate mothers of children with ASD and/or ID from those of mothers in the general population. Further, these attributes often vary by the disability group of their child. In Tables 2 to 4, these differences are grouped into categories according to their associations with groups of mothers. An examination of Table 2 shows that with socio-demographic factors,

than mothers with antibiotic treated urinary tract infections. [138]

408 Recent Advances in Autism Spectrum Disorders - Volume I

pregnancies were more than four times as likely to have a child with ASD.

impact of maternal medication use on the uterine environment.

**5.6. Summary**

Different associations of marital status were found with each of ASD and ID. With ASD, the only two studies found in the area had opposing results. With all but one study, single mothers were at increased risk of unspecified ID and mild or moderate ID, compared to women who were living with a partner.

In the majority of the studies, increased maternal age, along with increased paternal and parental age, were associated with ASD and ASD without ID. With ID, two associations emerged. Younger mothers had an increased risk of bearing a child with mild or moderate ID. But severe or profound ID was associated with increased maternal age.

Lower parity had a consistent positive association with ASD in most studies. With mild or moderate ID and unspecified ID, the relationship was reversed and the association was with greater parity. However, with severe or profound ID, there was no association.

In Table 3, the associations with immigrant status and ethnicity are summarized. Most often, immigrant mothers are more likely to have a child with ASD or ASD with ID than nonimmigrant mothers. On the other hand, ASD without ID was associated with non-immigrants, excepting those immigrants from nearby countries. The Mexican/Hispanic immigrant mothers in the US were a separate group since these mothers were less likely to have a child with ASD than Mexican/Hispanic non-immigrant mothers.

With ethnicity, the associations differed from those with immigrant status, in spite of the overlap between the groups. Except for Asian and black mothers, mothers from ethnic minority groups were at a lower risk of children with ASD compared to Caucasian mothers. With the exception of Asianmothers,therelationshipwithIDwasreversedsincemothersfromethnicminoritygroups, and particularly Aboriginal mothers, were at an increased risk of a child with ID.

Table 4 shows the many associations of health and behavioural traits with ASD and highlights the quite small proportion common to both ASD and ID. With mental health, ten research groups reported associations with ASD. Contrastingly, only one study found an association with the mothers of children with ID. Autistic-like traits were associated only with the parents of children with ASD.

As with other socio-demographic factors, ASD and ID had an overall reverse association with height. Taller and heavier women were more likely to have offspring with ASD and shorter women to have offspring with ID. The associations with maternal smoking during pregnancy were minimal. Excessive alcohol consumption during pregnancy was only associated with offspring with ID. Obesity though was associated with both ASD and ID.

Both ASD and ID had associations with immune function, though the association with ASD was broader. Both pre-existing diabetes and diabetes during pregnancy were associated with ASD and/or ID. Further, abnormal levels of cytokines during pregnancy were also associated with each of ASD and ID. Other associations were with only ASD and were auto-immune disorder generally, psoriasis, rheumatoid arthritis, celiac disease and maternal fetal brain antibodies.

Seven studies associated hypertension, oedema and pre-eclampsia with ASD whereas only one study associated pre-eclampsia with ID. Epilepsy and asthma had associations with both of ASD and ID but no other associations during pregnancy were common to both disorders. Medication use during pregnancy was only found to be associated with ASD.

**ASD ID**

+veassoc [17,22] -

+veassoc in

[22]

Somalis[77] & Africans

No assoc in Hispanics

[52]

ASD, autism spectrum disorder; ID, intellectual disability; Mild ID, Mild or moderate ID; Severe ID, Severe or profound ID; +ve, positive; -ve, negative;assoc, association; SE, south eastern; NE, north eastern; Aus, Australia; NHW, non-Hispanic

veassoc[17,20,2

http://dx.doi.org/10.5772/54488

411


+veassoc in Aboriginals [17,20]


+veassoc in Aboriginals [17,20]

1]

**Category ASD without ID Undifferentiated ASD ASD with ID Mild ID Severe ID**

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

+veassoc[17,22,30,57,62,7

Hispanic vs non-immigrant

[17,57]+veassoc in East



+veassoc in Asians [52] +veassoc in Blacks [52]

**Table 3.** Associations of immigrant status and ethnicity in the mothers of children with ASD and/or ID

[17,29]

Hispanics [78]

Asians[76]

5-77]

**Immigrant status** (Immigrant vs non-immigrant)

North Europe &

**Ethnicity**(Non-Caucasian vs Caucasians)

white.


US -veassoc immigrant

Asian +veassoc in SE & NE Asians

UK


ASD, autism spectrum disorder; ID, intellectual disability; Mild ID, Mild or moderate ID; Severe ID, Severe or profound ID; SES, socio-economic status; +ve, positive; -ve, negative; assoc, association.

**Table 2.** Associations of socio-demographic factors in the mothers of children with ASD and/or ID

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review http://dx.doi.org/10.5772/54488 411

Seven studies associated hypertension, oedema and pre-eclampsia with ASD whereas only

one study associated pre-eclampsia with ID. Epilepsy and asthma had associations with both

of ASD and ID but no other associations during pregnancy were common to both disorders.

**ID**

[17]

+veassoc [47] +veassoc [21,41,50] -veassoc [20,21] -veassoc

[17]

**ASD ID**




[21,52] -veassoc [25]

**Mild ID Unspecified ID Severe ID**

[20,21,32,44,45,51,


[21,68]



No assoc [46] +veassoc



53]

[55]


Medication use during pregnancy was only found to be associated with ASD.

**Undifferentiated ASD ASD with**

+veassoc [17,39-41,47] +veassoc

+veassoc [17] +veassoc

No assoc[42] -veassoc[43]


+veassoc

[17,21,29,47,56-61]

No assoc [42,43,66]

No assoc [42]

+veassoc [58]

SES, socio-economic status; +ve, positive; -ve, negative; assoc, association.

+veassoc [29,41,73] +veassoc

**Table 2.** Associations of socio-demographic factors in the mothers of children with ASD and/or ID

[17]

ASD, autism spectrum disorder; ID, intellectual disability; Mild ID, Mild or moderate ID; Severe ID, Severe or profound ID;

+veassoc [17,56,58,61]

**Category ASD without ID**

[17,47]

410 Recent Advances in Autism Spectrum Disorders - Volume I

**SES** +veassoc

In Denmark & Sweden

Education as a measure of SES

**Marital status at child's birth** (Women with partners)

Paternal & maternal

Maternal & paternal (Denmark, Sweden & UK)

**Age & lower parity**

**Age** Maternal +veassoc

**Lower parity** +veassoc

[17,47]

[17,74]

Only paternal +veassoc [65] +veassoc [58,62-65]


ASD, autism spectrum disorder; ID, intellectual disability; Mild ID, Mild or moderate ID; Severe ID, Severe or profound ID; +ve, positive; -ve, negative;assoc, association; SE, south eastern; NE, north eastern; Aus, Australia; NHW, non-Hispanic white.

**Table 3.** Associations of immigrant status and ethnicity in the mothers of children with ASD and/or ID


**ASD ID**

Hypertension[24,30,54] Oedema[92]

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

Allergies,[124] bleeding,[30] & high temperature[93] UTI[93] & any

medications[141] Anticonvulsants[140] &

ASD, autism spectrum disorder; ID, intellectual disability; Mild ID, mild or moderate ID; Severe ID, severe or profound ID;

This chapter provides a review of the research pertaining to the pre-existing characteristics of mothers of a child with ASD and/or ID. Some consistent and enduring associations have emerged across the published reports. With socio-demographic factors, these are the con‐ trasting associations of maternal education, age, immigrant status and ethnicity with ASD and ID. With maternal health; aspects of mental health, personality traits, immune function and the use of medication during pregnancy have stronger associations with the mothers of children with ASD than ID. Some of these differences may be reflections of distinct aetiolo‐ gies for ASD and/or ID of unknown cause and provide directions for future research. As such, primary and secondary prevention strategies may be refined and/or developed which will contribute to lower prevalence, reduced levels of severity and better outcomes for af‐

infection[93,136]

Anti-depressants,[64,139] prescribed[54,93] & other

psycho-active drugs[64]

**Table 5.** Associations of health during pregnancy in the mothers of children with ASD and/or ID

**Undifferentiated ASD Unspecified ID[Mild ID], [Severe**

Pre-eclampsia[25,29,134] Pre-eclampsia[135]

Asthma [124] Asthma (Mild ID) [127]

**ID]**

Epilepsy(Mild ID)[127]

Renal/urinary conditions,[127] [Mild ID][126] Anaemia [Severe ID] [127]Trichomoniasis[137] & untreated UTI[138]

http://dx.doi.org/10.5772/54488

413

**Category** ASD without ID[ASD with ID]

[127]

UTI, urinary tract infection.

**6. Conclusion**

fected children.

Epilepsy[ASD with ID)

**Other areas during pregnancy**

ASD, autism spectrum disorder; ID, intellectual disability; Mild ID, mild or moderate ID; Severe ID, severe or profound ID; UTI, urinary tract infection,

**Table 4.** Associations of mental health, personality traits, physical characteristics, health behaviours and physical health in the mothers of children with ASD and/or ID

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review http://dx.doi.org/10.5772/54488 413


ASD, autism spectrum disorder; ID, intellectual disability; Mild ID, mild or moderate ID; Severe ID, severe or profound ID; UTI, urinary tract infection.

**Table 5.** Associations of health during pregnancy in the mothers of children with ASD and/or ID

#### **6. Conclusion**

**ASD ID**

**Undifferentiated ASD Unspecified ID[Mild ID], [Severe ID]**

Depression [27,64,89] Unipolar major depression [95] or

Bipolar disorder [95]

ID in mother [95]

Shorter, medium height [20]Shortest[Severe ID] [20] & shorter[Mild ID] [17]

Alcohol[Severe ID] [112]

ASD)[24]

[130]

Higher conc of 3 cytokines[130] Higher conc of 3 other cytokines(DD)

Diabetes[126] & diabetes during pregnancy(Mild ID)[127] & (DD no

In male children with ≥ 20 cigs/day in mother[107]Smoking (no assoc)[46] Alcohol[85]Alcohol[Mild ID] [111, 112]

**Category ASD without ID,**

**Personality traits**

**Physical characteristics**

**Health behaviours** During pregnancy

**Immune function** **[Asperger syndrome] [ASD with ID]**

412 Recent Advances in Autism Spectrum Disorders - Volume I

Bipolar disorder [ASD with ID] [95]

Taller[ASD without ID] [17 [17]Taller[ASD with ID] [17]

Smoking[Asperger syndrome] [76]

Diabetes during pregnancy [ASD with

health in the mothers of children with ASD and/or ID

ID] [127]

UTI, urinary tract infection,

**Physical health** Obesity[ASD with ID] [24]

**Mental health** Schizophrenia [42,89,91] Schizophrenia [95] or

pregnancy [92,93]

Autistic-like traits [97,100,102,103]

Smoking [30]Smoking(-veassoc) [76] Smoking(no assoc) [29,105,106]

smoking mothers only) [29]

Early menarche[120]

pregnancy[25]

[128]

Diabetes[24,29] & diabetes during

Any auto-immune disorder, [256,26,123] psoriasis,[124] & rheumatoid arthritis[125] celiac disease, [125] &fetal brain antibodies

ASD, autism spectrum disorder; ID, intellectual disability; Mild ID, mild or moderate ID; Severe ID, severe or profound ID;

**Table 4.** Associations of mental health, personality traits, physical characteristics, health behaviours and physical

Taller and heavier [93] Taller and heavier (non-

Obesity [24,54,120] Obesity [24,46]

Psychiatric, [62,64,89] personality disorders, [62,89,90] affective [42] & obsessive compulsive disorders,[27] anxiety, [27,94] & paranoia [27]Somatization, [27] psychosis,[42] depression,[ 27, 64, 89] & depression during

> This chapter provides a review of the research pertaining to the pre-existing characteristics of mothers of a child with ASD and/or ID. Some consistent and enduring associations have emerged across the published reports. With socio-demographic factors, these are the con‐ trasting associations of maternal education, age, immigrant status and ethnicity with ASD and ID. With maternal health; aspects of mental health, personality traits, immune function and the use of medication during pregnancy have stronger associations with the mothers of children with ASD than ID. Some of these differences may be reflections of distinct aetiolo‐ gies for ASD and/or ID of unknown cause and provide directions for future research. As such, primary and secondary prevention strategies may be refined and/or developed which will contribute to lower prevalence, reduced levels of severity and better outcomes for af‐ fected children.

#### **Author details**

Jenny Fairthorne\* , Amanda Langridge, Jenny Bourke and Helen Leonard\*

\*Address all correspondence to: jfairthorne@ichr.uwa.edu.au

Centre for Child Health, University of Western Australia, Australia

#### **References**

[1] Filipek, P., et al., The screening and diagnosis of autistic spectrum disorders. Journal of Autism and Developmental Disorders, 1999. 29(6): p. 439-84.

[13] Maher, P., Methylglyoxal, advanced glycation end products and autism: Is there a

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

415

[14] Young, D., et al., The diagnosis of autism in a female: Could it be Rett syndrome? Eu‐

[15] Oberlé, I., et al., Instability of a 550-base pair DNA segment and abnormal methyla‐

[16] Fombonne, E., Epidemiology of pervasive developmental disorders. Pediatric Re‐

[17] Leonard, H., et al., Autism and intellectual disability are differentially related to soci‐

[18] Matson, J. and M. Shoemaker, Intellectual disability and its relationship to autism spectrum disorders. Research in Developmental Disabilities, 2009. 30(6): p. 1107-14.

[19] Leonard, H. and X. Wen, The epidemiology of mental retardation: challenges and op‐ portunities in the new millennium. Mental Retardation and Developmental Disabili‐

[20] Leonard, H., et al., Association of sociodemographic characteristics of children with intellectual disability in Western Australia. Social Science and Medicine, 2005. 60(7):

[21] Croen, L., J. Grether, and S. Selvin, The epidemiology of mental retardation of un‐

[22] Magnusson, C., et al., Migration and autism spectrum disorder: population-based

[23] Pinborough-Zimmerman, J., et al., Sociodemographic risk factors associated with au‐ tism spectrum disorders and intellectual disability. Autism Research, 2011. 4(5). [24] Krakowiak, P., et al., Maternal metabolic conditions and risk for autism and other

[25] Lyall, K., et al., Pregnancy complications and obstetric suboptimality in association with autism spectrum disorders in children of the Nurses' Health Study II. Autism

[26] Keil, A., et al., Parental autoimmune diseases associated with autism spectrum disor‐

[27] Hodge, D., C. Hoffman, and D. Sweeney, Increased psychopathology in parents of children with autism: genetic liability or burden of caregiving? Journal of Develop‐

tion in Fragile X syndrome. Science, 1991. 252(5009): p. 1097-102.

odemographic background at birth. PLoS ONE, 2011. 6(3): p. e17875.

connection? Medical Hypotheses, 2012.

search, 2009. 65(6): p. 591-8.

p. 1499-513.

ropean Journal of Pediatrics, 2008. 167(6): p. 661-9.

ties Research Reviews, 2002. 8(3): p. 117-34.

known cause. Pediatrics, 2001. 107(6): p. e86.

neurodevelopmental disorders. Pediatrics, 2012. 129(5).

ders in offspring. Epidemiology, 2010. 21(6): p. 805-8.

mental and Physical Disabilities, 2011. 23(3): p. 227-39.

study. British Journal of Psychiatry, 2012.

Research, 2012. 5(1): p. 21-30.


[13] Maher, P., Methylglyoxal, advanced glycation end products and autism: Is there a connection? Medical Hypotheses, 2012.

**Author details**

414 Recent Advances in Autism Spectrum Disorders - Volume I

Jenny Fairthorne\*

**References**

, Amanda Langridge, Jenny Bourke and Helen Leonard\*

[1] Filipek, P., et al., The screening and diagnosis of autistic spectrum disorders. Journal

[2] American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disor‐ ders, Fourth Edition, 2000, American Psychiatric Association: Washington, DC.

[3] Rutter, M., Aetiology of autism: findings and questions. Journal of Intellectual Disa‐

[4] Robinson, P., et al., Genetically determined low maternal serum dopamine hydroxy‐ lase levels and the etiology of autism spectrum disorders. American Journal of Medi‐

[5] Trajkovski, V., Etiology of autism. Journal of Special Education, 2004. 5(1-2): p. 61-74.

[6] Bass, M., et al., Genetic studies in autistic disorder and chromosome 15. Neurogenet‐

[7] Brune, C., et al., 5-HTTLPR genotype-specific phenotype in children and adolescents

[8] Newschaffer, C., et al., The epidemiology of autism spectrum disorders. Annual Re‐

[9] Mefford, H., M. Batshaw, and E. Hoffman, Genomics, intellectual disability, and au‐

[10] Stoltenberg, C., et al., The autism birth cohort (ABC): a paradigm for gene-environ‐

[11] Kubota, T., et al., Novel etiological and therapeutic strategies for neurodiseases: epi‐ genetic understanding of gene-environment interactions. Journal of Pharmacological

[12] Dodge, K. and M. Rutter, Gene-environment interactions: state of the science, in Gene-environment interactions in developmental psychopathology, K. Dodge and

with autism. American Journal of Psychiatry, 2006. 163(12): p. 2148-56.

tism. New England Journal of Medicine, 2012. 366(8): p. 733-43.

ment-timing research. Molecular Psychiatry, 2011. 15(7): p. 676-80.

\*Address all correspondence to: jfairthorne@ichr.uwa.edu.au

bility Research, 2005. 49(4): p. 231-38.

cal Genetics, 2001. 100(1): p. 30-6.

view of Public Health, 2007. 28(21): p. 235-58.

M. Rutter, Editors. 2011, Guilford Press: New York.

ics, 2000. 2(4): p. 219-26.

Sciences, 2010. 113: p. 3-8.

Centre for Child Health, University of Western Australia, Australia

of Autism and Developmental Disorders, 1999. 29(6): p. 439-84.


[28] Morgan, V., et al., What impact do obstetric complications have on the risk of ad‐ verse psychiatric outcomes for the high risk children of mothers with schizophrenia and other psychoses? Schizophrenia Research, 2008. 102(Supplement 2): p. 167-8.

[42] Larsson, H., et al., Risk factors for autism: perinatal factors, parental psychiatric his‐ tory, and socioeconomic status. American Journal of Epidemiology, 2005. 161(10): p.

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

417

[43] Rai, D., et al., Parental socioeconomic status and risk of offspring autism spectrum disorders in a Swedish population-based study. Journal of the American Academy of

[44] Gissler, M., et al., Social class differences in health until the age of seven years among the Finnish 1987 birth cohort. Social Science and Medicine, 1998. 46(12): p. 1543-52.

[45] Zheng, X., et al., Socioeconomic status and children with intellectual disability in

[46] Heikura, U., et al., Variations in prenatal sociodemographic factors associated with intellectual disability: a study of the 20-year interval between two birth cohorts in

[47] Bhasin, T. and D. Schendel, Sociodemographic risk factors for autism in a US metro‐ politan area. Journal of Autism and Developmental Disorders, 2007. 37(4): p. 667-77.

[48] Emerson, E., Deprivation, ethnicity and the prevalence of intellectual and develop‐ mental disabilities. Journal of Epidemiology and Community Health, 2012. 66(3): p.

[49] Harris, J., Autism risk factors: moving from epidemiology to translational epidemiol‐ ogy. Journal of the American Academy of Child and Adolescent Psychiatry, 2012.

[50] Van Meter, K., et al., Geographic distribution of autism in California: a retrospective

[51] Yaqoob, M., et al., Mild intellectual disability in children in Lahore, Pakistan: aetiolo‐ gy and risk factors. Journal of Intellectual Disability Research, 2004. 48(7): p. 663-71.

[52] Jelliffe-Pawlowski, L., et al., Risks for severe mental retardation occurring in isolation and with other developmental disabilities. American Journal of Medical Genetics,

[53] Singhi, P., et al., Psychosocial problems in families of disabled children. British Jour‐

[54] Dodds, L., et al., The role of prenatal, obstetric and neonatal factors in the develop‐ ment of autism. Journal of Autism and Developmental Disorders, 2011. 41(7): p.

[55] Hatton, E., et al., Changes in family composition and marital status in families with a young child with cognitive delay. Journal of Applied Research in Intellectual Disabil‐

birth cohort analysis. Autism Research, 2010. 3(1): p. 19-29.

nal of Medical Psychology, 1990. 63(2): p. 173-82.

Northern Finland. American Journal of Epidemiology, 2008. 167(2): p. 169-77.

China. Journal of Intellectual Disability Research, 2012. 56(2): p. 212-20.

916-25.

218-24.

51(5).

2005. 136(2): p. 152-7.

ities, 2010. 23(1): p. 14-26.

891-902.

Child and Adolescent Psychiatry, 2012.


[42] Larsson, H., et al., Risk factors for autism: perinatal factors, parental psychiatric his‐ tory, and socioeconomic status. American Journal of Epidemiology, 2005. 161(10): p. 916-25.

[28] Morgan, V., et al., What impact do obstetric complications have on the risk of ad‐ verse psychiatric outcomes for the high risk children of mothers with schizophrenia and other psychoses? Schizophrenia Research, 2008. 102(Supplement 2): p. 167-8.

[29] Burstyn, I., F. Sithole, and L. Zwaigenbaum, Autism spectrum disorders, maternal characteristics and obstetric complications among singletons born in Alberta, Cana‐

[30] Hultman, C., P. Sparen, and S. Cnattingius, Perinatal risk factors for infantile autism.

[31] Losh, M., et al., Neuropsychological profile of autism and the broad autism pheno‐

[32] Losh, M., et al., Defining key features of the broad autism phenotype: a comparison across parents of multiple and single incidence autism families. American Journal of

[33] Piven, J., The broad autism phenotype: a complementary strategy for molecular ge‐ netic studies of autism. American Journal of Medical Genetics, 2001. 105(1): p. 34-5.

[34] Harvey, J., M. O'Callaghan, and B. Vines, Prevalence of maternal depression and its relationship to ADL skills in children with developmental delay. Journal of Paediat‐

[35] Hertz-Picciotto, I., et al., The CHARGE Study: an epidemiologic investigation of ge‐ netic and environmental factors contributing to autism. Environmental Health Per‐

[36] Spitzer, R. and B. Siegel, The DSM-III-R field trial of pervasive developmental disor‐ ders. Journal of the American Academy of Child and Adolescent Psychiatry, 1990.

[37] Western Australian Autism Diagnosticians' Forum. Diagnosis in Western Australia 2012; Available from: http://waadf.org.au/Waitlist\_times\_1\_December\_2011.pdf.

[38] Shattuck, P. and S. Grosse, Issues related to the diagnosis and treatment of autism spectrum disorders. Mental Retardation and Developmental Disabilities Research

[39] Durkin, M., et al., Socioeconomic inequality in the prevalence of autism spectrum disorder: evidence from a US cross-sectional study. PLoS ONE, 2010. 5(7): p. e11551.

[40] Liptak, G., et al., Disparities in diagnosis and access to health services for children with autism: data from the National Survey of Children's Health. Journal of Develop‐

[41] King, M. and P. Bearman, Socioeconomic status and the increased prevalence of au‐

tism in California. American Sociological Review, 2011. 76(2): p. 320-46.

mental and Behavioral Pediatrics, 2008. 29(3): p. 152-60.

da. Chronic Diseases in Canada, 2010. 30(4): p. 125-34.

type. Archives of General Psychiatry, 2009. 66(5): p. 518-26.

Epidemiology, 2002. 13(4): p. 417-23.

416 Recent Advances in Autism Spectrum Disorders - Volume I

Medical Genetics, 2008. 147(4): p. 424-33.

rics and Child Health, 1997. 33(1): p. 42-6.

spectives, 2006. 114(7): p. 1119-25.

Reviews, 2007. 13(2): p. 129-35.

29(6): p. 855-62.


[56] King, M., et al., Estimated autism risk and older reproductive age. American Journal of Public Health, 2009. 99(9): p. 1673-9.

[71] Hultman, C., et al., Advancing paternal age and risk of autism: new evidence from a population-based study and a meta-analysis of epidemiological studies. Molecular

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

419

[73] Glasson, E., et al., Perinatal factors and the development of autism: a population

[74] Schmidt, K., et al., Brief report: Asperger's syndrome and sibling birth order. Journal

[75] Keen, D., F. Reid, and D. Arnone, Autism, ethnicity and maternal immigration. Brit‐

[76] Haglund, N. and K. Källén, Risk factors for autism and Asperger syndrome. Autism,

[77] Barnevik–Olsson, M., C. Gillberg, and E. Fernell, Prevalence of autism in children born to Somali parents living in Sweden: a brief report. Developmental Medicine and

[78] Schieve, L., et al., Association between parental nativity and autism spectrum disor‐ der among US-born non-Hispanic white and Hispanic children, 2007 National Sur‐

[79] Fernell, E., et al., Serum levels of 25-hydroxyvitamin D in mothers of Swedish and of Somali origin who have children with and without autism. Acta Pædiatrica, 2010.

[81] Zhou, M. and Y. Sao Xiong, The multifaceted American experiences of the children of Asian immigrants: lessons for segmented assimilation. Ethnic and Racial Studies,

[82] Grulich, A., M. McCredie, and M. Coates, Cancer incidence in Asian migrants to New South Wales, Australia. British Journal of Cancer, 1995. 71(2): p. 400-8.

[83] Ip, D., C.-T. Wu, and C. Inglis, Settlement experiences of Taiwanese immigrants in

[84] Pedersen, A., et al., Prevalence of autism spectrum disorders in Hispanic and non-

[85] O'Leary, C., et al., Intellectual disability: population-based estimates of the propor‐ tion attributable to heavy prenatal alcohol exposure. Developmental Medicine and

[86] O'Leary, C., Fetal alcohol syndrome: diagnosis, epidemiology and developmental

outcomes. Journal of Paediatrics and Child Health, 2004. 40(1-2): p. 2-7.

vey of Children's Health. Disability and Health Journal, 2012. 5(1): p. 18-25.

[80] Cannell, J., Autism and vitamin D. Medical Hypotheses, 2008. 70: p. 750-9.

Australia. Asian Studies Review, 1998. 22(1): p. 79-97.

Hispanic white children. Pediatrics, 2012.

Psychiatry, 2011. 16(12): p. 1203-12.

[72] Mosby's Medical Dictionary 2009: Elsevier. 8th edition.

of Autism and Developmental Disorders, 2012.

ish Journal of Psychiatry, 2010. 196: p. 274-81.

Child Neurology, 2008. 50(8): p. 598-601.

2011. 15(2): p. 163-83.

99(5): p. 743-7.

2005. 28(6): p. 1119-52.

Child Neurology, 2012.

study. Archives of General Psychiatry, 2004. 61(6): p. 618-27.


[56] King, M., et al., Estimated autism risk and older reproductive age. American Journal

[57] Williams, K., et al., Perinatal and maternal risk factors for autism spectrum disorders in New South Wales, Australia. Child-care, Health and Development, 2008. 34(2): p.

[58] Durkin, M., et al., Advanced parental age and the risk of autism spectrum disorder.

[59] Windham, G., et al., Birth prevalence of autism spectrum disorders in the San Fran‐ cisco Bay area by demographic and ascertainment source characteristics. Journal of

[60] Stein, D., et al., Obstetric complications in individuals diagnosed with autism and in

[61] El-Baz , F., et al., Risk factors for autism: an Egyptian study. Egyptian Journal of

[62] Lauritsen, M., C. Pedersen, and P. Mortensen, Effects of familial risk factors and place of birth on the risk of autism: a nationwide register-based study. Journal of

[63] Reichenberg, A., R. Gross, and M. Weiser, Advancing paternal age and autism. Ar‐

[64] Eriksson, M., et al., First-degree relatives of young children with autism spectrum disorders: some gender aspects. Research in Developmental Disabilities, 2012. 33(5):

[65] Tsuchiya, K., et al., Paternal age at birth and high-functioning autistic-spectrum dis‐

[66] Robinson, E., et al., Brief report: no association between parental age and extreme so‐ cial-communicative autistic traits in the general population. Journal of Autism and

[67] Frenette, P., et al., Factors affecting the age at diagnosis of autism spectrum disorders

[68] Drews, C., et al., Variation in the influence of selected sociodemographic risk factors for mental retardation. American Journal of Public Health, 1995. 85(3): p. 329-34.

[69] Hook, E. and A. Lindsjö, Down syndrome in live births by single year maternal age interval in a Swedish study: comparison with results from a New York State study.

[70] Liu, K., N. Zerubavel, and P. Bearman, Social demographic change and autism. De‐

order in offspring. British Journal of Psychiatry, 2008. 193(4): p. 316-21.

American Journal of Epidemiology, 2008. 168(11): p. 1268-76.

Autism and Developmental Disorders, 2011. 41(10): p. 1362-72.

healthy controls. Comprehensive Psychiatry, 2006. 47(1): p. 69-75.

of Public Health, 2009. 99(9): p. 1673-9.

418 Recent Advances in Autism Spectrum Disorders - Volume I

Medical Human Genetics, 2011. 12: p. 31-8.

Child Psychology and Psychiatry, 2005. 46(9): p. 963-71.

chives of General Psychiatry, 2006. 63(9): p. 1026-32.

Developmental Disorders, 2011. 41(12): p. 1733-7.

American Journal of Human Genetics, 1978. 30(1): p. 19-27.

in Nova Scotia, Canada. Autism, 2011: p. 1-12.

mography, 2010. 47(2): p. 327-43.

249-56.

p. 1642-8.


[87] Wilson, K. and L. Watson, Autism spectrum disorder in Australian Indigenous fami‐ lies: issues of diagnosis, support and funding. Aboriginal and Islander Health Work‐ er Journal, 2011. 35(5): p. 17-8.

[102] Wheelwright, S., et al., Defining the broader, medium and narrow autism phenotype among parents using the Autism Spectrum Quotient (AQ). Molecular Autism, 2010.

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

421

[103] Bernier, R., et al., Evidence for broader autism phenotype characteristics in parents

[104] Marques-Vidal, P., et al., Secular trends in height and weight among children and adolescents of the Seychelles, 1956-2006. BioMed Central Public Health, 2008. 8(1): p.

[105] Kalkbrenner, A., et al., Maternal smoking during pregnancy and the prevalence of autism spectrum disorders, using data from the autism and developmental disabili‐ ties monitoring network. Environmental Health Perspectives, 2012. 120(7): p. 1042-8.

[106] Lee, B., et al., Brief report: maternal smoking during pregnancy and autism spectrum disorders. Journal of Autism and Developmental Disorders, 2011: p. 1-6.

[107] Braun, J., et al., The effect of maternal smoking during pregnancy on intellectual dis‐ abilities among 8 year old children. Paediatric and Perinatal Epidemiology, 2009.

[108] Spohr, H., J. Willms, and H. Steinhausen, Fetal alcohol spectrum disorders in young

[109] Spohr, H. and H. Steinhausen, Fetal alcohol spectrum disorders and their persisting

[110] Malbin, D., Fetal alcohol spectrum disorder (FASD) and the role of family court judg‐ es in improving outcomes for children and families. Juvenile and Family Court Jour‐

[111] Hagberg, B. and M. Kyllerman, Epidemiology of mental retardation-a Swedish sur‐

[112] Yeargin-Allsopp, M., et al., Reported biomedical causes and associated medical con‐ ditions for mental retardation among 10 year old children, metropolitan Atlanta, 1985 to 1987. Developmental Medicine and Child Neurology, 1997. 39: p. 142-9.

[113] Quattlebaum, J. and M. O'Connor, Higher functioning children with prenatal alcohol exposure: Is there a specific neurocognitive profile? Child Neuropsychology, 2012: p.

[114] Eyal, R. and M. O'Connor, Psychiatry trainees' training and experience in fetal alco‐

[115] Cnattingius, S., The epidemiology of smoking during pregnancy: smoking preva‐ lence, maternal characteristics, and pregnancy outcomes. Nicotine and Tobacco Re‐

hol spectrum disorders. Academic Psychiatry, 2011. 35: p. 238-40.

sequelae in adult life. Deutsches Arzteblatt, 2008. 105(41): p. 693-8.

adulthood. Journal of Pediatrics, 2007. 150(2): p. 175-9.

vey. Brain and Development, 1983. 5(5): p. 441-9.

search, 2004. 6(Suppl 2): p. S125-S140.

from multiple incidence autism families. Autism Research, 2011.

1(1): p. 10.

166.

23(5): p. 482-91.

nal, 2004. 55(2): p. 53-63.

1-18.


[102] Wheelwright, S., et al., Defining the broader, medium and narrow autism phenotype among parents using the Autism Spectrum Quotient (AQ). Molecular Autism, 2010. 1(1): p. 10.

[87] Wilson, K. and L. Watson, Autism spectrum disorder in Australian Indigenous fami‐ lies: issues of diagnosis, support and funding. Aboriginal and Islander Health Work‐

[88] World Health Organisation. Mental health. 2012 [2012 September 3]; Available from:

[89] Daniels, J., et al., Parental psychiatric disorders associated with autism spectrum dis‐

[90] Mouridsen, S., et al., Psychiatric disorders in the parents of individuals with infantile

[91] Sullivan, P., et al., Family history of schizophrenia and bipolar disorder as risk fac‐

[92] Zhang, X., et al., Prenatal and perinatal risk factors for autism in China. Journal of

[93] Wilkerson, D., et al., Perinatal complications as predictors of infantile autism. Inter‐

[94] Piven, J., et al., Psychiatric disorders in the parents of autistic individuals. Journal of the American Academy of Child and Adolescent Psychiatry, 1991. 30(3): p. 471-8. [95] Morgan, V., et al., Intellectual disability and other neuropsychiatric outcomes in high-risk children of mothers with schizophrenia, bipolar disorder and unipolar ma‐

[96] Gokcen, S., et al., Theory of mind and verbal working memory deficits in parents of

[97] Hurley, R., et al., The broad autism phenotype questionnaire. Journal of Autism and

[98] Wong, D., et al., Profiles of executive function in parents and siblings of individuals with autism spectrum disorders. Genes, Brain and Behavior, 2006. 5(8): p. 561-76. [99] Hughes, C., M. Leboyer, and M. Bouvard, Executive function in parents of children

[100] Bishop, D., et al., Using self-report to identify the broad phenotype in parents of chil‐ dren with autistic spectrum disorders: a study using the Autism Spectrum Quotient.

[101] Baron-Cohen, S., et al., The Autism Spectrum Quotient (AQ): evidence from Asperg‐ er syndrome/high-functioning autism, males and females, scientists and mathemati‐

cians. Journal of Autism and Developmental Disorders, 2001. 31(1): p. 5-17.

autism: a case-control study. Psychopathology, 2007. 40(3): p. 166-71.

er Journal, 2011. 35(5): p. 17-8.

420 Recent Advances in Autism Spectrum Disorders - Volume I

http://www.who.int/topics/mental\_health/en/.

orders in the offspring. Pediatrics, 2008. 121(5): p. 1357-62.

tors for autism. Archives of General Psychiatry, 2012: p. 1-5.

Autism and Developmental Disorders, 2010. 40(11): p. 1311-21.

national Journal of Neuroscience, 2002. 112(9): p. 1085-98.

autistic children. Psychiatry Research, 2009. 166(1): p. 46-53.

with autism. Psychological Medicine, 1997. 27(1): p. 209-20.

Journal of Child Psychology and Psychiatry, 2004. 45(8): p. 1431-6.

jor depression. British Journal of Psychiatry, 2012.

Developmental Disorders, 2007. 37(9): p. 1679-90.


[116] Naeye, R., Effects of maternal cigarette smoking on the fetus and placenta. British Journal of Obstetrics and Gynaecology, 1978. 85(10): p. 732-7.

[131] Derecki, N., E. Privman, and J. Kipnis, Rett syndrome and other autism spectrum disorders-brain diseases of immune malfunction? Molecular Psychiatry, 2010. 15(4):

Pre-Existing Differences in Mothers of Children with Autism Spectrum Disorder and/or Intellectual Disability: A Review

http://dx.doi.org/10.5772/54488

423

[132] McDonough, J., Stedman's Concise Medical Dictionary, 1994: Williams & Wilkins.

[133] Rudra, C. and M. Williams, Monthly variation in preeclampsia prevalence: Washing‐ ton State, 1987-2001. Journal of Maternal-Fetal and Neonatal Medicine, 2005. 18(5): p.

[134] Mann, J., et al., Pre-eclampsia, birth weight, and autism spectrum disorders. Journal

[135] Griffith, M., J. Mann, and S. McDermott, The risk of intellectual disability in children born to mothers with preeclampsia or eclampsia with partial mediation by low birth

[136] Atladóttir, H., et al., Maternal infection requiring hospitalization during pregnancy and autism spectrum disorders. Journal of Autism and Developmental Disorders,

[137] Mann, J., et al., Trichomoniasis in pregnancy and mental retardation in children. An‐

[138] McDermott, S., et al., Urinary tract infections during pregnancy and mental retarda‐ tion and developmental delay. Obstetrics and Gynecology, 2000. 96(1): p. 113-9. [139] Croen, L., et al., Antidepressant use during pregnancy and childhood autism spec‐ trum disorders. Archives of General Psychiatry, 2011. 68(11): p. 11104-12.

[140] Rasalam, A., et al., Characteristics of fetal anticonvulsant syndrome associated autis‐ tic disorder. Developmental Medicine and Child Neurology, 2005. 47(8): p. 551-5. [141] Maimburg, R. and M. Væth, Perinatal risk factors and infantile autism. Acta Psy‐

of Autism and Developmental Disorders, 2010. 40(5): p. 548-54.

weight. Hypertension in Pregnancy, 2011. 30(1): p. 108-15.

nals of Epidemiology, 2009. 19(12): p. 891-99

chiatrica Scandinavica, 2006. 114(4): p. 257-64.

p. 355-63.

319-24.

2010. 40(12): p. 1423-30.


[116] Naeye, R., Effects of maternal cigarette smoking on the fetus and placenta. British

[117] Wakschlag, L., et al., Maternal smoking during pregnancy and severe antisocial be‐ havior in offspring: a review. American Journal of Public Health, 2002. 92(6): p.

[118] Leonard, H., et al., Relation between intrauterine growth and subsequent intellectual disability in a ten-year population cohort of children in Western Australia. American

[119] Ornoy, A. and Z. Ergaz, Alcohol abuse in pregnant women: effects on the fetus and newborn, mode of action and maternal treatment. International Journal of Environ‐

[120] Lyall, K., et al., Maternal early life factors associated with hormone levels and the risk of having a child with an autism spectrum disorder in the Nurses Health Study

[121] McLaren, L., Socioeconomic status and obesity. Epidemiologic Reviews, 2007. 29(1):

[122] Mokdad, A., et al., The spread of the obesity epidemic in the United States, 1991-1998. Journal of the American Medical Association, 1999. 282(16): p. 1519-22.

[123] Comi, A., et al., Familial clustering of autoimmune disorders and evaluation of medi‐ cal risk factors in autism. Journal of Child Neurology, 1999. 14(6): p. 388-94.

[124] Croen, L., et al., Maternal autoimmune diseases, asthma and allergies, and childhood autism spectrum disorders: a case-control study. Archives of Pediatrics and Adoles‐

[125] Atladóttir, H., et al., Association of family history of autoimmune diseases and au‐

[126] Mann, J., et al., Children born to diabetic mothers may be more likely to have intel‐

[127] Leonard, H., et al., Maternal health in pregnancy and intellectual disability in the off‐ spring: a population-based study. Annals of Epidemiology, 2006. 16(6): p. 448-54.

[128] Braunschweig, D., et al., Autism: maternally derived antibodies specific for fetal

[129] Ashwood, P., S. Wills, and J. Van de Water, The immune response in autism: a new frontier for autism research. Journal of Leukocyte Biology, 2006. 80(1): p. 1-15.

[130] Goines, P., et al., Increased midgestational IFN-g, IL-4 and IL-5 in women bearing a child with autism: a case-control study. Molecular Autism, 2011. 2(13): p. e1-e11.

tism spectrum disorders. Pediatrics, 2009. 124(2): p. 687-94.

brain proteins. Neurotoxicology, 2008. 29(2): p. 226-31.

lectual disability. Maternal and Child Health Journal, 2012: p. 1-5.

II. Journal of Autism and Developmental Disorders, 2011. 41(5): p. 618-27.

Journal of Obstetrics and Gynaecology, 1978. 85(10): p. 732-7.

Journal of Epidemiology, 2008. 167(1): p. 103-11.

cent Medicine, 2005. 159(2): p. 151-7.

mental Research and Public Health, 2010. 7(2): p. 364-79.

966-72.

422 Recent Advances in Autism Spectrum Disorders - Volume I

p. 29-48.


**Section 5**

**Aetiological Factors - Sensory Issues, Foetal**

**Alcohol Syndrome and Relationships**

**Aetiological Factors - Sensory Issues, Foetal Alcohol Syndrome and Relationships**

**Chapter 19**

**Relationships, Sexuality, and**

Maria R. Urbano, Kathrin Hartmann,

Gina M. Bondi Polychronopoulos and

Additional information is available at the end of the chapter

ders and sexuality while contributing to the existing literature.

The purpose of this chapter is to provide a brief overview of Autism Spectrum Disorders (ASD) and sexuality, as there is a paucity of this information in the literature. Specific attention is giv‐ en to sexuality involving the self, others, and interpersonal relationships. Problematic sexual behaviors, legal concerns, and sexual abuse (including victimization and perpetration) are also discussed. Finally, intervention strategies for ASD children, adults, and families are addressed. The overall aim of this chapter is to highlight major themes regarding Autism Spectrum Disor‐

Autism Spectrum Disorders, as currently defined by the Diagnostic and Statistical Manual (DSM-IV-TR) criteria, include the diagnoses of Autistic Disorder, Asperger's Disorder and Per‐ vasive Developmental Disorder NOS. The three major diagnostic categories include the fol‐ lowing: 1) language impairment, 2) social impairment, and 3) repetitive behaviors/restricted interests, with the impairments present prior to the age of three. Autism has been conceptual‐ ized under this diagnostic rubric as a spectrum of disorders with symptoms ranging from se‐ vere to minimally impaired [1]. With the advent of the DSM-5, only two major criteria will be included: 1) social communication impairment, and 2) repetitive behaviors/restricted interests.

and reproduction in any medium, provided the original work is properly cited.

© 2013 Urbano et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

Stephen I. Deutsch,

http://dx.doi.org/10.5772/53954

Vanessa Dorbin

**1. Introduction**

**2. Autism overview**

**Intimacy in Autism Spectrum Disorders**

**Chapter 19**
