The Experts below are selected from a list of 69 Experts worldwide ranked by ideXlab platform
Karen H Friderici - One of the best experts on this subject based on the ideXlab platform.
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confirmation and extension of association of blood lead with attention deficit hyperactivity disorder adhd and adhd symptom domains at population typical exposure levels
Journal of Child Psychology and Psychiatry, 2010Co-Authors: Joel T Nigg, Molly A Nikolas, Mark G Knottnerus, Kevin Cavanagh, Karen H FridericiAbstract:Attention deficit hyperactivity disorder (ADHD) occurs in 3 to 7% of children, with etiology believed to be multifactorial. The DSM-IV (APA, 2000) specifies three clinical subtypes: predominantly hyperactive (ADHD-PH), predominantly inattentive (ADHD-PI), and combined (ADHD-C). The subtypes are arrived at through combinations of two primary symptom dimensions: inattention-disorganization, and hyperactivity-impulsivity. These symptom domains may have partially distinct etiological inputs (Nigg, 2006). Because they appear to be an extreme of a behavioral continuum, the symptom dimensions also serve as useful foci to study etiology. Indeed, a factor analytic tradition has arrived at related but slightly different item sets than DSM-IV to capture population variation in “cognitive problems” and hyperactivity/impulsivity (e.g., Conners et al., 2007). Lead exposure via water, soil, and other sources remains a worldwide health concern (Centers for Disease Control, 2005). Blood lead above 10 μg/dL has been associated reliably with ADHD and related behaviors, with the only real dispute being the magnitude of the effect (Burns et al., 1999; Silva, Hughes, Williams, & Faed, 1988; Thomson et al. 1989). Regulation of commercial uses of lead has markedly reduced the incidence of frank lead poisoning in recent decades in the U.S. (CDC, 2005), Western Europe (e.g., Delschen, Machtolf, Sugiri, & Wilhelm, 2008), and Scandinavia (Stromberg, Lundh, & Skerfving, 2008). Perhaps as a result, lead exposure has not been highlighted as an ongoing concern related to ADHD. This reassuring picture, however, is eroding. Even at lower blood levels ( 2 μg/dL were more like to have ADHD than children with blood lead <0.7 μg/dL). One year later, Chiodo et al. (2007) reported that blood lead was related to teacher rated symptoms of inattention and activity, but not impulsivity, using the Conners Rating Scales and other standard Scales in a high-risk sample. The next year Nigg et al (2008) conducted the first low-level lead study of children formally diagnosed with ADHD. Blood lead was related to ADHD and to parent reported DSM-IV symptoms of hyperactivity but not inattention. Those results supported an association to ADHD but appeared partially to contradict Chiodo et al (2007) as to the affected symptom domain. The present study sought more definitive evaluation in a larger, well-diagnosed sample. The aim was to scrutinize relations with both DSM-IV and Conners Ratings, by both parent and teacher report, so as to confirm and extend prior findings as well as to clarify the apparent contradiction in the last two studies reported. Dozens of potential confounds have been ruled out in relation to lead exposure and ADHD (Chiodo et al. 2007; Silva, et al., 1988; Thomson et al. 1989), but mostly at higher lead exposure levels. Thus, an expanded set of confounders and covariates was also considered here, as outlined in Methods. Confirmation of the association of ADHD with lead exposure even at very low blood lead levels would be of major importance to public health, because exposure levels in the range of 1–5 μg/dL remain very common. Yet, most public authorities continue to use 10 μg/dL as the criterion of concern. If the association of low levels of lead exposure with ADHD is verified, it opens the potential for new insights into the etiology of ADHD, because lead can serve as a model insult affecting frontal-striatal circuitry in ways that are relatively well understood. It also could open potential new opportunities for study of susceptibility-insult or gene by experience models. It could also provide clues to prevention via dietary supplementation (Kordas et al., 2007), via renewed caution before introducing new toxins into children’s environments, or via aggressive efforts to continue to eliminate all lead exposure.
Joel T Nigg - One of the best experts on this subject based on the ideXlab platform.
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confirmation and extension of association of blood lead with attention deficit hyperactivity disorder adhd and adhd symptom domains at population typical exposure levels
Journal of Child Psychology and Psychiatry, 2010Co-Authors: Joel T Nigg, Molly A Nikolas, Mark G Knottnerus, Kevin Cavanagh, Karen H FridericiAbstract:Attention deficit hyperactivity disorder (ADHD) occurs in 3 to 7% of children, with etiology believed to be multifactorial. The DSM-IV (APA, 2000) specifies three clinical subtypes: predominantly hyperactive (ADHD-PH), predominantly inattentive (ADHD-PI), and combined (ADHD-C). The subtypes are arrived at through combinations of two primary symptom dimensions: inattention-disorganization, and hyperactivity-impulsivity. These symptom domains may have partially distinct etiological inputs (Nigg, 2006). Because they appear to be an extreme of a behavioral continuum, the symptom dimensions also serve as useful foci to study etiology. Indeed, a factor analytic tradition has arrived at related but slightly different item sets than DSM-IV to capture population variation in “cognitive problems” and hyperactivity/impulsivity (e.g., Conners et al., 2007). Lead exposure via water, soil, and other sources remains a worldwide health concern (Centers for Disease Control, 2005). Blood lead above 10 μg/dL has been associated reliably with ADHD and related behaviors, with the only real dispute being the magnitude of the effect (Burns et al., 1999; Silva, Hughes, Williams, & Faed, 1988; Thomson et al. 1989). Regulation of commercial uses of lead has markedly reduced the incidence of frank lead poisoning in recent decades in the U.S. (CDC, 2005), Western Europe (e.g., Delschen, Machtolf, Sugiri, & Wilhelm, 2008), and Scandinavia (Stromberg, Lundh, & Skerfving, 2008). Perhaps as a result, lead exposure has not been highlighted as an ongoing concern related to ADHD. This reassuring picture, however, is eroding. Even at lower blood levels ( 2 μg/dL were more like to have ADHD than children with blood lead <0.7 μg/dL). One year later, Chiodo et al. (2007) reported that blood lead was related to teacher rated symptoms of inattention and activity, but not impulsivity, using the Conners Rating Scales and other standard Scales in a high-risk sample. The next year Nigg et al (2008) conducted the first low-level lead study of children formally diagnosed with ADHD. Blood lead was related to ADHD and to parent reported DSM-IV symptoms of hyperactivity but not inattention. Those results supported an association to ADHD but appeared partially to contradict Chiodo et al (2007) as to the affected symptom domain. The present study sought more definitive evaluation in a larger, well-diagnosed sample. The aim was to scrutinize relations with both DSM-IV and Conners Ratings, by both parent and teacher report, so as to confirm and extend prior findings as well as to clarify the apparent contradiction in the last two studies reported. Dozens of potential confounds have been ruled out in relation to lead exposure and ADHD (Chiodo et al. 2007; Silva, et al., 1988; Thomson et al. 1989), but mostly at higher lead exposure levels. Thus, an expanded set of confounders and covariates was also considered here, as outlined in Methods. Confirmation of the association of ADHD with lead exposure even at very low blood lead levels would be of major importance to public health, because exposure levels in the range of 1–5 μg/dL remain very common. Yet, most public authorities continue to use 10 μg/dL as the criterion of concern. If the association of low levels of lead exposure with ADHD is verified, it opens the potential for new insights into the etiology of ADHD, because lead can serve as a model insult affecting frontal-striatal circuitry in ways that are relatively well understood. It also could open potential new opportunities for study of susceptibility-insult or gene by experience models. It could also provide clues to prevention via dietary supplementation (Kordas et al., 2007), via renewed caution before introducing new toxins into children’s environments, or via aggressive efforts to continue to eliminate all lead exposure.
Dorret I Boomsma - One of the best experts on this subject based on the ideXlab platform.
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the genetic and environmental contributions to attention deficit hyperactivity disorder as measured by the Conners Rating Scales revised
American Journal of Psychiatry, 2005Co-Authors: James J Hudziak, Eske M Derks, Robert R Althoff, David C Rettew, Dorret I BoomsmaAbstract:Objective: The majority of published reports on twin studies of attention deficit hyperactivity disorder (ADHD) have indicated robust additive genetic influences and unique environmental influences. These studies typically used DSM ADHD symptoms collected by telephone or interviews with mothers. The purpose of this study was to test the genetic architecture of ADHD by using the ADHD index from Conners’ Rating Scales—Revised. Method: From the Conners’ scale forms, data for the ADHD index were collected from the mothers of 1,595 7-year-old twin pairs from the Netherlands Twin Registry. Rates of ADHD diagnoses were computed by using Conners’ gender- and age-specific cutoff points. Contributions from additive, dominant, unique environmental, interaction, and gender effects were computed by using gender-genetic models. Results: The prevalence of ADHD across the sample of 7-year-old twin pairs was about 4% according to the mothers’ reports, consistent with other reported rates of ADHD. However, using the gender norms provided with the ADHD index, the authors found slightly higher rates of ADHD in girls than previously reported. Genetic analyses yielded a model that includes genetic dominance (48%), additive genetic factors (30%), and unique environmental factors (22%). Conclusions: The ADHD index from Conners’ Rating Scales—Revised identified an appropriate percentage of children across this epidemiologic twin sample as being at risk for ADHD. The results of the genetic analyses are consistent with prior reports that ADHD is predominantly influenced by genetic factors that are both dominant and additive.
Sushma Jani - One of the best experts on this subject based on the ideXlab platform.
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cross cultural studies with the Conners Rating Scales
Journal of Clinical Psychology, 1995Co-Authors: Leon A Rosenberg, Sushma JaniAbstract:The teacher and parent forms of the Conners Rating Scales were completed by the parents and teachers of 863 children who were living in an area of Bombay, India. Two socioeconomic strata were sampled. The results were compared to American norms for Ratings done by parents and teachers. The teacher Ratings demonstrated some clear differences from American norms. Correlational analysis suggested that the Conners Scales showed greater overlap, and, hence, less independence, than has been reported in the American research literature.
Kevin Cavanagh - One of the best experts on this subject based on the ideXlab platform.
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confirmation and extension of association of blood lead with attention deficit hyperactivity disorder adhd and adhd symptom domains at population typical exposure levels
Journal of Child Psychology and Psychiatry, 2010Co-Authors: Joel T Nigg, Molly A Nikolas, Mark G Knottnerus, Kevin Cavanagh, Karen H FridericiAbstract:Attention deficit hyperactivity disorder (ADHD) occurs in 3 to 7% of children, with etiology believed to be multifactorial. The DSM-IV (APA, 2000) specifies three clinical subtypes: predominantly hyperactive (ADHD-PH), predominantly inattentive (ADHD-PI), and combined (ADHD-C). The subtypes are arrived at through combinations of two primary symptom dimensions: inattention-disorganization, and hyperactivity-impulsivity. These symptom domains may have partially distinct etiological inputs (Nigg, 2006). Because they appear to be an extreme of a behavioral continuum, the symptom dimensions also serve as useful foci to study etiology. Indeed, a factor analytic tradition has arrived at related but slightly different item sets than DSM-IV to capture population variation in “cognitive problems” and hyperactivity/impulsivity (e.g., Conners et al., 2007). Lead exposure via water, soil, and other sources remains a worldwide health concern (Centers for Disease Control, 2005). Blood lead above 10 μg/dL has been associated reliably with ADHD and related behaviors, with the only real dispute being the magnitude of the effect (Burns et al., 1999; Silva, Hughes, Williams, & Faed, 1988; Thomson et al. 1989). Regulation of commercial uses of lead has markedly reduced the incidence of frank lead poisoning in recent decades in the U.S. (CDC, 2005), Western Europe (e.g., Delschen, Machtolf, Sugiri, & Wilhelm, 2008), and Scandinavia (Stromberg, Lundh, & Skerfving, 2008). Perhaps as a result, lead exposure has not been highlighted as an ongoing concern related to ADHD. This reassuring picture, however, is eroding. Even at lower blood levels ( 2 μg/dL were more like to have ADHD than children with blood lead <0.7 μg/dL). One year later, Chiodo et al. (2007) reported that blood lead was related to teacher rated symptoms of inattention and activity, but not impulsivity, using the Conners Rating Scales and other standard Scales in a high-risk sample. The next year Nigg et al (2008) conducted the first low-level lead study of children formally diagnosed with ADHD. Blood lead was related to ADHD and to parent reported DSM-IV symptoms of hyperactivity but not inattention. Those results supported an association to ADHD but appeared partially to contradict Chiodo et al (2007) as to the affected symptom domain. The present study sought more definitive evaluation in a larger, well-diagnosed sample. The aim was to scrutinize relations with both DSM-IV and Conners Ratings, by both parent and teacher report, so as to confirm and extend prior findings as well as to clarify the apparent contradiction in the last two studies reported. Dozens of potential confounds have been ruled out in relation to lead exposure and ADHD (Chiodo et al. 2007; Silva, et al., 1988; Thomson et al. 1989), but mostly at higher lead exposure levels. Thus, an expanded set of confounders and covariates was also considered here, as outlined in Methods. Confirmation of the association of ADHD with lead exposure even at very low blood lead levels would be of major importance to public health, because exposure levels in the range of 1–5 μg/dL remain very common. Yet, most public authorities continue to use 10 μg/dL as the criterion of concern. If the association of low levels of lead exposure with ADHD is verified, it opens the potential for new insights into the etiology of ADHD, because lead can serve as a model insult affecting frontal-striatal circuitry in ways that are relatively well understood. It also could open potential new opportunities for study of susceptibility-insult or gene by experience models. It could also provide clues to prevention via dietary supplementation (Kordas et al., 2007), via renewed caution before introducing new toxins into children’s environments, or via aggressive efforts to continue to eliminate all lead exposure.