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Shareghfarid E, Sangsefidi Z S, Hosseinzadeh M, Salehi-Abargouei A, Mohammadi M. Comparison of Nutrients' Intakes in Children with and without Attention Deficit Hyperactivity Disorder. JNFS 2020; 5 (2) :132-140
URL: http://jnfs.ssu.ac.ir/article-1-207-en.html
URL: http://jnfs.ssu.ac.ir/article-1-207-en.html
Elham Shareghfarid 
, Zohreh Sadat Sangsefidi , Mahdieh Hosseinzadeh , Amin Salehi-Abargouei * , Mohammad Mohammadi
, Zohreh Sadat Sangsefidi , Mahdieh Hosseinzadeh , Amin Salehi-Abargouei * , Mohammad Mohammadi
Department of Nutrition, School of Public Health, Shahid Sadughi University of Medical Sciences, Yazd, Iran.
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Comparison of Nutrients' Intakes in Children with and without Attention Deficit Hyperactivity Disorder
Elham Shareghfarid; MSc1, Zohreh Sadat Sangsefidi; MSc1, Mahdieh Hosseinzadeh; PhD*1
Amin Salehi-Abargouei; PhD1 & Mohammad Mohammadi; MSc1
1 Department of Nutrition, School of Public Health, Shahid Sadughi University of Medical Sciences, Yazd, Iran.
Elham Shareghfarid; MSc1, Zohreh Sadat Sangsefidi; MSc1, Mahdieh Hosseinzadeh; PhD*1
Amin Salehi-Abargouei; PhD1 & Mohammad Mohammadi; MSc1
1 Department of Nutrition, School of Public Health, Shahid Sadughi University of Medical Sciences, Yazd, Iran.
| ARTICLE INFO | ABSTRACT | |
| ORIGINAL ARTICLE | Background: Attention deficit hyperactivity disorder (ADHD) is the most common chronic mental disorder among children. Children with ADHD may be at risk for a variety of nutrients' deficiencies. We aimed to assess the nutrients' intakes among ADHD children and compare them with the healthy ones. Methods: This was a hospital-based case-control survey over 120 ADHD as the cases and 240 non-ADHD children as the control participants aged 6-13 years. Usual dietary intakes were assessed using a validated semi quantitative food-frequency questionnaire (FFQ). The P-values were considered significant if they were < 0·05. Results: Energy: 2812.2 ± 1029.9 kcal/day vs. 3136.4 ± 1360.3 kcal/day, P = 0.001), fat: 78.3 ± 28.8 g/day vs. 87.2 ± 44.9 g/day, P > 0.001), and carbohydrate: 436.8 ± 192.6 g/day vs. 479.9 ± 244.2 g/day, P = 0.009) intakes were significantly lower in ADHD than healthy children. Similarly, consumption of calcium: 968.5 ± 358.3 mg/day vs. 1055.7 ± 453.4 mg/day, P = 0.03) and magnesium: 363.1 ± 173.9 mg/day vs. 411.9 ± 220.8 mg/day, P = 0.01) were significantly lower in the cases than control group. However, intakes of thiamin: 34.4±18.8 mg/day vs. 40.4 ± 25.6 mg/day, P = 0.002), riboflavin: 1.99 ± 0.76 mg/day vs. 2.21 ± 0.95 mg/day, P = 0.01), niacin: 24.9 ± 10.6 mg/day vs. 27.5 ± 13.2 mg/day, P = 0.01), and vitamin B5: 6.85 ± 3.35 mg/day vs. 7.49 ± 3.84 mg/day, P = 0.02) were significantly lower in the case than control group. Conclusion: Children with ADHD consumed significantly lower quantities of energy, macronutrients, calcium, magnesium, B vitamins (B1, B2, B3, B5), and vitamin C compared with the healthy children. Key words: Nutrients; Dietary assessment; Nutritional status; ADHD; Children |
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| Article history: Received: 21 Sep 2018 Revised: 12 Nov 2018 Accepted: 20 Feb 2019 |
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| *Corresponding author Hoseinzadeh.Mahdieh@gmail.com Department of Nutrition, School of Public Health, Shahid Sadughi University of Medical Sciences. Yazd, Iran. Postal code: 891-6978477 Tel: +98-353-8203232 |
Introduction
Attention deficit hyperactivity disorder (ADHD) is the most common chronic mental and behavioral disorder among children (Izquierdo-Pulido et al., 2015). The prevalence of ADHD was 7.2% all over the world, while its prevalence was 17% in Iran (Meysamie et al., 2011). This disorder has a growing trend every year around the world (Thomas et al., 2015, Visser et al., 2010). Unlike those showing simple hyperactivity features, children with ADHD have three subtype symptoms of predominantly hyperactive-impulsive, predominantly inattentive, and combined hyperactive-impulsive and inattentive (Lahey et al., 2006, Rader et al., 2009, Schnoll et al., 2003). Children with ADHD may be at risk for a variety of nutrients' deficiencies due to their disorderd attention and appetite suppressant effects of treatment (Goldfield et al., 2007). Increased availability of the processed food, rich in sugar and fat, has increased the consumption rate by children and adolescents (Øverby et al., 2004).
Nutritional status is very important during childhood, which is a period of vigorous growth, increased activity, and developed body functions, and social cognitive ability. As showed in previous studies, ADHD children are at risk for different nutrients' deficiencies including zinc (Bilici et al., 2004), iron (Konofal et al., 2008), magnesium (Mousain-Bosc et al., 2004), copper (Kiddie et al., 2010) vitamin D (Kamal et al., 2014), and long-chain polyunsaturated fatty acids (Chang et al., 2016). Poly unsaturated fatty acids have fundamental role in neurotransmitters' function (Erikson et al., 2001, Neuringer et al., 1988, Solanto, 2002). Vitamin C and iron are also needed in synthesis of the serotonin and dopamine, respectively (Gershoff, 1993, Konofal et al., 2004). A recent study on sugar consumption suggested that higher consumption of sugar was significantly correlated with a higher level of hyperactivity and attention deficiency (Choi et al., 2008, Dykman and Dykman, 1998, Kavale and Forness, 1983, Lee and Rhie, 2008).
Considering assessment of the nutrients' intake in ADHD, seven studies have been conducted (Arnold et al., 2005, Bekaroǧlu et al., 1996, Chang et al., 2016, Chen et al., 2004, Jang and Bu, 2017, Kaplan et al., 1989, Kiddie et al., 2010). A Korean study reported that overweight ADHD participants consumed significantly less amounts of iron in comparison to the normal weight individuals with ADHD. Serum ferritin level was also lower in the overweight group (59.0 ng/ml) than the normal weight group (47.9 ng/ml). After adjusting for the total energy intake, total vegetable consumption was 14.3% lower in overweight group compared with the normal weight group (Jang and Bu, 2017). Another research assessing dietary intakes and nutrients status among children with ADHD indicated that 66% of children had zinc and 23% had copper deficiency (Kiddie et al., 2010). A study among ADHD Korean children found that these children consumed protein twice higher than the recommended level (Kim and Chang, 2011); whereas, another case-control study showed no significant difference in terms of macronutrients intake between ADHD and non ADHD children (Kiddie et al., 2010). Moreover, a Chinese research reported an inverse association between ADHD and the mineral-protein nutrient pattern rich in zinc, protein, phosphorus, selenium, calcium, and riboflavin (Zhou et al., 2016).
Methodological limitations existed in the former research, including use of dietary assessment tools not validated for pediatric use (Arnold et al., 2005). Furthermore, inconsistent results were observed regarding the nutrients' intakes. Regarding the above-mentioned ideas and the fact that dietary habits of Iranians are very different from western countries, it is worth to explore the nutritional status of children and adolescents with ADHD in Iran.
Materials and methods
Study design and participants: We conducted a hospital-based case-control study using elementary school students (aged 6 to 13 years) who visited clinics of Shahid Sadoughi University of medical sciences from June to February, 2016.
The ADHD group was recruited from two clinics (Khatam al Anbia and Imam Hossein). Inclusion criterion was having ADHD diagnosed by psychiatrists based on the Text Revision of Statistical Manual of Mental Disorders-Fourth Edition (DSM-IV-TR). Exclusion criterion included having concurrent condition, such as tic disorder (motor type), anxiety disorder, oppositional defiant disorder, Tourette’s disorder, depression, and learning disability. A total of 120 patients were selected as the case group
Control group members were recruited from four elementary schools. Exclusion criteria were having a history of ADHD, any mental disorder, and tic disorder. The test used to confirm lack of ADHD in controls was DSM-IV-TR. All questionnaires were completed and a total of 240 controls were recruited.
ADHD diagnosis: The presence of ADHD was confirmed using the DSM-IV TR by a psychiatrist (Owens and Hoza, 2003). According to the DSM-IV TR, a person with ADHD must have at least six symptoms of inattention or hyperactivity–impulsivity persisted for at least 6 months to a maladaptive and inconsistent degree with the person’s developmental level (Owens and Hoza, 2003). The reliability and validity of this questionnaire was confirmed previously (Owens and Hoza, 2003). Newly and previously diagnosed patients participated in the present study.
Measurements: Usual dietary intakes were assessed using a semi quantitative food-frequency questionnaire (FFQ), which consisted of supplement intake and 186 food items commonly consumed by the Iranian and local foods specify for children. The validity and reliability of the FFQ was evaluated in Tehran lipid and glucose study (TLGS) (Asghari et al., 2012). All questionnaires were administered by a trained dietitian in face-to-face interviews. Parents were interviewed with their children and were requested to report the frequency intakes of food items by their children on a daily (i.e., fruits), weekly (i.e., cruciferous vegetables), and monthly (i.e., pizza) basis during the previous year.
The reported frequency for each food item was converted to daily intake. Portion sizes of the consumed foods were converted into grams using household measures. Each food and beverage was then coded according to the protocol and analyzed for its content of energy and other nutrients using Nutritionist IV (N-Squared Computing, Salem, OR, USA) designed for Iranian foods.
Weight was measured while participants were minimally clothed and without shoes using digital seca scales (Seca, Germany) to the nearest 100 g. Height was measured using a tape measure while the children were standing in a normal position
and were not wearing shoes. The participants' BMI was calculated by dividing weight (kilograms) by the square of height (in meters). Obesity was defined according to the definition provided
by the international obesity task force (IOTF) for children (Cole et al., 2000).
To address the important confounding factors, we employed a pair-match design on age and gender. Variables including age, gender, medical history, socioeconomic status current use of medications and drug therapy, family history of ADHD, and screen exposure were obtained by a general information questionnaire. Family history of ADHD was assessed by asking parents about existence of any ADHD case diagnosed by a psychotherapist in the first and second order family members. Socioeconomic status was determined as low, moderate, or high based on the parents' education (undergraduate, postgraduate, and doctorate) and acquisition (house ownership or not). Physical activity was also evaluated using a validate questionnaire (Aadahl and Jørgensen, 2003, Kelishadi et al., 2007) and categorized to less than one a week 2-3 times a week, 3-5 times a week, and more than 5 times a week.
Data analysis: The analyses were performed using the IBM SPSS version 22·0. Values were expressed in mean and standard error for continuous variables and percentages for categorical variables. Chi-square tests were run to determine differences in categorical data between cases and controls. Independent sample t-tests were also applied to evaluate differences between groups of continuous normally distributed variables. P-values were considered significant if they were < 0·05.
Ethical considerations: Written informed consent forms were collected from all participants and their parents. Furthermore, participants of the two study groups were matched in terms of age, gender, and residential area. The study was approved by the Nutrition & Food Security Research Center, Yazd Shahid Sadoughi University of Medical Sciences and Health Services as well as the Ethics Committee of Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
Results
Of the 120 children with ADHD diagnosed in clinics, a total of 110 ADHD participants were retained in this analysis, including 85 boys and 25 girls. Additionally, 232 eligible age- and gender-matched controls were recruited from the schools selected from the same region of clinics. In the study process, 18 children from cases and controls were excluded because of unreasonable energy intakes. The general characteristics of study participants are shown in Table 1. Compared with the controls, participants with ADHD were more likely to use medication and screen use; they were also more physically active than the healthy controls. The possibility of having a family history of ADHD was also higher in the intervention group. Children with and without ADHD were similar regarding their BMI, household income, parental education, and sleep hours per day.
The macronutrients intakes of the ADHD and non-ADHD children are compared in Table 2. As shown in Table 2, energy intake, fat, and carbohydrate intakes were significantly higher in controls than the case group.
The vitamins and mineral intakes between ADHD and non-ADHD children are compared in Table 3. Although zinc, calcium, and magnesium intakes were significantly lower in cases than controls, iodine intake was significantly higher in ADHD children in comparison to the controls. No significant differences were observed in terms of iron intake between the two groups. Consumption of vitamins including thiamin, riboflavin, niacin, vitamin B5, and vitamin C were also significantly lower in ADHD children than non-ADHD ones. However, vitamin E intake was significantly greater in than controls.
Nutritional status is very important during childhood, which is a period of vigorous growth, increased activity, and developed body functions, and social cognitive ability. As showed in previous studies, ADHD children are at risk for different nutrients' deficiencies including zinc (Bilici et al., 2004), iron (Konofal et al., 2008), magnesium (Mousain-Bosc et al., 2004), copper (Kiddie et al., 2010) vitamin D (Kamal et al., 2014), and long-chain polyunsaturated fatty acids (Chang et al., 2016). Poly unsaturated fatty acids have fundamental role in neurotransmitters' function (Erikson et al., 2001, Neuringer et al., 1988, Solanto, 2002). Vitamin C and iron are also needed in synthesis of the serotonin and dopamine, respectively (Gershoff, 1993, Konofal et al., 2004). A recent study on sugar consumption suggested that higher consumption of sugar was significantly correlated with a higher level of hyperactivity and attention deficiency (Choi et al., 2008, Dykman and Dykman, 1998, Kavale and Forness, 1983, Lee and Rhie, 2008).
Considering assessment of the nutrients' intake in ADHD, seven studies have been conducted (Arnold et al., 2005, Bekaroǧlu et al., 1996, Chang et al., 2016, Chen et al., 2004, Jang and Bu, 2017, Kaplan et al., 1989, Kiddie et al., 2010). A Korean study reported that overweight ADHD participants consumed significantly less amounts of iron in comparison to the normal weight individuals with ADHD. Serum ferritin level was also lower in the overweight group (59.0 ng/ml) than the normal weight group (47.9 ng/ml). After adjusting for the total energy intake, total vegetable consumption was 14.3% lower in overweight group compared with the normal weight group (Jang and Bu, 2017). Another research assessing dietary intakes and nutrients status among children with ADHD indicated that 66% of children had zinc and 23% had copper deficiency (Kiddie et al., 2010). A study among ADHD Korean children found that these children consumed protein twice higher than the recommended level (Kim and Chang, 2011); whereas, another case-control study showed no significant difference in terms of macronutrients intake between ADHD and non ADHD children (Kiddie et al., 2010). Moreover, a Chinese research reported an inverse association between ADHD and the mineral-protein nutrient pattern rich in zinc, protein, phosphorus, selenium, calcium, and riboflavin (Zhou et al., 2016).
Methodological limitations existed in the former research, including use of dietary assessment tools not validated for pediatric use (Arnold et al., 2005). Furthermore, inconsistent results were observed regarding the nutrients' intakes. Regarding the above-mentioned ideas and the fact that dietary habits of Iranians are very different from western countries, it is worth to explore the nutritional status of children and adolescents with ADHD in Iran.
Materials and methods
Study design and participants: We conducted a hospital-based case-control study using elementary school students (aged 6 to 13 years) who visited clinics of Shahid Sadoughi University of medical sciences from June to February, 2016.
The ADHD group was recruited from two clinics (Khatam al Anbia and Imam Hossein). Inclusion criterion was having ADHD diagnosed by psychiatrists based on the Text Revision of Statistical Manual of Mental Disorders-Fourth Edition (DSM-IV-TR). Exclusion criterion included having concurrent condition, such as tic disorder (motor type), anxiety disorder, oppositional defiant disorder, Tourette’s disorder, depression, and learning disability. A total of 120 patients were selected as the case group
Control group members were recruited from four elementary schools. Exclusion criteria were having a history of ADHD, any mental disorder, and tic disorder. The test used to confirm lack of ADHD in controls was DSM-IV-TR. All questionnaires were completed and a total of 240 controls were recruited.
ADHD diagnosis: The presence of ADHD was confirmed using the DSM-IV TR by a psychiatrist (Owens and Hoza, 2003). According to the DSM-IV TR, a person with ADHD must have at least six symptoms of inattention or hyperactivity–impulsivity persisted for at least 6 months to a maladaptive and inconsistent degree with the person’s developmental level (Owens and Hoza, 2003). The reliability and validity of this questionnaire was confirmed previously (Owens and Hoza, 2003). Newly and previously diagnosed patients participated in the present study.
Measurements: Usual dietary intakes were assessed using a semi quantitative food-frequency questionnaire (FFQ), which consisted of supplement intake and 186 food items commonly consumed by the Iranian and local foods specify for children. The validity and reliability of the FFQ was evaluated in Tehran lipid and glucose study (TLGS) (Asghari et al., 2012). All questionnaires were administered by a trained dietitian in face-to-face interviews. Parents were interviewed with their children and were requested to report the frequency intakes of food items by their children on a daily (i.e., fruits), weekly (i.e., cruciferous vegetables), and monthly (i.e., pizza) basis during the previous year.
The reported frequency for each food item was converted to daily intake. Portion sizes of the consumed foods were converted into grams using household measures. Each food and beverage was then coded according to the protocol and analyzed for its content of energy and other nutrients using Nutritionist IV (N-Squared Computing, Salem, OR, USA) designed for Iranian foods.
Weight was measured while participants were minimally clothed and without shoes using digital seca scales (Seca, Germany) to the nearest 100 g. Height was measured using a tape measure while the children were standing in a normal position
and were not wearing shoes. The participants' BMI was calculated by dividing weight (kilograms) by the square of height (in meters). Obesity was defined according to the definition provided
by the international obesity task force (IOTF) for children (Cole et al., 2000).
To address the important confounding factors, we employed a pair-match design on age and gender. Variables including age, gender, medical history, socioeconomic status current use of medications and drug therapy, family history of ADHD, and screen exposure were obtained by a general information questionnaire. Family history of ADHD was assessed by asking parents about existence of any ADHD case diagnosed by a psychotherapist in the first and second order family members. Socioeconomic status was determined as low, moderate, or high based on the parents' education (undergraduate, postgraduate, and doctorate) and acquisition (house ownership or not). Physical activity was also evaluated using a validate questionnaire (Aadahl and Jørgensen, 2003, Kelishadi et al., 2007) and categorized to less than one a week 2-3 times a week, 3-5 times a week, and more than 5 times a week.
Data analysis: The analyses were performed using the IBM SPSS version 22·0. Values were expressed in mean and standard error for continuous variables and percentages for categorical variables. Chi-square tests were run to determine differences in categorical data between cases and controls. Independent sample t-tests were also applied to evaluate differences between groups of continuous normally distributed variables. P-values were considered significant if they were < 0·05.
Ethical considerations: Written informed consent forms were collected from all participants and their parents. Furthermore, participants of the two study groups were matched in terms of age, gender, and residential area. The study was approved by the Nutrition & Food Security Research Center, Yazd Shahid Sadoughi University of Medical Sciences and Health Services as well as the Ethics Committee of Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
Results
Of the 120 children with ADHD diagnosed in clinics, a total of 110 ADHD participants were retained in this analysis, including 85 boys and 25 girls. Additionally, 232 eligible age- and gender-matched controls were recruited from the schools selected from the same region of clinics. In the study process, 18 children from cases and controls were excluded because of unreasonable energy intakes. The general characteristics of study participants are shown in Table 1. Compared with the controls, participants with ADHD were more likely to use medication and screen use; they were also more physically active than the healthy controls. The possibility of having a family history of ADHD was also higher in the intervention group. Children with and without ADHD were similar regarding their BMI, household income, parental education, and sleep hours per day.
The macronutrients intakes of the ADHD and non-ADHD children are compared in Table 2. As shown in Table 2, energy intake, fat, and carbohydrate intakes were significantly higher in controls than the case group.
The vitamins and mineral intakes between ADHD and non-ADHD children are compared in Table 3. Although zinc, calcium, and magnesium intakes were significantly lower in cases than controls, iodine intake was significantly higher in ADHD children in comparison to the controls. No significant differences were observed in terms of iron intake between the two groups. Consumption of vitamins including thiamin, riboflavin, niacin, vitamin B5, and vitamin C were also significantly lower in ADHD children than non-ADHD ones. However, vitamin E intake was significantly greater in than controls.
Discussion
Energy, fat, and carbohydrate intakes were significantly lower in ADHD than healthy children. Similarly, consumption of calcium and magnesium were significantly lower in cases than controls. However, intakes of thiamin, riboflavin, niacin, vitamin B5, and vitamin C were significantly lower in cases than controls.
Based on the findings, macronutrient intakes were significantly lower in ADHD children. On the contrary, Stevens reported significantly higher intakes of total fat (g) in ADHD participants when compared to controls (Stevens et al., 1995). Another study showed that ADHD adolescents consumed more energy and fat than controls (Colter et al., 2008). ADHD children in the current study consumed less amounts of high nutrient density foods than normal gender-age matched children. Moreover, the mean age of children in this study was 8 years, but it was 14 in Colter study.
Results of vitamin intakes in this study showed that vitamin intakes were significantly lower in ADHD children than healthy ones. Similar to our results, previous studies showed that consumption of thiamin, riboflavin, niacin, vitamin B5, and vitamin C among ADHD children were lower than non-ADHD participants (Colter et al., 2008, Kiddie et al., 2010). In contrast to our conclusion, a case-control study demonstrated that ADHD participants consumed higher levels of at least 10 different nutrients, than their control counterparts (Colter et al., 2008). Furthermore, Chen et al. reported significantly increased vitamin C (mg) consumption in participants with ADHD versus controls (Chen et al., 2004). The difference between our results and previous studies may be due to higher energy intake in normal children than ADHD children. Considering that Iran has undergone a nutritional transition caused by a Westernization in lifestyle (Ghassemi et al., 2002), the availability of low nutrients' density has extended the related problems (Azadbakht and Esmaillzadeh, 2008). Dietary habits and lifestyle characteristics of Iranian children across different cities may be different from those in the present study (Azadbakht et al., 2006, Azadbakht et al., 2005). B vitamins have the main role in brain function, so that niacinamide (vitamin B3) transfers tryptophan to serotonin (Imbalance, 2009, Kaplan et al., 2007). Micronutrient administration and nutritional status are important in ADHD children due to their role in regulating homocysteine metabolism (Huskisson et al., 2007), mood (Taylor et al., 2004, Wilkins et al., 2006), and neurotransmitter synthesis (Bottiglieri et al., 2000). Cobalt included in vitamin B12 (cyancobalamin) can create behavioral disturbances especially due to its lack of body. It improves functions of the frontal lobe and language in those with cognitive dysfunctions (Tudosie et al., 2017).
According to our results, magnesium and calcium intakes were significantly lower in cases than controls. However, in a case-control study, 11 ADHD participants reported slightly higher intakes of magnesium compared to the controls (Colter et al., 2008). Although the mechanisms linking low-quality diet and ADHD are still unknown, an unbalanced diet can lead to deficiencies in essential nutrients or higher intakes of certain food components (i.e, food additives) (Izquierdo-Pulido et al., 2015). Enzymes involved in the process of ATP hydrolysis by brain microsomes were activated in the presence of Mg and Ca (Nakamaru et al., 1967).
We observed that ADHD children were more active regarding physical activity, had allergies more frequently, used more medication, and had more frequent family history of ADHD than Iranian children without ADHD. Our finding is consistent with previous reports indicating that ADHD children had increased rates of allergic sensitization and allergic rhinitis than non ADHD children (Suwan et al., 2011). Another study also found that neuropsychological performance in ADHD was significantly affected by familial status (Seidman et al., 1995). However, a case-control study about physical activity experiences of 12 age-matched boys with and without ADHD revealed that boys with ADHD were not as proficient movers as their peers without ADHD (Harvey et al., 2009).
This was the first study in Iran that demonstrated significantly lower dietary intakes of micronutrients in ADHD children compared to non-ADHD children. In the current study, we assessed nutrient intakes in a large sample size of Iranian children. Children in the case and control groups did not have any significant difference with regard to their socioeconomic status. Vitamin and mineral supplementations were also recorded in the present research.
The present study has several limitations. As this was a case-control study, it is possible that dietary intake was affected by an individual’s health status. Results could differ by ADHD types, but information about ADHD type was not gathered for subgroup analysis.
Further research is needed to identify the etiology, impact, and possible therapeutic implications of low micronutrient status in ADHD given the essential nature of these micronutrients in producing neurotransmitters involved in ADHD.
Conclusion
This study established the dietary intake of ADHD children from Iranian population in taking nutrients. We found that ADHD children consumed significantly lower quantities of calcium, magnesium, vitamin C, and B vitamins except B6. Similarly, energy, carbohydrate, and fat intakes were lower in ADHD children.
Future studies are required on comparing dietary intakes and nutrients status, controlling for medication and supplementation, and including normal controls. Such research should be conducted to determine if micronutrient deficiency is a cause, effect, or related to a third variable involved in ADHD.
Acknowledgments
Authors appreciate Shahid Sadoughi University of Medical Sciences to support this research.
Authors’ contributions
Shareghfarid E and Hosseinzadeh M design the study and implementation of it, Shareghfarid E and Mohammadi M contributed to the data analysis with supervised of Salehi-abarguei A, all authors participated in writing manuscript and discussed the results and commented on the manuscript.
Conflicts of interest
Authors declared no conflict of interest.
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Kelishadi R, et al. 2007. Association of physical activity and dietary behaviours in relation to the body mass index in a national sample of Iranian children and adolescents: CASPIAN Study. Bulletin of the World Health Organization. 85 (1): 19-26.
Kiddie JY, Weiss MD, Kitts DD, Levy-Milne R & Wasdell MB 2010. Nutritional status of children with attention deficit hyperactivity disorder: a pilot study. International journal of pediatrics. 2010.
Kim Y & Chang H 2011. Correlation between attention deficit hyperactivity disorder and sugar consumption, quality of diet, and dietary behavior in school children. Nutrition research and practice. 5 (3): 236-245.
Konofal E, Lecendreux M, Arnulf I & Mouren M-C 2004. Iron deficiency in children with attention-deficit/hyperactivity disorder. Archives of pediatrics & adolescent medicine. 158 (12): 1113-1115.
Konofal E, et al. 2008. Effects of iron supplementation on attention deficit hyperactivity disorder in children. Pediatric neurology. 38 (1): 20-26.
Lahey BB, et al. 2006. Predictive validity of ICD‐10 hyperkinetic disorder relative to DSM‐IV attention‐deficit/hyperactivity disorder among younger children. Journal of child psychology and psychiatry. 47 (5): 472-479.
Lee J-K & Rhie S-G 2008. The effect of carbohydrate processed snacks on middle school students' emotional intelligence. Korean journal of community living science. 19 (3): 335-351.
Meysamie A, Fard MD & Mohammadi M-R 2011. Prevalence of attention-deficit/hyperactivity disorder symptoms in preschool-aged Iranian children. Iranian journal of pediatrics. 21 (4): 467.
Mousain-Bosc M, Roche M, Rapin J & Bali J-P 2004. Magnesium VitB6 intake reduces central nervous system hyperexcitability in children. Journal of the American college of nutrition. 23 (5): 545S-548S.
Nakamaru Y, Kosakai M & Konishi K 1967. Some properties of brain microsome adenosine triphosphatases activated by magnesium and calcium. Archives of biochemistry and biophysics. 120 (1): 15-21.
Neuringer M, Anderson GJ & Connor WE 1988. The essentiality of n-3 fatty acids for the development and function of the retina and brain. Annual review of nutrition. 8 (1): 517-541.
Øverby NC, Lillegaard IT, Johansson L & Andersen LF 2004. High intake of added sugar among Norwegian children and adolescents. Public health nutrition. 7 (2): 285-293.
Owens J & Hoza B 2003. Diagnostic utility of DSM-IV-TR symptoms in the prediction of DSM-IV-TR ADHD subtypes and ODD. Journal of attention disorders. 7 (1): 11-27.
Rader R, McCauley L & Callen EC 2009. Current strategies in the diagnosis and treatment of childhood attention-deficit/hyperactivity disorder. American family physician. 79 (8).
Schnoll R, Burshteyn D & Cea-Aravena J 2003. Nutrition in the treatment of attention-deficit hyperactivity disorder: a neglected but important aspect. Applied psychophysiology and biofeedback. 28 (1): 63-75.
Seidman LJ, et al. 1995. Effects of family history and comorbidity on the neuropsychological performance of children with ADHD: Preliminary findings. Journal of the American academy of child & adolescent psychiatry. 34 (8): 1015-1024.
Solanto MV 2002. Dopamine dysfunction in AD/HD: integrating clinical and basic neuroscience research. Behavioural brain research. 130 (1): 65-71.
Stevens LJ, et al. 1995. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. American journal of clinical nutrition. 62 (4): 761-768.
Suwan P, Akaramethathip D & Noipayak P 2011. Association between allergic sensitization and attention deficit hyperactivity disorder (ADHD). Asian Pacific journal of allergy and immunology. 29 (1): 57.
Taylor MJ, Carney SM, Goodwin GM & Geddes JR 2004. Folate for depressive disorders: systematic review and meta-analysis of randomized controlled trials. Journal of psychopharmacology. 18 (2): 251-256.
Thomas R, Sanders S, Doust J, Beller E & Glasziou P 2015. Prevalence of attention-deficit/hyperactivity disorder: a systematic review and meta-analysis. Pediatrics. 135 (4): e994-e1001.
Tudosie M, Truţă E, Daviţoiu AM, Mitu AM & Bojescu AA 2017. Optoelectronics method for determining the cobalt involved in symptoms of attention deficit hyperactivity disorder. In Electronics, Computers and Artificial Intelligence (ECAI), 2017 9th International Conference on, pp. 1-4. IEEE.
Visser SN, Bitsko RH, Danielson ML, Perou R & Blumberg SJ 2010. Increasing prevalence of parent-reported attention-deficit/hyperactivity disorder among children—United States, 2003 and 2007. Morbidity and mortality weekly report. 59 (44): 1439-1443.
Wilkins CH, Sheline YI, Roe CM, Birge SJ & Morris JC 2006. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. American journal of geriatric psychiatry. 14 (12): 1032-1040.
Zhou F, et al. 2016. Dietary, Nutrient Patterns and Blood Essential Elements in Chinese Children with ADHD. Nutrients. 8 (6): 352.
Energy, fat, and carbohydrate intakes were significantly lower in ADHD than healthy children. Similarly, consumption of calcium and magnesium were significantly lower in cases than controls. However, intakes of thiamin, riboflavin, niacin, vitamin B5, and vitamin C were significantly lower in cases than controls.
Based on the findings, macronutrient intakes were significantly lower in ADHD children. On the contrary, Stevens reported significantly higher intakes of total fat (g) in ADHD participants when compared to controls (Stevens et al., 1995). Another study showed that ADHD adolescents consumed more energy and fat than controls (Colter et al., 2008). ADHD children in the current study consumed less amounts of high nutrient density foods than normal gender-age matched children. Moreover, the mean age of children in this study was 8 years, but it was 14 in Colter study.
Results of vitamin intakes in this study showed that vitamin intakes were significantly lower in ADHD children than healthy ones. Similar to our results, previous studies showed that consumption of thiamin, riboflavin, niacin, vitamin B5, and vitamin C among ADHD children were lower than non-ADHD participants (Colter et al., 2008, Kiddie et al., 2010). In contrast to our conclusion, a case-control study demonstrated that ADHD participants consumed higher levels of at least 10 different nutrients, than their control counterparts (Colter et al., 2008). Furthermore, Chen et al. reported significantly increased vitamin C (mg) consumption in participants with ADHD versus controls (Chen et al., 2004). The difference between our results and previous studies may be due to higher energy intake in normal children than ADHD children. Considering that Iran has undergone a nutritional transition caused by a Westernization in lifestyle (Ghassemi et al., 2002), the availability of low nutrients' density has extended the related problems (Azadbakht and Esmaillzadeh, 2008). Dietary habits and lifestyle characteristics of Iranian children across different cities may be different from those in the present study (Azadbakht et al., 2006, Azadbakht et al., 2005). B vitamins have the main role in brain function, so that niacinamide (vitamin B3) transfers tryptophan to serotonin (Imbalance, 2009, Kaplan et al., 2007). Micronutrient administration and nutritional status are important in ADHD children due to their role in regulating homocysteine metabolism (Huskisson et al., 2007), mood (Taylor et al., 2004, Wilkins et al., 2006), and neurotransmitter synthesis (Bottiglieri et al., 2000). Cobalt included in vitamin B12 (cyancobalamin) can create behavioral disturbances especially due to its lack of body. It improves functions of the frontal lobe and language in those with cognitive dysfunctions (Tudosie et al., 2017).
According to our results, magnesium and calcium intakes were significantly lower in cases than controls. However, in a case-control study, 11 ADHD participants reported slightly higher intakes of magnesium compared to the controls (Colter et al., 2008). Although the mechanisms linking low-quality diet and ADHD are still unknown, an unbalanced diet can lead to deficiencies in essential nutrients or higher intakes of certain food components (i.e, food additives) (Izquierdo-Pulido et al., 2015). Enzymes involved in the process of ATP hydrolysis by brain microsomes were activated in the presence of Mg and Ca (Nakamaru et al., 1967).
We observed that ADHD children were more active regarding physical activity, had allergies more frequently, used more medication, and had more frequent family history of ADHD than Iranian children without ADHD. Our finding is consistent with previous reports indicating that ADHD children had increased rates of allergic sensitization and allergic rhinitis than non ADHD children (Suwan et al., 2011). Another study also found that neuropsychological performance in ADHD was significantly affected by familial status (Seidman et al., 1995). However, a case-control study about physical activity experiences of 12 age-matched boys with and without ADHD revealed that boys with ADHD were not as proficient movers as their peers without ADHD (Harvey et al., 2009).
This was the first study in Iran that demonstrated significantly lower dietary intakes of micronutrients in ADHD children compared to non-ADHD children. In the current study, we assessed nutrient intakes in a large sample size of Iranian children. Children in the case and control groups did not have any significant difference with regard to their socioeconomic status. Vitamin and mineral supplementations were also recorded in the present research.
The present study has several limitations. As this was a case-control study, it is possible that dietary intake was affected by an individual’s health status. Results could differ by ADHD types, but information about ADHD type was not gathered for subgroup analysis.
Further research is needed to identify the etiology, impact, and possible therapeutic implications of low micronutrient status in ADHD given the essential nature of these micronutrients in producing neurotransmitters involved in ADHD.
Conclusion
This study established the dietary intake of ADHD children from Iranian population in taking nutrients. We found that ADHD children consumed significantly lower quantities of calcium, magnesium, vitamin C, and B vitamins except B6. Similarly, energy, carbohydrate, and fat intakes were lower in ADHD children.
Future studies are required on comparing dietary intakes and nutrients status, controlling for medication and supplementation, and including normal controls. Such research should be conducted to determine if micronutrient deficiency is a cause, effect, or related to a third variable involved in ADHD.
Acknowledgments
Authors appreciate Shahid Sadoughi University of Medical Sciences to support this research.
Authors’ contributions
Shareghfarid E and Hosseinzadeh M design the study and implementation of it, Shareghfarid E and Mohammadi M contributed to the data analysis with supervised of Salehi-abarguei A, all authors participated in writing manuscript and discussed the results and commented on the manuscript.
Conflicts of interest
Authors declared no conflict of interest.
References
Aadahl M & Jørgensen T 2003. Validation of a new self-report instrument for measuring physical activity. Medicine and science in sports and exercise. 35 (7): 1196-1202.
Arnold LE, et al. 2005. Serum zinc correlates with parent-and teacher-rated inattention in children with attention-deficit/hyperactivity disorder. Journal of child & adolescent psychopharmacology. 15 (4): 628-636.
Asghari G, et al. 2012. Reliability, comparative validity and stability of dietary patterns derived from an FFQ in the Tehran Lipid and Glucose Study. British journal of nutrition. 108 (6): 1109-1117.
Azadbakht L & Esmaillzadeh A 2008. Fast foods and risk of chronic diseases. Journal of research in medical sciences. 13 (1): 1-2.
Azadbakht L, Mirmiran P & Azizi F 2006. Predictors of cardiovascular risk factors in Tehranian adults: diet and lifestyle. Eastern mediterranean health journal. 12 (1-2): 88-97.
Azadbakht L, Mirmiran P, Hosseini F & Azizi F 2005. Diet quality status of most Tehranian adults needs improvement. Asia Pacific journal of clinical nutrition. 14 (2).
Bekaroǧlu M, et al. 1996. Relationships between serum free fatty acids and zinc, and attention deficit hyperactivity disorder: a research note. Journal of child psychology and psychiatry. 37 (2): 225-227.
Bilici M, et al. 2004. Double-blind, placebo-controlled study of zinc sulfate in the treatment of attention deficit hyperactivity disorder. Progress in neuro-psychopharmacology and biological psychiatry. 28 (1): 181-190.
Bottiglieri T, et al. 2000. Homocysteine, folate, methylation, and monoamine metabolism in depression. Journal of neurology, neurosurgery & psychiatry. 69 (2): 228-232.
Chang JP-C, Jingling L, Huang Y-T, Lu Y-J & Su K-P 2016. Delay Aversion, Temporal Processing, and N-3 Fatty Acids Intake in Children With Attention-Deficit/Hyperactivity Disorder (ADHD). Clinical psychological science. 4 (6): 1094-1103.
Chen J-R, Hsu S-F, Hsu C-D, Hwang L-H & Yang S-C 2004. Dietary patterns and blood fatty acid composition in children with attention-deficit hyperactivity disorder in Taiwan. Journal of nutritional biochemistry. 15 (8): 467-472.
Choi M-H, et al. 2008. Monitoring of total sugar contents in processed foods and noncommercial foodservice foods. Korean journal of food science and technology. 40 (3): 337-342.
Cole TJ, Bellizzi MC, Flegal KM & Dietz WH 2000. Establishing a standard definition for child overweight and obesity worldwide: international survey. British medical journal. 320 (7244): 1240.
Colter AL, Cutler C & Meckling KA 2008. Fatty acid status and behavioural symptoms of attention deficit hyperactivity disorder in adolescents: a case-control study. Nutrition journal. 7 (1): 8.
Dykman KD & Dykman RA 1998. Effect of nutritional supplements on attentional-deficit hyperactivity disorder. Integrative physiological and behavioral science. 33 (1): 49-60.
Erikson KM, Jones BC, Hess EJ, Zhang Q & Beard JL 2001. Iron deficiency decreases dopamine D 1 and D 2 receptors in rat brain. Pharmacology biochemistry and behavior. 69 (3): 409-418.
Gershoff SN 1993. Vitamin C (ascorbic acid): new roles, new requirements? Nutrition reviews. 51 (11): 313-326.
Ghassemi H, Harrison G & Mohammad K 2002. An accelerated nutrition transition in Iran. Public health nutrition. 5 (1a): 149-155.
Goldfield GS, Lorello C & Doucet É 2007. Methylphenidate reduces energy intake and dietary fat intake in adults: a mechanism of reduced reinforcing value of food? American journal of clinical nutrition. 86 (2): 308-315.
Harvey WJ, et al. 2009. Physical activity experiences of boys with and without ADHD. Adapted physical activity quarterly. 26 (2): 131-150.
Huskisson E, Maggini S & Ruf M 2007. The influence of micronutrients on cognitive function and performance. Journal of international medical research. 35 (1): 1-19.
Imbalance A 2009. Nutrients and botanicals for treatment of stress: adrenal fatigue, neurotransmitter imbalance, anxiety, and restless sleep. Alternative medicine review. 14 (2): 114-140.
Izquierdo-Pulido M, Ríos A, Farran-Codina A & Alda JÁ 2015. The role of diet and physical activity in children and adolescents with ADHD'. In Recent advances in pharmaceutical V (ed. M. Diego Muñoz Torrero, V. Pilar and P. Javier), pp. 51-64.
Jang BY & Bu SY 2017. Nutritional Status of Korean Children and Adolescents with Attention Deficit Hyperactivity Disorder (ADHD). Clinical nutrition research. 6 (2): 112-121.
Kamal M, Bener A & Ehlayel MS 2014. Is high prevalence of vitamin D deficiency a correlate for attention deficit hyperactivity disorder? Attention deficit and hyperactivity disorders. 6 (2): 73-78.
Kaplan BJ, Crawford SG, Field CJ & Simpson JSA 2007. Vitamins, minerals, and mood. Psychological bulletin. 133 (5): 747.
Kaplan BJ, McNicol J, Conte RA & Moghadam H 1989. Overall nutrient intake of preschool hyperactive and normal boys. Journal of abnormal child psychology. 17 (2): 127-132.
Kavale KA & Forness SR 1983. Hyperactivity and diet treatment: a meta-analysis of the Feingold hypothesis. Journal of learning disabilities. 16 (6): 324-330.
Kelishadi R, et al. 2007. Association of physical activity and dietary behaviours in relation to the body mass index in a national sample of Iranian children and adolescents: CASPIAN Study. Bulletin of the World Health Organization. 85 (1): 19-26.
Kiddie JY, Weiss MD, Kitts DD, Levy-Milne R & Wasdell MB 2010. Nutritional status of children with attention deficit hyperactivity disorder: a pilot study. International journal of pediatrics. 2010.
Kim Y & Chang H 2011. Correlation between attention deficit hyperactivity disorder and sugar consumption, quality of diet, and dietary behavior in school children. Nutrition research and practice. 5 (3): 236-245.
Konofal E, Lecendreux M, Arnulf I & Mouren M-C 2004. Iron deficiency in children with attention-deficit/hyperactivity disorder. Archives of pediatrics & adolescent medicine. 158 (12): 1113-1115.
Konofal E, et al. 2008. Effects of iron supplementation on attention deficit hyperactivity disorder in children. Pediatric neurology. 38 (1): 20-26.
Lahey BB, et al. 2006. Predictive validity of ICD‐10 hyperkinetic disorder relative to DSM‐IV attention‐deficit/hyperactivity disorder among younger children. Journal of child psychology and psychiatry. 47 (5): 472-479.
Lee J-K & Rhie S-G 2008. The effect of carbohydrate processed snacks on middle school students' emotional intelligence. Korean journal of community living science. 19 (3): 335-351.
Meysamie A, Fard MD & Mohammadi M-R 2011. Prevalence of attention-deficit/hyperactivity disorder symptoms in preschool-aged Iranian children. Iranian journal of pediatrics. 21 (4): 467.
Mousain-Bosc M, Roche M, Rapin J & Bali J-P 2004. Magnesium VitB6 intake reduces central nervous system hyperexcitability in children. Journal of the American college of nutrition. 23 (5): 545S-548S.
Nakamaru Y, Kosakai M & Konishi K 1967. Some properties of brain microsome adenosine triphosphatases activated by magnesium and calcium. Archives of biochemistry and biophysics. 120 (1): 15-21.
Neuringer M, Anderson GJ & Connor WE 1988. The essentiality of n-3 fatty acids for the development and function of the retina and brain. Annual review of nutrition. 8 (1): 517-541.
Øverby NC, Lillegaard IT, Johansson L & Andersen LF 2004. High intake of added sugar among Norwegian children and adolescents. Public health nutrition. 7 (2): 285-293.
Owens J & Hoza B 2003. Diagnostic utility of DSM-IV-TR symptoms in the prediction of DSM-IV-TR ADHD subtypes and ODD. Journal of attention disorders. 7 (1): 11-27.
Rader R, McCauley L & Callen EC 2009. Current strategies in the diagnosis and treatment of childhood attention-deficit/hyperactivity disorder. American family physician. 79 (8).
Schnoll R, Burshteyn D & Cea-Aravena J 2003. Nutrition in the treatment of attention-deficit hyperactivity disorder: a neglected but important aspect. Applied psychophysiology and biofeedback. 28 (1): 63-75.
Seidman LJ, et al. 1995. Effects of family history and comorbidity on the neuropsychological performance of children with ADHD: Preliminary findings. Journal of the American academy of child & adolescent psychiatry. 34 (8): 1015-1024.
Solanto MV 2002. Dopamine dysfunction in AD/HD: integrating clinical and basic neuroscience research. Behavioural brain research. 130 (1): 65-71.
Stevens LJ, et al. 1995. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. American journal of clinical nutrition. 62 (4): 761-768.
Suwan P, Akaramethathip D & Noipayak P 2011. Association between allergic sensitization and attention deficit hyperactivity disorder (ADHD). Asian Pacific journal of allergy and immunology. 29 (1): 57.
Taylor MJ, Carney SM, Goodwin GM & Geddes JR 2004. Folate for depressive disorders: systematic review and meta-analysis of randomized controlled trials. Journal of psychopharmacology. 18 (2): 251-256.
Thomas R, Sanders S, Doust J, Beller E & Glasziou P 2015. Prevalence of attention-deficit/hyperactivity disorder: a systematic review and meta-analysis. Pediatrics. 135 (4): e994-e1001.
Tudosie M, Truţă E, Daviţoiu AM, Mitu AM & Bojescu AA 2017. Optoelectronics method for determining the cobalt involved in symptoms of attention deficit hyperactivity disorder. In Electronics, Computers and Artificial Intelligence (ECAI), 2017 9th International Conference on, pp. 1-4. IEEE.
Visser SN, Bitsko RH, Danielson ML, Perou R & Blumberg SJ 2010. Increasing prevalence of parent-reported attention-deficit/hyperactivity disorder among children—United States, 2003 and 2007. Morbidity and mortality weekly report. 59 (44): 1439-1443.
Wilkins CH, Sheline YI, Roe CM, Birge SJ & Morris JC 2006. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. American journal of geriatric psychiatry. 14 (12): 1032-1040.
Zhou F, et al. 2016. Dietary, Nutrient Patterns and Blood Essential Elements in Chinese Children with ADHD. Nutrients. 8 (6): 352.
Type of article: orginal article |
Subject:
public specific
Received: 2018/09/21 | Published: 2020/05/1 | ePublished: 2020/05/1
Received: 2018/09/21 | Published: 2020/05/1 | ePublished: 2020/05/1
References
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2. Arnold LE, et al. 2005. Serum zinc correlates with parent-and teacher-rated inattention in children with attention-deficit/hyperactivity disorder. Journal of child & adolescent psychopharmacology. 15 (4): 628-636.
3. Asghari G, et al. 2012. Reliability, comparative validity and stability of dietary patterns derived from an FFQ in the Tehran Lipid and Glucose Study. British journal of nutrition. 108 (6): 1109-1117.
4. Azadbakht L & Esmaillzadeh A 2008. Fast foods and risk of chronic diseases. Journal of research in medical sciences. 13 (1): 1-2.
5. Azadbakht L, Mirmiran P & Azizi F 2006. Predictors of cardiovascular risk factors in Tehranian adults: diet and lifestyle. Eastern mediterranean health journal. 12 (1-2): 88-97.
6. Azadbakht L, Mirmiran P, Hosseini F & Azizi F 2005. Diet quality status of most Tehranian adults needs improvement. Asia Pacific journal of clinical nutrition. 14 (2).
7. Bekaroǧlu M, et al. 1996. Relationships between serum free fatty acids and zinc, and attention deficit hyperactivity disorder: a research note. Journal of child psychology and psychiatry. 37 (2): 225-227.
8. Bilici M, et al. 2004. Double-blind, placebo-controlled study of zinc sulfate in the treatment of attention deficit hyperactivity disorder. Progress in neuro-psychopharmacology and biological psychiatry. 28 (1): 181-190.
9. Bottiglieri T, et al. 2000. Homocysteine, folate, methylation, and monoamine metabolism in depression. Journal of neurology, neurosurgery & psychiatry. 69 (2): 228-232.
10. Chang JP-C, Jingling L, Huang Y-T, Lu Y-J & Su K-P 2016. Delay Aversion, Temporal Processing, and N-3 Fatty Acids Intake in Children With Attention-Deficit/Hyperactivity Disorder (ADHD). Clinical psychological science. 4 (6): 1094-1103.
11. Chen J-R, Hsu S-F, Hsu C-D, Hwang L-H & Yang S-C 2004. Dietary patterns and blood fatty acid composition in children with attention-deficit hyperactivity disorder in Taiwan. Journal of nutritional biochemistry. 15 (8): 467-472.
12. Choi M-H, et al. 2008. Monitoring of total sugar contents in processed foods and noncommercial foodservice foods. Korean journal of food science and technology. 40 (3): 337-342.
13. Cole TJ, Bellizzi MC, Flegal KM & Dietz WH 2000. Establishing a standard definition for child overweight and obesity worldwide: international survey. British medical journal. 320 (7244): 1240.
14. Colter AL, Cutler C & Meckling KA 2008. Fatty acid status and behavioural symptoms of attention deficit hyperactivity disorder in adolescents: a case-control study. Nutrition journal. 7 (1): 8.
15. Dykman KD & Dykman RA 1998. Effect of nutritional supplements on attentional-deficit hyperactivity disorder. Integrative physiological and behavioral science. 33 (1): 49-60.
16. Erikson KM, Jones BC, Hess EJ, Zhang Q & Beard JL 2001. Iron deficiency decreases dopamine D 1 and D 2 receptors in rat brain. Pharmacology biochemistry and behavior. 69 (3): 409-418.
17. Gershoff SN 1993. Vitamin C (ascorbic acid): new roles, new requirements? Nutrition reviews. 51 (11): 313-326.
18. Ghassemi H, Harrison G & Mohammad K 2002. An accelerated nutrition transition in Iran. Public health nutrition. 5 (1a): 149-155.
19. Goldfield GS, Lorello C & Doucet É 2007. Methylphenidate reduces energy intake and dietary fat intake in adults: a mechanism of reduced reinforcing value of food? American journal of clinical nutrition. 86 (2): 308-315.
20. Harvey WJ, et al. 2009. Physical activity experiences of boys with and without ADHD. Adapted physical activity quarterly. 26 (2): 131-150.
21. Huskisson E, Maggini S & Ruf M 2007. The influence of micronutrients on cognitive function and performance. Journal of international medical research. 35 (1): 1-19.
22. Imbalance A 2009. Nutrients and botanicals for treatment of stress: adrenal fatigue, neurotransmitter imbalance, anxiety, and restless sleep. Alternative medicine review. 14 (2): 114-140.
23. Izquierdo-Pulido M, Ríos A, Farran-Codina A & Alda JÁ 2015. The role of diet and physical activity in children and adolescents with ADHD'. In Recent advances in pharmaceutical V (ed. M. Diego Muñoz Torrero, V. Pilar and P. Javier), pp. 51-64.
24. Jang BY & Bu SY 2017. Nutritional Status of Korean Children and Adolescents with Attention Deficit Hyperactivity Disorder (ADHD). Clinical nutrition research. 6 (2): 112-121.
25. Kamal M, Bener A & Ehlayel MS 2014. Is high prevalence of vitamin D deficiency a correlate for attention deficit hyperactivity disorder? Attention deficit and hyperactivity disorders. 6 (2): 73-78.
26. Kaplan BJ, Crawford SG, Field CJ & Simpson JSA 2007. Vitamins, minerals, and mood. Psychological bulletin. 133 (5): 747.
27. Kaplan BJ, McNicol J, Conte RA & Moghadam H 1989. Overall nutrient intake of preschool hyperactive and normal boys. Journal of abnormal child psychology. 17 (2): 127-132.
28. Kavale KA & Forness SR 1983. Hyperactivity and diet treatment: a meta-analysis of the Feingold hypothesis. Journal of learning disabilities. 16 (6): 324-330.
29. Kelishadi R, et al. 2007. Association of physical activity and dietary behaviours in relation to the body mass index in a national sample of Iranian children and adolescents: CASPIAN Study. Bulletin of the World Health Organization. 85 (1): 19-26.
30. Kiddie JY, Weiss MD, Kitts DD, Levy-Milne R & Wasdell MB 2010. Nutritional status of children with attention deficit hyperactivity disorder: a pilot study. International journal of pediatrics. 2010.
31. Kim Y & Chang H 2011. Correlation between attention deficit hyperactivity disorder and sugar consumption, quality of diet, and dietary behavior in school children. Nutrition research and practice. 5 (3): 236-245.
32. Konofal E, Lecendreux M, Arnulf I & Mouren M-C 2004. Iron deficiency in children with attention-deficit/hyperactivity disorder. Archives of pediatrics & adolescent medicine. 158 (12): 1113-1115.
33. Konofal E, et al. 2008. Effects of iron supplementation on attention deficit hyperactivity disorder in children. Pediatric neurology. 38 (1): 20-26.
34. Lahey BB, et al. 2006. Predictive validity of ICD‐10 hyperkinetic disorder relative to DSM‐IV attention‐deficit/hyperactivity disorder among younger children. Journal of child psychology and psychiatry. 47 (5): 472-479.
35. Lee J-K & Rhie S-G 2008. The effect of carbohydrate processed snacks on middle school students' emotional intelligence. Korean journal of community living science. 19 (3): 335-351.
36. Meysamie A, Fard MD & Mohammadi M-R 2011. Prevalence of attention-deficit/hyperactivity disorder symptoms in preschool-aged Iranian children. Iranian journal of pediatrics. 21 (4): 467.
37. Mousain-Bosc M, Roche M, Rapin J & Bali J-P 2004. Magnesium VitB6 intake reduces central nervous system hyperexcitability in children. Journal of the American college of nutrition. 23 (5): 545S-548S.
38. Nakamaru Y, Kosakai M & Konishi K 1967. Some properties of brain microsome adenosine triphosphatases activated by magnesium and calcium. Archives of biochemistry and biophysics. 120 (1): 15-21.
39. Neuringer M, Anderson GJ & Connor WE 1988. The essentiality of n-3 fatty acids for the development and function of the retina and brain. Annual review of nutrition. 8 (1): 517-541.
40. Øverby NC, Lillegaard IT, Johansson L & Andersen LF 2004. High intake of added sugar among Norwegian children and adolescents. Public health nutrition. 7 (2): 285-293.
41. Owens J & Hoza B 2003. Diagnostic utility of DSM-IV-TR symptoms in the prediction of DSM-IV-TR ADHD subtypes and ODD. Journal of attention disorders. 7 (1): 11-27.
42. Rader R, McCauley L & Callen EC 2009. Current strategies in the diagnosis and treatment of childhood attention-deficit/hyperactivity disorder. American family physician. 79 (8).
43. Schnoll R, Burshteyn D & Cea-Aravena J 2003. Nutrition in the treatment of attention-deficit hyperactivity disorder: a neglected but important aspect. Applied psychophysiology and biofeedback. 28 (1): 63-75.
44. Seidman LJ, et al. 1995. Effects of family history and comorbidity on the neuropsychological performance of children with ADHD: Preliminary findings. Journal of the American academy of child & adolescent psychiatry. 34 (8): 1015-1024.
45. Solanto MV 2002. Dopamine dysfunction in AD/HD: integrating clinical and basic neuroscience research. Behavioural brain research. 130 (1): 65-71.
46. Stevens LJ, et al. 1995. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. American journal of clinical nutrition. 62 (4): 761-768.
47. Suwan P, Akaramethathip D & Noipayak P 2011. Association between allergic sensitization and attention deficit hyperactivity disorder (ADHD). Asian Pacific journal of allergy and immunology. 29 (1): 57.
48. Taylor MJ, Carney SM, Goodwin GM & Geddes JR 2004. Folate for depressive disorders: systematic review and meta-analysis of randomized controlled trials. Journal of psychopharmacology. 18 (2): 251-256.
49. Thomas R, Sanders S, Doust J, Beller E & Glasziou P 2015. Prevalence of attention-deficit/hyperactivity disorder: a systematic review and meta-analysis. Pediatrics. 135 (4): e994-e1001.
50. Tudosie M, Truţă E, Daviţoiu AM, Mitu AM & Bojescu AA 2017. Optoelectronics method for determining the cobalt involved in symptoms of attention deficit hyperactivity disorder. In Electronics, Computers and Artificial Intelligence (ECAI), 2017 9th International Conference on, pp. 1-4. IEEE.
51. Visser SN, Bitsko RH, Danielson ML, Perou R & Blumberg SJ 2010. Increasing prevalence of parent-reported attention-deficit/hyperactivity disorder among children—United States, 2003 and 2007. Morbidity and mortality weekly report. 59 (44): 1439-1443.
52. Wilkins CH, Sheline YI, Roe CM, Birge SJ & Morris JC 2006. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. American journal of geriatric psychiatry. 14 (12): 1032-1040.
53. Zhou F, et al. 2016. Dietary, Nutrient Patterns and Blood Essential Elements in Chinese Children with ADHD. Nutrients. 8 (6): 352.
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