Attention-Deficit Hyperactivity Disorder (ADHD) is a neurobehavioral disorder, and one of the most common neurodevelopmental disorders in childhood that is characterized by developmentally inappropriate behaviors of inattention, and/or impulsivity and hyperactivity. These behavioral manifestations contribute to diminish academic, occupational and social functioning (American Psychiatric Association (APA) 2013).
In this study, 40.5% of children were normal weight, 40.5% were overweight and 19% were obese before diet modification (˃ ½ of patients were overweight and obese) going with the systematic review and meta-analysis by Cortese and Vincenzi (2011) who found that the prevalence of ADHD in clinical samples of patients seeking treatment for their obesity is higher than that in the general population. Also, Cortese and Tessari (2017) showed a significant association between ADHD and obesity with a possible explanation that obesity and factors associated with it (such as sleep-disordered breathing and deficits in arousal/alertness) manifest as ADHD-like symptoms or that ADHD and obesity share common genetics and neurobiological dysfunctions, involving the dopaminergic system.
After diet modification program, 53% became normal weight, 32% overweight and 7% obese with significant reduction in weight and body mass index (BMI) implicating effectiveness of diet modification intervention in weight reduction.
The obese patients had higher scores of hyperactivity index of Conner’s parent rating scale (CPR-RS) at baseline period as shown by ANOVA test (F = 6.8 and sig.003). A study of Hamid et al. (2015) on Egyptian children found that childhood obesity was associated with serum levels of monocyte chemoattractant protein-1 (MCP-1) and interlukin-6 (IL-6) predisposing to systemic inflammation including neuroinflammation causing foggy brain and development of neuropsychiatric disorders and this is also reported by a study performed by Theoharides et al. (2015).
In comparison to Tong et al. (2017) who concluded that ADHD contributed to emotional eating and bulimia nervosa but there was no significant relationship between ADHD and BMI.
The present study showed positive effect of the diet modification on ADHD outcome, it was noted that there was a decrease in the behavioral disturbance as assessed by CPR-RS. All subscales of CPR-RS decreased statistically significantly after diet modification. There was statistically significant decrease in hyperactivity index scores, hyperactivity/impulsivity scores and learning problems after diet program (66.21 ± 12.95 vs. 64.06 ± 11.98), (65.93 ± 7.36 vs. 64.31 ± 6.93), (71.85 ± 12.58 vs.70.14 ± 11.82).
There is notable similarities between these findings and another study performed by Pelsser et al. (2011) in which children aged 4–8 year diagnosed with ADHD were randomly assigned to 5 weeks of a restricted elimination diet (diet group) or to instructions for a healthy diet (control group), the difference between the diet group and the control group in the mean of abbreviated Conner’s scale (ACS) score at end of the 5 weeks was significant (p < 0·0001) showing effectiveness of this diet in improving symptomatology of ADHD.
In line with this study, Benton (2007) and Nigg and Holton (2014) reported that few foods diet (FFD) which consists of “lamb, chicken, potatoes, rice, banana, apple and cabbage; foods for a period of one week has a positive effect in case of comorbid food allergy with ADHD. That was in accordance with Beela abd Raji (2017) who detected improvement in ADHD symptoms after reduction in carbohydrate intake in group of Korean children aged from (4–12) years in comparison to control group who are diagnosed with ADHD but did not follow carbohydrate restriction. Also, Lien et al. (2006) found that the odds ratios for mental difficulties, hyperactivity and conduct problems were highest in those reporting the greatest levels of simple sugar consumption.
In this study, the energy intake after diet modification decreased with no significant difference from energy intake before diet modification (p value .08). But, there was statistically significant reduction in carbohydrate intake of patients after diet modification (t = 4.1, p = .000).
Significant positive correlation existed between both carbohydrate intake of the patients during baseline and hyperactivity index scores of CPR scale and learning problem scores of CPR scale during baseline (r = 0.3and 0.29, respectively, and p value = .03 and.04, respectively). This can be explained by the intake of foods high on the glycemic index lead to oscillating blood sugar levels that are reflected in behavior, as blood sugar goes up, and then crashes, triggering the release of stress hormones like adrenaline and in the same time homeostasis of blood and cellular glucose is very important for the functioning of the central nervous system (CNS), that fits the same research by Cryer (2008) and Akaltun et al. (2019).
While another study of Kim and Chang (2011) which was performed on Korean fifth grade children found no relationship between consumption of carbohydrates and hyperactivity behavior.
In this study, any food containing artificial colorings, additives, preservatives or gluten were excluded and eliminated from the diet modification program and that was associated with improvement in behavior as measured by CPR going with many studies evaluated the effect of food color restriction as Schab and Trinh (2004), Nigg et al. (2012), Sonuga-Barke et al. (2013) and Stevenson et al. (2014) who concluded that there was reliable effect when synthetic food colors were restricted.
Also, Bateman et al. (2004) found that children when subjected to a diet eliminating artificial colorings and benzoate preservatives for 1 week showed significant reduction in hyperactive behavior; in the subsequent 3 weeks and when they received random order periods of dietary challenge with a drink containing artificial colorings (20 mg daily) and sodium benzoate, they showed greater increase in hyperactive behavior.
This could be explained by that sulfotransferase inhibitors found in artificial food colors lead to increment of catechol amines, with negative effects on proper functioning of the prefrontal cortex where ADHD behavior can arise as mentioned by Eagle (2014) and Nigg and Holton (2014) or due to erythrosine-induced inhibition of serotonergic activity and corticosterone effects of erythrosine which could affect brain function without crossing the blood–brain barrier as explained with Dalal and Podar (2010).
In current study, the protein intake of patients decreased significantly after diet modification (p = 0.000 and t test = 6.41), As with Kim and Chang (2011), who found that at risk children for ADHD had higher protein intakes than non-risk group. Also Niederhofer (2011) found that gluten free diet improved ADHD symptoms.
Czaja-Bulsa (2015) explained that gluten-related disorders (celiac disease, gluten allergy, non-celiac gluten sensitivity) are associated with behavioral disorders as disturbance in attention and hyperactivity. Also, Zelnik et al. (2004) found that 20.7% of celiac disease (CD) patients had evidence of learning disability/ADHD compared with only 10.5% of control patients which necessitate further checking for celiac disease in the ADHD symptom checklist.
The elimination of milk, eggs and dairy products in this study come in line with some studies as Elder et al. (2006) and Taylor et al. (2018) which showed that a diet free of cow milk, egg and related by-products, and several histamine-releasers foods, produced a notable improvement of both attention and hyperkinesia in 79% of cases.
Yaghmaie et al. (2013) reported that allergic response to milk, eggs and dairy products was paralleled by increasing prevalence of mental health problems such as attention-deficit/hyperactivity disorder (ADHD) and depression. On the contrary, a study of Park et al. (2012) found that high intake of dairy products is associated with less learning, attention, and behavioral problems.
In current study, fat intake increased after diet modification, the mean of fat intake was 73 ± 21.6 g while after diet modification, it is 84.9 ± 12.5 g with statistically significant increment (p = 0.007). Maalouf et al. (2009) and Bostock et al. (2017) showed that calorie restriction and high fat intake diet possess broad therapeutic potential in various neurological diseases.
In this study, mean dietary intake of vitamin A and vitamin C decreased statistically significantly after diet modification and there was significant negative correlation between vitamin A intakes during baseline and hyperactivity index scores of CPR scale during baseline (Pearson correlation − 0.318 and significance 0.03).
In the same context are Kim and Chang (2011) who reported that vitamin A and C intakes in risk group of Korean children did not reach the daily recommended level and Mikirova (2015) who found that subjects with ADHD were deficient in nutrients such as zinc, vitamin B3, magnesium, and vitamin C.
Annelies et al. (2018) showed that vitamin A and C have some antioxidant and neuroprotective effect. That can be explained by that vitamin C is critical component of the antioxidant system. Oxidative stress caused by chronic inflammation, heavy metal or other environmental exposures, and hyperexcited neurons place heavy demands on the brain’s antioxidant system as fit with Lopresti (2015).