Attention Deficit/Hyperactivity Disorder (ADHD)
Causes and Risk Factors
No single factor has been identified as a definitive cause of ADHD. Instead, most scientists believe that several variables influence ADHD risk. For example, genetics, exposure to stressors during pregnancy or infancy, early social interactions, and environmental toxins all appear to affect ADHD risk (Thapar 2013).
A considerable portion of ADHD cases are thought to be attributable to genetics and heritability (Neale 2010). A number of specific genetic variations are associated with ADHD. These are predominantly related to the regulation of dopamine (ie, a chemical messenger used by brain cells) (Faraone 2006; Thapar 2013; Franke 2012). The importance of dopamine in ADHD is highlighted by the fact that methylphenidate is thought to treat ADHD symptoms in part by increasing dopamine signaling in the brain (Volkow 2005).
Environmental toxins such as polychlorinated biphenyls, some pesticides, and lead have been linked to ADHD development, but no studies have proven that they directly cause the condition (Thapar 2013).Other external factors, such as negative child-parent interactions and poor or lacking early social contact, have been found to have a contributory effect in ADHD onset (McLaughlin 2010; Thapar 2013). Some variables in utero (in the womb) are seen as risk factors, but not causative links to ADHD. These include maternal smoking during pregnancy, premature birth and/or low birth weight, and/or maternal stress (Thapar 2013).
Traumatic brain injury has been linked to behaviors similar to those observed in ADHD (Eme 2012; NIH 2013a). Approximately 20–50% of children who suffer a traumatic brain injury develop a form of clinically relevant attention disorder termed secondary ADHD (Senior 2013; Ornstein 2013; Sinopoli 2011).
There is some evidence that deficiencies in certain nutrients, such as zinc, magnesium, and polyunsaturated fatty acids may be linked to ADHD (Thapar 2013). As will be discussed later in this protocol, studies have found evidence for insufficiency or imbalance of omega-3 and omega-6 fatty acids in people with ADHD (Colter 2008). Zinc and magnesium intake have also been found to be reduced in those with ADHD (Dura Trave 2013). Additionally, there is some evidence that high levels of ingested food additives such as artificial coloring (eg, tartrazine (E103), quinolone yellow (E104), sunset yellow (E110), carmoisine (E122), ponceau 4R (E124) and allura red (E129)) correlate with increased activity in children and therefore may exacerbate this symptom in those with ADHD (Stevens 2013). Excessive sugar intake has often been linked to ADHD as well, although the majority of research has largely debunked this as unsubstantiated; definitive evidence for a causal relationship is currently lacking (Johnson 2011). Nevertheless, it is generally advisable to limit sugar intake, as high sugar consumption may contribute to numerous other health detriments.
Sleep Disorders and ADHD
Several lines of evidence suggest a relationship between ADHD and sleep disorders such as sleep apnea. It has been reported that up to 95% of obstructive sleep apnea sufferers experience attentional deficits, and obstructive sleep apnea has been observed in up to 30% of individuals with ADHD. Moreover, successfully treating obstructive sleep apnea appears to relieve ADHD symptoms in some individuals (Youssef 2011). Overall, sleep disorders have been observed in up to 30% of children and 80% of adults with ADHD (Yoon 2012).
It is important for physicians to realize that symptoms of sleep disorders such as sleep apnea or restless leg syndrome can resemble those of ADHD in both children and adults. Otherwise, a person may be misdiagnosed with ADHD when their symptoms are actually the consequence of a sleep disorder (Philipsen 2006; Owens 2005).
Despite intensive study and an active body of research, it is not entirely clear whether sleep disorders directly cause ADHD or vise-versa, or if the conditions have a high rate of concurrence yet remain distinct entities (Stein 2012; Yoon 2012).
Sleep and ADHD must also be contemporaneously considered since stimulant medications like methylphenidate, which are used to treat ADHD, may contribute to impaired sleep patterns. In a study on 93 children with ADHD, methylphenidate treatment was shown to considerably delay bedtimes and lead to reduced total sleep duration (Lee 2012). On the other hand, some studies have found that methylphenidate treatment does not disrupt sleep habits and may lead to better sleep quality in certain populations (Tomas Vila 2010; Faraone 2009). Since the impact of methylphenidate on sleep patterns appears not to be uniform in all individuals, a reasonable approach is to carefully monitor sleep habits following treatment initiation. If signs of diminished sleep duration or quality emerge, consult with a healthcare provider about dose-adjustment or pursuing a different treatment option.