Most cited article - PubMed ID 21859418
Salivary melatonin rhythm as a marker of the circadian system in healthy children and those with attention-deficit/hyperactivity disorder
BACKGROUND: Adult attention-deficit/hyperactivity disorder (ADHD) has been added as a diagnosis to the Diagnostic and Statistical Manual of Mental Disorders version 5 (DSM5) in 2013, thus making ADHD, which has been classically known as a childhood disorder, a life-long disorder. Those suffering from the condition show very specific behavioral traits, which manifest as lifestyle habits; they also show comorbidities that can be the symptoms and/or consequences of certain lifestyles. MATERIALS AND METHODS: The targeted population was adults aged 18-65 years. The total sample was 1,012 (507 males and 505 females). The Adult ADHD Self-Report Scale (ASRS V. 1.1) was administered to evaluate the current symptoms of ADHD and a questionnaire regarding lifestyles that are pertinent to ADHD, exercise, drug use, and diet. RESULTS: An ASRS score of 4-6 points was found in 11.4% of the male population and 9.7% of the female population (5-6 points indicate very high-intensity symptoms). A score of 6, the highest intensity of symptomatology, was found in 1.18% of males and 0.99% of females. Gender differences in scores were not statistically significant. In terms of self-reported lifestyles, we calculated an ordered logistic regression and the odds ratios of those with ASRS scores >4. Those with higher ASRS scores had higher rates of self-reported unhealthy lifestyles and poor diets with high consumption of sweets. We also ascertained a paradoxical finding that is not in line with the current literature on the disorder - lower rates of cigarette smoking among people with higher ADHD symptomatology. CONCLUSION: Several specific lifestyles were found to be associated with higher ADHD symptoms such as poor diet and cannabis use. Other factors classically associated with the disorder such as cocaine addiction and nicotinism were either insignificant or surprisingly less prominent among the Czech sample. However, ADHD-prone respondents reported to be more physically active, which fits the clinical picture of hyperactivity but contrasts with literature that reports sedentary ADHD lifestyle.
The review examines Attention Deficit Hyperactivity Disorder (ADHD in its Child and Adult form) and its various presentations (Hyperactive Impulsive, Inattentive, and Combined) with a particular focus on environmental (incl. social factors), lifestyles and comorbidities. It is argued that ADHD is best understood in a holistic and interactive context and a vast empirical literature is presented to illustrate the point: Environmental factors include stress in general as well as exposure to toxins (phthalates, bisphenol A). Social factors are illustrated by effects of social deprivation and seduction to unhealthy lifestyles. Maternal lifestyle during pregnancy is pointed out (particularly her exposure to nicotine, alcohol, caffeine, and drugs, even seemingly benign medications like acetaminophen), which all tend to be related to ADHD. Family environment is discussed with respect to protective effect of (mainly authoritative and autocratic) parenting styles. Societal factors include mainly economic and political issues: income inequality and poverty (low SES is an ADHD risk factor) and a growing moral dilemma between a humanistic effort to globally spread the knowledge of ADHD and the medicalization and commercialization of the disorder. The second part of the review is devoted to ADHD related lifestyles and resulting comorbidities (e.g., food addiction and obesity, substance abuse, electronic media dependencies and conduct and personality disorders). Although ADHD is a neurodevelopmental disorder, its assessment and treatment are also linked to environmental, behavioral and social factors and their interactions.
- Keywords
- ADHD, alcohol, childhood, comorbidities, obesity, pollution, smoking, substance abuse,
- Publication type
- Journal Article MeSH
- Review MeSH
Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder that often persists in adulthood. It is defined by inattention and/or hyperactivity-impulsivity. ADHD is associated with many comorbidities, including eating disorders (EDs). In the last decade, studies have reported that ADHD is linked with binge EDs, bulimia nervosa, and anorexia nervosa. Many postulates have been proposed to explain the association: 1) impulsive behavior in ADHD patients leads to disordered eating behavior; 2) other psychologic comorbidities present in ADHD patients account for eating behavior; 3) poor eating habits and resulting nutritional deficiencies contribute to ADHD symptoms; and 4) other risk factors common to both ADHD and EDs contribute to the coincidence of both diseases. Additionally, sex differences become a significant issue in the discussion of EDs and ADHD because of the higher incidence of bulimia nervosa and anorexia nervosa in females and the ability of females to mask the symptoms of ADHD. Interestingly, both EDs and ADHD rely on a common neural substrate, namely, dopaminergic signaling. Dopaminergic signaling is critical for motor activity and emotion, the latter enabling the former into a combined motivated movement like eating. This linkage aids in explaining the many comorbidities associated with ADHD. The interconnection of ADHD and EDs is discussed from both a historical perspective and the one based on the revealing nature of its comorbidities.
- Keywords
- ADHD, disordered eating, dopamine, eating disorders, motivation, obesity,
- Publication type
- Journal Article MeSH
- Review MeSH
Alzheimer's disease (AD) is a neurodegenerative disease often accompanied with disruption of sleep-wake cycle. The sleep-wake cycle is controlled by mechanisms involving internal timekeeping (circadian) regulation. The aim of our present pilot study was to assess the circadian system in patients with mild form of AD in their home environment. In the study, 13 elderly AD patients and 13 age-matched healthy control subjects (the patient's spouses) were enrolled. Sleep was recorded for 21 days by sleep diaries in all participants and checked by actigraphy in 4 of the AD patient/control couples. The samples of saliva and buccal mucosa were collected every 4 hours during the same 24 h-interval to detect melatonin and clock gene (PER1 and BMAL1) mRNA levels, respectively. The AD patients exhibited significantly longer inactivity interval during the 24 h and significantly higher number of daytime naps than controls. Daily profiles of melatonin levels exhibited circadian rhythms in both groups. Compared with controls, decline in amplitude of the melatonin rhythm in AD patients was not significant, however, in AD patients more melatonin profiles were dampened or had atypical waveforms. The clock genes PER1 and BMAL1 were expressed rhythmically with high amplitudes in both groups and no significant differences in phases between both groups were detected. Our results suggest moderate differences in functional state of the circadian system in patients with mild form of AD compared with healthy controls which are present in conditions of their home dwelling.
- MeSH
- Actigraphy MeSH
- Alzheimer Disease complications physiopathology MeSH
- Housing MeSH
- Medical Records MeSH
- Period Circadian Proteins biosynthesis genetics MeSH
- Circadian Rhythm physiology MeSH
- Humans MeSH
- Melatonin analysis MeSH
- RNA, Messenger analysis biosynthesis MeSH
- Sleep Disorders, Intrinsic complications physiopathology MeSH
- Gene Expression Regulation MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Saliva chemistry MeSH
- Case-Control Studies MeSH
- ARNTL Transcription Factors biosynthesis genetics MeSH
- Mouth Mucosa chemistry MeSH
- Environment MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- BMAL1 protein, human MeSH Browser
- Period Circadian Proteins MeSH
- Melatonin MeSH
- RNA, Messenger MeSH
- PER1 protein, human MeSH Browser
- ARNTL Transcription Factors MeSH