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Circadian Rhythms and Neuroendocrine Dysregulation in ADHD: Therapeutic…
Circadian Rhythms and Neuroendocrine Dysregulation in ADHD: Therapeutic Insights from Omega-3 Fatty Acids
Genetic variations and single-nucleotide polymorphisms in the CLOCK gene have been associated with adult ADHD symptoms and increased vulnerability to major depressive disorder
Animals with CLOCK gene knockouts exhibit ADHD-like behaviors, such as hyperactivity, impulsivity, lower dopamine levels, and attention deficits which further evidences the link between circadian dysfunction and ADHD
The circadian clock regulates dopamine synthesis and, when disrupted, shows a link between reduced dopamine levels, circadian system dysregulation, and ADHD-like symptoms
Some interventions to improve sleep in those with ADHD include weighted blankets, light therapy, acupuncture, supplemental melatonin intake, and supplemental omega-3 polyunsaturated fatty acid (n-3 PUFA) intake
n-3 PUFAs modulate the CLOCK gene to regulate neurological, inflammatory, metabolic, and cardiovascular processes
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Auroculasin (a bioactive prenylated isoflavonoid) therapy was shown to reduce hyperactivity, increase melatonin and dopamine levels, and regulate the circadian clock gene PER1b in a zebrafish model
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Hypothalamic-pituitary adrenal (HPA) axis dysregulation has been reported in both circadian rhythm disorders and ADHD
Cortisol is a key hormone in the HPA axis and follows the circadian rhythm; it rises before waking up in the morning, peaks within an hour, and gradually declines throughout the day
Lower cortisol levels in response to stress are associated with certain ADHD traits in children, but are unchanged in adults with ADHD
Studies indicate that ADHD is linked with changes in cortisol secretion patterns, including lower overall cortisol levels compared to controls and higher morning and afternoon cortisol levels in individuals with ADHD
omega-3 Polyunsaturated Fatty Acid (n-3 PUFA) deficiency may be linked to ADHD and circadian rhythm disorders
ADHD children and adults with low levels of n-3 PUFAs were shown to have more severe symptoms, including inattention, hyperactivity-impulsivity, dry eyes, and skin problems
Supplementation with n-3 PUFAs showed significant improvement in symptoms and cognitive performance in children and adolescents with ADHD
Diets poor in n-3 PUFAs have shown to cause sleep pattern disruption and disruption of circadian CLOCK gene expression
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Sleep-wake cycles and fatty acid metabolism may be correlated, and n-3 PUFAs may counteract the circadian disrupting effects of saturated fats
HPA-axis activity affects fatty acid metabolism in that cortisol plays a role in mobilizing, lysis, oxidation, and synthesis of fatty acids
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Supplementation of long-chain n-3 PUFAs in both animal and human studies leads to a reduction in cortisol levels
While no clinical studies have been conducted, an animal study showed that hamsters deficient in n-3 PUFAs exhibited chronic locomotor hyperactivity and a disturbed melatonin rhythm
Human studies have shown that supplementation of n-3 and n-6 PUFAs, along with magnesium and zinc, improved symptoms associated with ADHD, but no significant improvement in sleep dysfunction
Adding additional supplements aside from n-3 PUFAs can muddy results as it’s harder to tell what specifically contributed to a study’s outcomes
A study conducted on preterm toddlers showed that supplementation of n-3, n-6, and n-9 PUFAs led to improvement in socioemotional outcomes, but there was no effect on sleep or behavior symptoms
Higher EPA (a type of n-3 PUFAs) content in supplementation seems to be more effective for core ADHD symptoms, while DHA (another type of n-3 PUFA) is more directly linked to melatonin synthesis, as well as circadian gene modulation and membrane stability
Emphasis of one type of fatty acid, as well as duration of studies (some may be too short to see effects of sustained n-3 PUFAs supplementation) may lead to different outcomes and conclusions