Related Experiment Videos
A lack of essential fatty acids as a possible cause of hyperactivity in children
Insights
Many children with hyperactivity may have essential fatty acid (EFA) deficiencies due to metabolic or absorption issues. Supplementation shows promising results for improving symptoms in these children.
Area of Science:
- Nutritional Science
- Pediatric Health
- Biochemistry
Background:
- Hyperactive Children's Support Group (HCSG) surveyed children and families.
- Literature review on hyperactivity and essential fatty acids (EFAs).
Purpose of the Study:
- Investigate potential EFA deficiency in children with hyperactivity.
- Explore the link between EFA metabolism and hyperactivity symptoms.
Main Methods:
- Survey of child and family characteristics.
- Analysis of food constituents affecting EFA conversion.
- Observation of symptoms like thirst, eczema, allergies, and asthma.
- Assessment of zinc levels and reactions to wheat/milk.
Main Results:
- Children exhibit potential EFA deficiency linked to metabolism or absorption.
- Food components and zinc deficiency may inhibit EFA conversion to prostaglandins (PGs).
- Higher EFA requirements in males align with higher prevalence in boys.
- Symptoms like thirst, eczema, allergies, and asthma are noted.
- Preliminary EFA supplementation trials yielded positive outcomes.
Conclusions:
- Hypothesize EFA deficiency as a contributing factor in hyperactivity.
- Suggest further research into EFA supplementation for hyperactive children.
Abstract:
The Hyperactive Children's Support Group (HCSG) in an organisation with over 70 branches in Britain devoted to helping such children and their families. We have carried out a detailed survey of the characteristics of many of our children and their families and have studied the literature in detail. We have come to the conclusion that many of these children have a deficiency of essential fatty acids (EFAs) either because they cannot metabolise linoleic acid normally, or because they cannot absorb EFAs normally from the gut, or because their EFA requirements are higher than normal. The main pieces of evidence are: 1. Most of the food constituents which cause trouble in these children are weak inhibitors of the conversion of EFAs to prostaglandins (PGs). 2. Boys are much more commonly effected than girls and males are known to have much higher requirements for EFAs than females. 3. A high proportion of our children have abnormal thirst and thirst is one of the cardinal signs of EFA deficiency. 4. Many of our children have eczema, allergies and asthma which some reports suggest can be alleviated by EFAs. 5. Many of our children are deficient in zinc which is required for conversion of EFAs to PGs. 6. Some of of our children are badly affected by wheat and milk which are known to give rise to exorphins in the gut which can block conversion of EFAs to PGE1. A preliminary study of EFA supplementation in a number of our children has given promising results. We hope that others with better facilities will be encouraged to test out this hypothesis.