Out of all nutrients known for their effects on brain functions, two groups are assumed being of particular importance for the process of learning therefore being of even more importance for children with learning disabilities. Here is what they are and why.
The process of learning is believed to rely on mechanisms providing contacts between brain cells called, as you know, neurons. These contacts take place in highly specialised tiny places where two neurons physically contact each other called synapses. One of the neurons initiates the contact by releasing a chemical substance, called neurotransmitter, into the narrow cleft separating pre-synapse from post-synapse.
As soon as the neuron-recipient feels this substance, it gets all excited and became electrically active. The more often the contact the easier the recipient gets excited. Under one important condition: if there’s enough of the substance-neurotransmitter. More synapses involved mean a higher probability of newly formed communication pathways – “learned” ones. There are enzymes and their helpers co-enzymes that work facilitating the production of neurotransmitters. Many vitamins are involved in enzymes’ work. The good example of co-enzymes is the well-known supplement co-enzyme Q10.
Another way to help the process of learning is to supply the brain with neuronal metabolites that promote neuronal growth and activity and enrich the brain architecture.
This is the list of nutrients, which were under investigation whether they work for children with learning disabilities (Alternative Therapies in Health and Medicine, 2000, 6(3): 85-91):
1. Magnesium Chelate 100 mg (at bedtime since it causes drowsiness)
2. Pure Vitamin C 100 mg (bioflavanoids were excluded due to their adverse effects on learning disabilities)
3. Vitamin B1 Thiamine 50 mg
4. Vitamin B3 Niacinamide 50 mg
5. Vitamin B6 Pyridoxine 100 mg
6. Vitamin B12 500 mcg
7. Folic Acid 400 mcg
8. Manganese Chelate 20 mg
9. Zinc Chelate22.5 mg
10. L-tyrosine 500 mg
11. L-glutamine 500 mg
12. Linoleic Acid as evening primrose oil 500 mg
13. Co-enzyme Q10 10 mg
These nutrients were tested on a group of 19 children with learning disabilities for 4 years resulting in dramatic improvement in behavior and academic grades. All the participating children were able to join the mainstream school classes. Those who discontinued the program remained in normal range of school performance for almost one year, however their grades were gradually decreasing. Those who stayed on the program, continued improving their grades during this year so that in the end of the year 4, the difference in overage grades became very significant: 94.6 in those remaining versus 79 in those who discontinued.
Out of the nutrients on the list, the most prominent effect had magesium, vitamins B1 and B6, Zn, and folic acid, followed by vitamin C, L-glutamine, and primrose oil. Manganese was found to have mild adverse effects.
How can calorie restriction improve brain function
Researchers at the Internal Medicine & Gerontology and INSERM, Toulouse, France pointed to an array of ways that hopefully can lead to real managing of age-related diseases of the brain. They all concern calorie restriction. Thus, according to the review published by the Current Opinion in Clinical Nutrition and Metabolic Care, calorie restriction (CR) can protect the brain by the following mechanisms:
1. It’s a new way to improve brain health via induction of neurogenesis
2. It affects the risk for neurodegenerative disorders by increasing resistance to oxidative, metabolic or excitotoxic injuries
3. It results particularly in the upregulation of the brain-derived neurotrophic factor (BDNF) in hippocampal and cortical neurons of rats and mice, which may protect neurons against excitotoxic, oxidative and metabolic insults
4. It may prevent beta-amyloid neuropathology
5. It promote neuronal plasticity
The authors conclude: “It is now well established that caloric restriction could be used to promote successful brain aging. Data from randomized controlled trials in humans are limited. No positive effect on cognitive impairment was found probably due to methodological limitations. The long-term effects of caloric restriction in adults must be clarified before engaging in such preventive strategy. Additional animal studies must be conducted in the future to test the effects of ‘multidomain’ interventions (caloric restriction plus regular exercise) on age-related cognitive decline”
Source:
S. Gillette-Guyonneta, and B. VellasaCaloric restriction and brain function. Current Opinion in Clinical Nutrition and Metabolic Care 2008, 11:686–692
Researchers at the Internal Medicine & Gerontology and INSERM, Toulouse, France pointed to an array of ways that hopefully can lead to a real management of age-related diseases of the brain. They all concern calorie restriction. Thus, according to the review published by the Current Opinion in Clinical Nutrition and Metabolic Care, calorie restriction (CR) can protect the brain by the following mechanisms:
1. It’s a new way to improve brain health via induction of neurogenesis
2. It affects the risk for neurodegenerative disorders by increasing resistance to oxidative, metabolic or excitotoxic injuries
3. It results particularly in the upregulation of the brain-derived neurotrophic factor (BDNF) in hippocampal and cortical neurons of rats and mice, which may protect neurons against excitotoxic, oxidative and metabolic insults
4. It may prevent beta-amyloid neuropathology
5. It promotes neuronal plasticity
The authors conclude: “It is now well established that caloric restriction could be used to promote successful brain aging. Data from randomized controlled trials in humans are limited. No positive effect on cognitive impairment was found probably due to methodological limitations. The long-term effects of caloric restriction in adults must be clarified before engaging in such preventive strategy. Additional animal studies must be conducted in the future to test the effects of ‘multidomain’ interventions (caloric restriction plus regular exercise) on age-related cognitive decline”
Source:
S. Gillette-Guyonneta, and B. VellasaCaloric restriction and brain function. Current Opinion in Clinical Nutrition and Metabolic Care 2008, 11:686–692
Combined deficiency in vitamins C and E is a risk factor for neuronal death and brain necrosis
Vitamin C easily crosses the blood brain barrier and its transport into the brain is mediated by glucose transporters. Vitamin C concentrations in the brain exceed those in blood by 10-fold. In humans, hypovitaminosis C correlated with brain damage in patients with head trauma (Stroke. 2001;32:898-902). The vitamin C has important functions in the brain, for example, protecting neuronal membranes from oxidative damage acting as a scavenger of free radicals.
Another free radical scavenger Vitamin E (-tocopherol) inhibits the amyloid peptide characteristic for Alzheimer’s disease known to induced cell death (Biochemical and Biophysical Research Communications Volume 186, Issue 2, 31 July 1992, Pages 944-950).
The results of a study of Guinea Pigs’s fed either on normal or vitamin-deficient diets showed that while moderate deficiencies of vitamins E or C didn’t result in serious brain changes, their combined moderate deficienciescaused degenerative changes in the guinea pig brains in only 5 days after vitamins were removed from the feed.
Interestingly, the deficiencies in either E or C vitamins had only moderate consequences, but their combination caused severe brain lesions – inflammation, cell death with necrosis and apoptosis and animals’ death (Nutr. 136:1576-1581, June 2006).
Combined deficiency in vitamins C and E is a risk factor for neuronal death and brain necrosis.
Vitamin C easily crosses the blood brain barrier and its transport into the brain is mediated by glucose transporters. Vitamin C concentrations in the brain exceed those in blood by 10-fold. In humans, hypovitaminosis C correlated with brain damage in patients with head trauma (Stroke. 2001;32:898-902). The vitamin C has important functions in the brain, for example, protecting neuronal membranes from oxidative damage acting as a scavenger of free radicals.
Another free radical scavenger Vitamin E (-tocopherol) inhibits the amyloid peptide characteristic for Alzheimer’s disease known to induced cell death (Biochemical and Biophysical Research Communications Volume 186, Issue 2, 31 July 1992, Pages 944-950).
The results of a study of Guinea Pigs’s fed either on normal or vitamin-deficient diets showed that while moderate deficiencies of vitamins E or C didn’t result in serious brain changes, their combined moderate deficienciescaused degenerative changes in the guinea pig brains in only 5 days after vitamins were removed from the feed.
Interestingly, the deficiencies in either E or C vitamins had only moderate consequences, but their combination caused severe brain lesions – inflammation, cell death with necrosis and apoptosis and animals’ death (Nutr. 136:1576-1581, June 2006).
