Archive for the ‘Brain Basics’ Category
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.
Phytochemical-rich foods have been shown to be effective at reversing age-related deficits in memory in both animals and humans. Specifically, blueberry were effective in reversing age-related deficits in neuronal signaling and behavioral parameters following 8 weeks of feeding, possibly due to their high flavonoid content. It has been reported that blueberry-supplemented diet may not only retard but also revert declining brain functions due to aging. Young and old rats were trained to memorize objects shown them an hour ago. Old rats receiving 2% of their meals as blueberries performed as young rats while old rats on regular diet failed to memorize the objects at al. In several regions of the brain, old control diet rats had significantly higher levels of so called nuclear factor-kappa B (NF-κB) than young animals on the control diet and old rats eating blueberries (Nutritional Neuroscience, V 7, No 2, 2004, 5-83-9). NF-κB is known for its involvement in vulnerability of neurons to “excitotoxicity” – a toxic biochemical condition occurring during neuronal hyperactivity (Synapse. 2000 Feb;35(2):151-9). Errors in regulation of NF-κB may lead to cancer, inflammation and improper immune development. To resist excitotoxicity, there’s so called Brain-derived neurotrophic factor or BDNF, which function is to help supporting the survival of neurons. Recent data (Free Radical Biology and Medicine, 45, 3, 008, 295-305) on blueberry supplementation may indicate that changes in working memory in aged animals are linked to the effects of flavonoids on BDNF.
It was unclear if phytonutrients from blueberries were able to cross the blood-brain barrier and directly access the brain. Researchers in Barcelona, Spain, investigated this issue. They took old rats and fed them a diet containing 2% blueberries for 2 to 2.5 months, than tested the rats for learning and memory. in the brain areas participating in learning and memory processing and storing – cerebellum, cortex, hippocampus or striatum, 14 antioxidant substances found. The antioxidant content correlated with improvements in learning and memory normally declined in old age rats (and humans). In control rats of same age fed on regular diet, there were no changes in bioche
Phytochemical-rich foods have been shown to be effective at reversing age-related deficits in memory in both animals and humans. Specifically, blueberry were effective in reversing age-related deficits in neuronal signaling and behavioral parameters following 8 weeks of feeding, possibly due to their high flavonoid content. It has been reported that blueberry-supplemented diet may not only retard but also revert declining brain functions due to aging. Young and old rats were trained to memorize objects shown them an hour ago. Old rats receiving 2% of their meals as blueberries performed as young rats while old rats on regular diet failed to memorize the objects at al. In several regions of the brain, old control diet rats had significantly higher levels of so called nuclear factor-kappa B (NF-κB) than young animals on the control diet and old rats eating blueberries (Nutritional Neuroscience, V 7, No 2, 2004, 5-83-9). NF-κB is known for its involvement in vulnerability of neurons to “excitotoxicity” – a toxic biochemical condition occurring during neuronal hyperactivity (Synapse. 2000 Feb;35(2):151-9). Errors in regulation of NF-κB may lead to cancer, inflammation and improper immune development. To resist excitotoxicity, there’s so called Brain-derived neurotrophic factor or BDNF, which function is to help supporting the survival of neurons. Recent data (Free Radical Biology and Medicine, 45, 3, 008, 295-305) on blueberry supplementation may indicate that changes in working memory in aged animals are linked to the effects of flavonoids on BDNF.
It was unclear if phytonutrients from blueberries were able to cross the blood-brain barrier and directly access the brain. Researchers in Barcelona, Spain, investigated this issue. They took old rats and fed them a diet containing 2% blueberries for 2 to 2.5 months, than tested the rats for learning and memory. in the brain areas participating in learning and memory processing and storing – cerebellum, cortex, hippocampus or striatum, 14 antioxidant substances found. The antioxidant content correlated with improvements in learning and memory normally declined in old age rats (and humans). In control rats of same age fed on regular diet, there were no changes in bioche
Flavonoids are water soluble plant pigments that plants produce to assist in photosynthesis and are believed to function as antioxidants.
Major dietary sources of flavonoids include fruits, vegetables, cereals, tea, wine and fruit juices.
The main groups of flavonoids and their food sources are:
flavonols – found in onions, leeks and broccoli;
flavones – found in parsley and celery;
isoflavones – found in soyabeans;
flavanones – found in citrus fruit and tomatoes;
flavanols – abundant in green tea, red wine and cocoa; anthocyanidins’ sources include red wine and red berries.
A recent study has provided strong evidence that dietary flavonoid intake preserved cognitive abilities with aging. Isoflavones from soy had positive effects on cognitive function, because they were able to mimic the actions of estrogens in the brain. Isoflavone supplementation had a favourable effect on verbal memory in post-menopausal women.
Brain-imaging studies in humans have demonstrated that the consumption of flavanol-rich cocoa may enhance blood flow to the brain cortex. Berries, in particular blueberries, are effective at reversing age-related deficits in movements and memory.
Animal studies with tea, grape juice or flavonols such as quercetin have shown that they all are beneficial in reversing the course of neuronal and behavioural ageing. Such beneficial effects have been attributed to antioxidant activities, however, there are growing body of evidence that their mechanisms involve a modulation of neurotransmitter release, a stimulation of neurogenesis and changes in neuronal signaling.
Source: Proceedings of the Nutrition Society (2008), 67: 238-252
Flavonoids are water soluble plant pigments that plants produce to assist in photosynthesis and are believed to function as antioxidants. Major dietary sources of flavonoids include fruits, vegetables, cereals, tea, wine and fruit juices.
The main groups of flavonoids and their food sources are:
- flavonols – found in onions, leeks and broccoli;
- flavones – found in parsley and celery;
- isoflavones – found in soyabeans;
- flavanones – found in citrus fruit and tomatoes;
- flavanols – abundant in green tea, red wine and cocoa; anthocyanidins’ sources include red wine and red berries.
A recent study has provided strong evidence that dietary flavonoid intake preserved cognitive abilities with aging. Isoflavones from soy had positive effects on cognitive function, because they were able to mimic the actions of estrogens in the brain. Isoflavone supplementation had a favourable effect on verbal memory in post-menopausal women.
Brain-imaging studies in humans have demonstrated that the consumption of flavanol-rich cocoa may enhance blood flow to the brain cortex. Berries, in particular blueberries, are effective at reversing age-related deficits in movements and memory.
Animal studies with tea, grape juice or flavonols such as quercetin have shown that they all are beneficial in reversing the course of neuronal and behavioural ageing. Such beneficial effects have been attributed to antioxidant activities, however, there are growing body of evidence that their mechanisms involve a modulation of neurotransmitter release, a stimulation of neurogenesis and changes in neuronal signaling.
Source: Proceedings of the Nutrition Society (2008), 67: 238-252
Severe endemic iodine deficiency such as in New Guinea, China, Indonesia, and Thailand causes the clinical picture of cretinism with dominant neurological pathologies; that the most detrimental is the combination of iodine and selenium deficiencies. In the rat fetuses in such condition, experiments showed the developmental failure of the central nervous system…
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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
Research results showed that when calories are restricted in older animals, an increase in life span is still observed; though not as great as that observed in the animals that were calorie restricted since they were young. The data of this research suggests there may be a level of maturity, or a stage in the aging process, after which caloric restriction no longer increases longevity. (6) Restricted nutrient intake may have beneficial effects on alults’ degenerative disease, autoimmune processes, susceptibility to infection and survival rate after infection. (New Horizons, 2(2):257-63, 1994).
Adult rats fed the calorie restricted yet nutritionally balanced diet ate fewer meals but consumed more food during each meal. They also spent more time eating during each meal. The average body temperature per day was significantly lower in restricted rats. However, they moved around significantly more than the rats that were fed as much as they pleased, so they spent more energy during the day.
Related: Neuroprotective effects of Coenzyme Q10
Is Q10 a fitness-enhancing or an anti-aging supplement in the long run?
When we talk about the energy level-enhancing and aging-hindering supplement, we mean Coenzyme Q or (2,3-dimethoxy-5 methyl-6-multiprenyl-1–4-benzoquinone) where Q stands for the quinone group, and 10 means the place the isoprenyl subunits occupies in the molecule. CoQ10 plays a very important role in the cellular power stations, mitochondria, participating in the electron transport chain. It’s a strong antioxidant since it is included in the oxidation-reduction cycle justifying its use for health-protecting purposes. Surprisingly, in the studies confirming that it’s good for you, low doses and short time intake protocols were used while it takes at least 14 weeks to observe increased levels of Q19 in mitochondria of heart, muscle, kidney, and brain.
A recent study published in The Journal of Nutrition (139: 1926–1932, 2009) was undertaken exactly in order to investigate the effects of long term intake of CoQ10 on the motor performance, sensory perception, and cognitive functions in doses either 0.68mg/g (low) or 2.6 mg/g (high). The high doses exacerbated, not prevented the cognitive and sensory impairments observed in old mice.
The authors conclude: “These findings do not support the notion that CoQ10 is a fitness-enhancing or an “antiaging” substance under normal physiological conditions.”
It is not clear, however, how these findings relate to human practice of using Q10 as a health-protecting supplement. The doses considered “low” in the study would mean almost 50 grams a day while only 50 to 200 mg (up to 1000 times lower) is recommended by health professionals. On the other hand, 300 mg/day effectively improved mitochondrial function in patients with ischaemic heart disease (comparing with patients receiving placebo), as shown in the study of Yuk-Ling Dai et al. (Atherosclerosis, 2011, online ahead of print)
139: 1926–1932, 2009
When we talk about the energy level-enhancing and aging-hindering supplement, we mean Coenzyme Q or (2,3-dimethoxy-5 methyl-6-multiprenyl-1–4-benzoquinone) where Q stands for the quinone group, and 10 means the place the isoprenyl subunits occupies in the molecule. CoQ10 plays a very important role in the cellular power stations, mitochondria, participating in the electron transport chain. It’s a strong antioxidant since it is included in the oxidation-reduction cycle justifying its use for health-protecting purposes. Surprisingly, in the studies confirming that it’s good for you, low doses and short time intake protocols were used while it takes at least 14 weeks to observe increased levels of Q19 in mitochondria of heart, muscle, kidney, and brain.
A recent study published in The Journal of Nutrition (139: 1926–1932, 2009) was undertaken exactly in order to investigate the effects of long term intake of CoQ10 on the motor performance, sensory perception, and cognitive functions in doses either 0.68mg/g (low) or 2.6 mg/g (high). The high doses exacerbated, not prevented the cognitive and sensory impairments observed in old mice.
The authors conclude: “These findings do not support the notion that CoQ10 is a fitness-enhancing or an “antiaging” substance under normal physiological conditions.”
It is not clear, however, how these findings relate to human practice of using Q10 as a health-protecting supplement. The doses considered “low” in the study would mean almost 50 grams a day while only 50 to 200 mg (up to 1000 times lower) is recommended by health professionals. On the other hand, 300 mg/day effectively improved mitochondrial function in patients with ischaemic heart disease (comparing with patients receiving placebo), as shown in the study of Yuk-Ling Dai et al. (Atherosclerosis, 2011, online ahead of print)
Thirty percent less calories equals thirty percent better memory
Calorie restriction benefits for the aging brain health have been proposed and the mechanisms were suggested but a direct evidence showing that it can improve memory function in elderly humans appeared only recently. The study conducted in Munster, Germany, showed that a three months calorie intake reduction by 30% compared with habitual diet or a Mediterranean style diet rich in unsaturated fatty acids (although known to positively influence memory) resulted in a highly significant, 30% improvement in memory scores of 60 something group of relatively healthy people.
A. Witte et al., 2009. Caloric restriction improves memory in elderly humans. PNAS, vol. 106 no. 4 1255–126
Calorie restriction benefits for the aging brain health have been proposed and the mechanisms were suggested but a direct evidence showing that it can improve memory function in elderly humans appeared only recently. The study conducted in Munster, Germany, showed that a three months calorie intake reduction by 30% compared with habitual diet or a Mediterranean style diet rich in unsaturated fatty acids (although known to positively influence memory) resulted in a highly significant, 30% improvement in memory scores of 60 something group of relatively healthy people.
A. Witte et al., 2009. Caloric restriction improves memory in elderly humans. PNAS, vol. 106 no. 4 1255–126
A calorie restriction effect on longevity is a very well documented topic of experimental biology. It is important to know that life span researchers deal mostly with small size any meals since their generations change much faster than in larger size animal species. It is also important that only restriction as serious as 30 to 60 percent of “all you can eat” amount can cause significant improvement in health and longevity.
It was first demonstrated in insects, where it yielded up to a 300% increase in life span; then in young small size mammals such as mice and rats, where results were more modest but still impressive. Later the results on adult animals appeared, yet more modest, but still significant. As to the human outcome, published epidemiological studies have reported evidence of reduced mortality rates in persons who have lost weight, regardless of whether the weight loss was due to decreased calorie intake or increased energy expenditure (1). These data are consistent with experimental results where exercise increased average longevity of female rats, despite increased food intake (2).
This consistency is probably the reason for hopes arising from numerous animal data showing benefits of calorie restriction in animals, including improvement in immune status, anti-cancer defense system and decrease in the occurrence of general disease. The hope, if not for increased longevity, is at least for decreased mortality.
Can we use calorie restriction to improve health and to live longer? A daily calorie
restriction of 30 to 60 percent seems to be too hard a sacrifice. Perhaps this is why new hope arose when preliminary information about developing an anti-aging drug mimicking effects of semi-starvation leaked into mass media.
Dr. Masoro from the Department of Physiology and Aging Research, University of Texas, reviewed 54 scientific articles and concluded: “A spectrum of findings indicates that dietary restriction retards the aging processes of mice and rats. It also maintains many physiological processes in a youthful state and, most strikingly, retards or prevents almost all age-associated disease processes.” (3) However, it’s too soon to use the calorie restriction as a strategy to improve health and prolong life.
“Due to the interrelationships between disease and older age, and the limitations of existing research in this area, most life extension strategies are untested hypotheses. Many strategies merit scientific inquiry, but they cannot be recommended for use. More extensive research is necessary to assess their safety, effectiveness, and socio-economic impact, and to resolve ethical controversies before they can be considered applicable in humans.” (Pharmacotherapy, 16(2):183-200, 1996)
A calorie restriction effect on longevity is a very well documented topic of experimental biology. It is important to know that life span researchers deal mostly with small size any meals since their generations change much faster than in larger size animal species. It is also important that only restriction as serious as 30 to 60 percent of “all you can eat” amount can cause significant improvement in health and longevity.
It was first demonstrated in insects, where it yielded up to a 300% increase in life span; then in young small size mammals such as mice and rats, where results were more modest but still impressive. Later the results on adult animals appeared, yet more modest, but still significant. As to the human outcome, published epidemiological studies have reported evidence of reduced mortality rates in persons who have lost weight, regardless of whether the weight loss was due to decreased calorie intake or increased energy expenditure (1). These data are consistent with experimental results where exercise increased average longevity of female rats, despite increased food intake (2).
This consistency is probably the reason for hopes arising from numerous animal data showing benefits of calorie restriction in animals, including improvement in immune status, anti-cancer defense system and decrease in the occurrence of general disease. The hope, if not for increased longevity, is at least for decreased mortality.
Can we use calorie restriction to improve health and to live longer? A daily calorie restriction of 30 to 60 percent seems to be too hard a sacrifice. Perhaps this is why new hope arose when preliminary information about developing an anti-aging drug mimicking effects of semi-starvation leaked into mass media.
Dr. Masoro from the Department of Physiology and Aging Research, University of Texas, reviewed 54 scientific articles and concluded: “A spectrum of findings indicates that dietary restriction retards the aging processes of mice and rats. It also maintains many physiological processes in a youthful state and, most strikingly, retards or prevents almost all age-associated disease processes.” (3) However, it’s too soon to use the calorie restriction as a strategy to improve health and prolong life.
“Due to the interrelationships between disease and older age, and the limitations of existing research in this area, most life extension strategies are untested hypotheses. Many strategies merit scientific inquiry, but they cannot be recommended for use. More extensive research is necessary to assess their safety, effectiveness, and socio-economic impact, and to resolve ethical controversies before they can be considered applicable in humans.” (Pharmacotherapy, 16(2):183-200, 1996)
Yes, but it seems to be a good stress. The mechanism of action of caloric restriction remains unknown; owever, data suggest that cellular functions are altered in such a way that destructive by-products of metabolism are reduced, and defense or repair systems are enhanced by this nutritional manipulation. (Clinics in Geriatric Medicine, 11(4):553-65, 1995)
The amount of oxidative damage increases as an organism ages and is postulated to be a major causal factor of senescence. Restriction of caloric intake lowers levels of oxidative stress and damage, retards age associated changes, and extends the maximum life span in mammals. Animal and human studies suggest potential benefits of dietary restriction, exercise, antioxidants, hormones and deprenyl.
Does deprenyl mimic at least some of calorie restriction effects? Probably, thinks Dr. Masoro. “Dietary restriction protects against oxidative damage and oxidative damage is probably an inevitable component of fuel use.” So does deprenil, though in rather narrow way. Deprenyl (selegiline) is a neuroprotective drug an inhibitor of brain monoamine oxidase B (MAO-B). That means it inhibits a very particular enzyme promoting oxidation of the brain chemical monoamines, which are very important in many vital functions, including cognition.
Dietary restriction was found to retard age associated decline of sensory and movement coordination, and improve performance of aged mice on learning problems. “Studies in aged calorie restricted mice indicated that lowering of protein oxidation by calorie restriction could be reversed within a time frame of three to six weeks. These findings suggest that the beneficial effects of dietary restriction upon brain function and life span may depend upon its ability to acutely reduce steady state levels of oxidative stress.” (Archives of Biochemistry & Biophysics, 333(1):189-97, 1996)
