Archive for the ‘- Brain Aging’ Category
Message: there are many supplements on the market believed to postpone brain aging but they are still on clinical trials. To wait until consensus is reached or to go for them since they wouldn’t hurt depends (mostly) whether you can afford them or not.
Vitamins E and C, alpha-lipoic acid, creatine, melatonin, omega-3 polyunsaturated fatty acids, CoQ10, curcumin, resveratrol, glucose, malate and other antioxidants and (and their combinations) are subjects of around 30 registered clinical trials investigating diseases blamed for the consequences of brain aging — Alzheimer’s and Parkinson’s diseases and amyotrophic lateral sclerosis.
Source: Journal of Alzheimer’s Disease 25 (2011) 187–208
Message: Meditation can prevent brain cortex loss
Magnetic resonance imaging to assess cortical thickness revealed that brain areas—such as the prefrontal cortex involved with memory, attention, and sensory processing—were approximately 5 percent thicker in the subjects who meditated compared with those who did not. This difference was most pronounced in older participants, suggesting that meditation might offset agerelated cortical thinning.
Source: Neuroreport 2005;16:1893–1897
Message: The sense of balance is important for intelligence
Exercise can help maintain balance, and balance in the elderly has been highly correlated with performance measures of mental abilities such as general intelligence, memory, and reaction time. Balance thus serves as a biomarker of cerebroarterial blood flow and age-related global neurophysiologic status.
Source: Neuropsychologia 2006;44:1978–1983).
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
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)
The growth hormone (GH) secretion declines as we age (by 14% per decade), the process called somatopause. Drugs like pyridostigmine (an acetylcholinesterase inhibitor) are able to enhance GH secretion, but its clinical use is limited due to the strong side effects. Rivastigmine, a drug for Alzheimer’s disease (AD), was found to enhance GH release (Gerontology. 2003;49:191–195).
Oral administration of certain amino acids (arginine, glutamine, glycine, and lysine) increased the release of endogenous GH (Nutrition. 2002;18:657–661); the doses of arginine were 0.5 or 1 g/kg body weight increased GH level (J Clin Endocrinol Metab, 2011 ; Vol. 43 (3): 582-586) or roughly 35 to 70 g a day.
Arginine dissolved in distilled water was infused over a thirty-minute period in doses 1/12, 1/6 and 1/4 g. per pound of body weight. Only the highest dose (average 37.5 g total) was found to be effective in this administration mode. Interestingly, the responses of GH among females remain significantly higher than those among males (N Engl J Med 1967; 276:434-439).
The mixture of L-arginine, L-glutamine, L-lysine, and glycine at a ratio of 37:30:18.5:14.5) added as 5% of the daily meals total has been found to increase the release of endogenous GH. When mice were fed a diet containing GH-releasing supplements they had significantly fewer memory impairments and changes in acetylcholine level in hippocampus induced by Alzheimer’s amyloid beta 1–42 (J Pharmacol Sci; 2005, 99, 117 – 120).
Recently, a clinical target for improving the conditions of AD may be the activation not of GH alone but the entire GH/insulin-like growth factor-I (IGF-I) brain axis. IGF-I alone is also considered a physiological regulator of brain amyloid levels with therapeutic potential (Nature Medicine, 2002; 8, 1390 – 1397)
The growth hormone (GH) secretion declines as we age (by 14% per decade), the process called somatopause. Drugs like pyridostigmine (an acetylcholinesterase inhibitor) are able to enhance GH secretion, but its clinical use is limited due to the strong side effects. Rivastigmine, a drug for Alzheimer’s disease (AD), was found to enhance GH release (Gerontology. 2003;49:191–195).
Oral administration of certain amino acids (arginine, glutamine, glycine, and lysine) increased the release of endogenous GH (Nutrition. 2002;18:657–661); the doses of arginine were 0.5 or 1 g/kg body weight increased GH level (J Clin Endocrinol Metab, 2011 ; Vol. 43 (3): 582-586) or roughly 35 to 70 g a day.
Arginine dissolved in distilled water was infused over a thirty-minute period in doses 1/12, 1/6 and 1/4 g. per pound of body weight. Only the highest dose (average 37.5 g total) was found to be effective in this administration mode. Interestingly, the responses of GH among females remain significantly higher than those among males (N Engl J Med 1967; 276:434-439).
The mixture of L-arginine, L-glutamine, L-lysine, and glycine at a ratio of 37:30:18.5:14.5) added as 5% of the daily meals total has been found to increase the release of endogenous GH. When mice were fed a diet containing GH-releasing supplements they had significantly fewer memory impairments and changes in acetylcholine level in hippocampus induced by Alzheimer’s amyloid beta 1–42 (J Pharmacol Sci; 2005, 99, 117 – 120).
Recently, a clinical target for improving the conditions of AD may be the activation not of GH alone but the entire GH/insulin-like growth factor-I (IGF-I) brain axis. IGF-I alone is also considered a physiological regulator of brain amyloid levels with therapeutic potential (Nature Medicine, 2002; 8, 1390 – 1397)
