Is calorie restriction stressful?

Age-protection, Calorie restriction, Oxidative damage — 8:46 am

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)

Can Adults Benefit from Calorie Restriction?

Age-protection, Calorie restriction — 8:43 am

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.

Dietary restriction and life span

Age-protection, Brain Aging, Calorie restriction — 8:41 am
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)

Epilepsy Drugs May Treat Alzheimer’s and Parkinson’s

Alzheimer's, Epilepsy, Parkinson's — 8:37 am

(WebMD) A group of drugs used to treat epilepsy may also treat Alzheimer’s and Parkinson’s disease.
New research shows treatment with T-type calcium channel blockers, used to treat epilepsy, protected nerve cells from the brains of mice that can be damaged by neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease.
Researchers say there aren’t any effective medications that protect brain cells from age-related damage and degeneration. If these findings hold up under further study in humans, they could lead to a new class of more effective treatments for age-related neurological diseases.
Calcium-signaling pathways play an important role in the survival of nerve cells (neurons) in the brain. As people age, this process can become disrupted and can lead to cognitive and functional decline.
Researchers say that opens up the possibility of using chemicals like calcium channel blockers that are involved in the calcium-signaling process to protect the nerve cells from death.
The study, published in Molecular Neurodegeneration, looked at the effects of treatment with calcium channel blockers on the brain cells of mice.
Researchers found neurons showed an increase in viability after treatment with the calcium channel blockers over both the long term and short term.
“Our data provides implications for the use of this family of anti-epileptic drugs in developing new treatments for neuronal injury, and for the need of further studies of the use of such drugs in age-related neurodegenerative disorders,” says researcher Jianxin Bao, PhD, of Washington University in St. Louis, in a news release.
(WebMD) A group of drugs used to treat epilepsy may also treat Alzheimer’s and Parkinson’s disease.

New research shows treatment with T-type calcium channel blockers, used to treat epilepsy, protected nerve cells from the brains of mice that can be damaged by neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease.

Researchers say there aren’t any effective medications that protect brain cells from age-related damage and degeneration. If these findings hold up under further study in humans, they could lead to a new class of more effective treatments for age-related neurological diseases. Calcium-signaling pathways play an important role in the survival of nerve cells (neurons) in the brain. As people age, this process can become disrupted and can lead to cognitive and functional decline.

Researchers say that opens up the possibility of using chemicals like calcium channel blockers that are involved in the calcium-signaling process to protect the nerve cells from death. The study, published in Molecular Neurodegeneration, looked at the effects of treatment with calcium channel blockers on the brain cells of mice.

Researchers found neurons showed an increase in viability after treatment with the calcium channel blockers over both the long term and short term.

“Our data provides implications for the use of this family of anti-epileptic drugs in developing new treatments for neuronal injury, and for the need of further studies of the use of such drugs in age-related neurodegenerative disorders,” says researcher Jianxin Bao, PhD, of Washington University in St. Louis, in a news release.

Why is fat so tasty?

Fats, Senses — 8:32 am
Why is fat so tasty?
Most animals, including humans, prefer high-fat food to low-fat food. Fatty foods are very palatable though the fatty acids, which make these foods fatty, are tasteless. On the other hand, sweet, sour, salty, or bitter foods are recognized by the corresponding receptors of the taste buds. The receptors then send information to the brain areas responsible for positive or negative sensations called hedonic or aversive. But how the tasteless fatty acids manage to make fatty foods so tasty?
Recently, it was suggested that long-chain fatty acids attaching to their specific transporter in the tongue. These long-chain fatty acids are recognized on the tongue, and then neuropeptides and neurotransmitters such as the famous “reward chemical” beta-endorphin is released in the brain.
Source: J Nutr Sci Vitaminol (Tokyo). 2007 Feb;53(1):1-4.

Most animals, including humans, prefer high-fat food to low-fat food. Fatty foods are very palatable though the fatty acids, which make these foods fatty, are tasteless. On the other hand, sweet, sour, salty, or bitter foods are recognized by the corresponding receptors of the taste buds. The receptors then send information to the brain areas responsible for positive or negative sensations called hedonic or aversive. But how the tasteless fatty acids manage to make fatty foods so tasty?

Recently, it was suggested that long-chain fatty acids attaching to their specific transporter in the tongue. These long-chain fatty acids are recognized on the tongue, and then neuropeptides and neurotransmitters such as the famous “reward chemical” beta-endorphin is released in the brain.

Source: J Nutr Sci Vitaminol (Tokyo). 2007 Feb;53(1):1-4.

Most fats seem to be protective against Alzheimer’s disease

Alzheimer's, Diet, Fats, Foods for the Brain, Prevention — 8:26 am
Most fats seem to be protective against Alzheimer disease
In 1989-99, an association was found, between dietary fat composition and cognitive performance in later adult years: the higher intake of monounsaturated and polyunsaturated fats and the lower intake of saturated fat — the higher cognitive performance. Another, epidemiologic study conducted in 1997 suggested that high intake of total fat, saturated fat, and dietary cholesterol may increase the risk of dementia.
However, researchers at St Luke’s Medical Center, Chicago, Ill found increased risk of Alzheimer’s disease among people with high intakes of saturated and trans-unsaturated fats and decreased risk with high intakes of polyunsaturated and monounsaturated fats. Consumption of vegetable fat and a high ratio of polyunsaturated to saturated fats were also protective, whereas total fat, animal fat, and dietary cholesterol had no association with Alzheimer disease.
Sources
Brain Res. 1989;505:302-305
Behav Neurosci. 1996;110:451-459
Behav Brain Res. 1999;101:153-161
Am J Epidemiol. 1997;145:33-41.
Arch Neurol. 2003;60:194-200

In 1989-99, an association was found, between dietary fat composition and cognitive performance in later adult years: the higher intake of monounsaturated and polyunsaturated fats and the lower intake of saturated fat — the higher cognitive performance. Another, epidemiologic study conducted in 1997 suggested that high intake of total fat, saturated fat, and dietary cholesterol may increase the risk of dementia.

However, researchers at St Luke’s Medical Center, Chicago, Ill found increased risk of Alzheimer’s disease among people with high intakes of saturated and trans-unsaturated fats and decreased risk with high intakes of polyunsaturated and monounsaturated fats. Consumption of vegetable fat and a high ratio of polyunsaturated to saturated fats were also protective, whereas total fat, animal fat, and dietary cholesterol had no association with Alzheimer disease.

Sources

  1. Brain Res. 1989;505:302-305
  2. Behav Neurosci. 1996;110:451-459
  3. Behav Brain Res. 1999;101:153-161
  4. Am J Epidemiol. 1997;145:33-41.
  5. Arch Neurol. 2003;60:194-200

Flavonoids: what they are, food sources, and brain aging

Age-protection, Foods for the Brain, Memory — 8:21 am
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

Blueberries, aging, learning, and memory

Age-protection, Alzheimer's, Foods for the Brain, Memory — 8:16 am

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

Anti-depressant supplements

Emotions/Mood, Supplements — 11:16 am
Deficiency of vitamin B12 can create disturbances in mood and B12 supplementation helps to normalize the mood. Vitamin B6, vitamin C, Folic Acid (Folate) and Zinc are all essential good mood nutrients. They are needed to make the feel-good brain chemical serotonin from the raw material – amino acid tryptophan. (New England Journal of Medicine 1988;318:1720–8.)
In a clinical trial of healthy young men, consumption of a high-selenium diet was associated with improved mood and decrease of anxiety.
Vitamin D supplementation may be associated with elevations in mood. In a double-blind controlled study, healthy people were given vitamin D3 supplements. Researchers found that D3 supplementation enhanced positive mood and there was some evidence of a reduction in negative mood.
The precursor of serotonin tryptophan is found in many foods, primarily turkey, chicken, fish, cottage cheese, bananas, eggs, nuts, wheat germ, avocados, milk, cheese and legumes and, in lesser amounts, breads, cereals, potatoes and rice. However, these foods also contain competing amino acids tyrosine, phenylalanine, valine, leucine and isoleucine. The solution? Take 5-hydroxytryptophan (5-HTP).
5-HTP is extracted from the seed of the Griffonia simplicifolia plant. L-tryptophan has to be converted to (5-HTP) before it becomes serotonin in the body. In a clinical trial, supplemental 5-HTP had antidepressant effects in bipolar patients. (Acta Psychiatr Scand Suppl 1981;290:191–201.)
Omega-3 Fatty Acids May Reduce the Risk of Depression in Pregnancy. Using British data compiled from pregnant women, the researchers analyzed the association between omega-3 fatty acids and depression. Their findings were supported by an additional analysis, which showed that in countries where omega-3 intake is the highest, the incidence of depression appears to be the lowest. (The Lancet Aug. 1998)

Deficiency of vitamin B12 can create disturbances in mood and B12 supplementation helps to normalize the mood. Vitamin B6, vitamin C, Folic Acid (Folate) and Zinc are all essential good mood nutrients. They are needed to make the feel-good brain chemical serotonin from the raw material – amino acid tryptophan. (New England Journal of Medicine 1988;318:1720–8.) In a clinical trial of healthy young men, consumption of a high-selenium diet was associated with improved mood and decrease of anxiety.

Vitamin D supplementation may be associated with elevations in mood. In a double-blind controlled study, healthy people were given vitamin D3 supplements. Researchers found that D3 supplementation enhanced positive mood and there was some evidence of a reduction in negative mood.

The precursor of serotonin tryptophan is found in many foods, primarily turkey, chicken, fish, cottage cheese, bananas, eggs, nuts, wheat germ, avocados, milk, cheese and legumes and, in lesser amounts, breads, cereals, potatoes and rice. However, these foods also contain competing amino acids tyrosine, phenylalanine, valine, leucine and isoleucine. The solution? Take 5-hydroxytryptophan (5-HTP).

5-HTP is extracted from the seed of the Griffonia simplicifolia plant. L-tryptophan has to be converted to (5-HTP) before it becomes serotonin in the body. In a clinical trial, supplemental 5-HTP had antidepressant effects in bipolar patients. (Acta Psychiatr Scand Suppl 1981;290:191–201.)

Omega-3 Fatty Acids May Reduce the Risk of Depression in Pregnancy. Using British data compiled from pregnant women, the researchers analyzed the association between omega-3 fatty acids and depression. Their findings were supported by an additional analysis, which showed that in countries where omega-3 intake is the highest, the incidence of depression appears to be the lowest. (The Lancet Aug. 1998)

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