July 29, 2010

Foods that heal, foods that harm

Foods for the brain and mind (resources)





July 23, 2010

Should we start exercising early in life to postpone or prevent age-related cognitive decline?

Exercise during midlife comparing with exercise during late life

Most of the studies into the protective effects of exercise against cognitive decline, dementia, and Alzheimer’s disease, followed the elderly people starting their 65s and watched the results, which were relevant to the beneficial effects in late life. However, there are some results where a large cohort of 65-79-year olds has been followed-up for around 21 years so information about physical activity during midlife was available. Those who who participated in at least “leisure-time physical activity” during midlife had significantly lower risks of dementia or Alzheimer’s disease comparing with those who did not exercise at all [1].

Another study has suggested that physical activity at even earlier ages (physical activity between ages 15 and 25 years was asked retrospectively) can improve or preserve cognitive ability in late life [2]. This cognitive decline risk reduction is at least comparable to the eisks reduction reported in studies of physical activity in older persons. Thus, midlife physical activity might be as important for preventing later cognitive decline as is physical activity at older ages.

Sources

  1. Rovio S, et al. Leisure-time physical activity at midlife and the risk of dementia and Alzheimer’s disease. Lancet Neurol 2005;4:705–11
  2. Dik M, Deeg DJ, Visser M, Jonker C. Early life physical activity and cognition at old age. J Clin Exp Neuropsychol 2003;25:643–53

July 15, 2010

Resveratrol and curcumin, plant’s own weapons that protect the brain

According to Michael Wong, MD, PhD (1), although there’s a noticeable progress in anti-epileptic drug development, two obstacles remain unchanged for many decades:
1. The number of cases resistant to the best and newest drugs does not decrease
2. The best drugs address symptoms and not the cause of the disease, namely, they might suppress the seizures but they cannot make them disappear. As a result of such a failure, we still have no anti-epileptic therapies.
Recent studies, however, addresses potential neuroprotective and anti-epileptogenic actions of substances naturally occurring in plants. For example, Resveratrol (a phytoalexin) is found in plants such as peanuts and grapes, but it’s especially abundant in red wine. In plants, Resveratrol defends the cells against the consequences of injury, parasitics, and infectious diseases — hence its antiinflammatory, antioxidant, anti-tumor, and, if given to animals, its neuroprotective effects.
In the article “Protective Effect of Resveratrol Against Kainate-Induced Temporal Lobe Epilepsy in Rats” Resveratrol is described as a potent anti-epilepsy agent, which protects against epileptogenesis (not just against seizures) in animal model of temporal lobe epilepsy (2).
Another success story was told about curcumin, which is the major ingredient in the popular Indian spice, tumeric. Tumeric has been used for centuries in parts of India as an herbal therapy; including treatment of Alzheimer’s disease and epilepsy. As resveratrol, curcumin has been shown to inhibit acute seizures. The recent study (3) studied the effect of curcumin on epileptogenesis in a rat model of post-traumatic epilepsy.  Curcumin decreased the development of and seizures and improved memory and learning.
1. M Wong. HERBS AND SPICES: UNEXPECTED SOURCES OF ANTIEPILEPTOGENIC DRUG TREATMENTS? Epilepsy Currents, Vol. 10, No. 1  2010 pp. 21–23
2. Protective Effect of Resveratrol Against Kainate-Induced Temporal Lobe Epilepsy in Rats. Wu Z, Xu Q, Zhang
L, Kong D, Ma R, Wang L. Neurochem Res 2009;34(8):1393–1400.
3. Curcumin Protects Against Electrobehavioral Progression of Seizures in the Iron-Induced Experimental Model
of Epileptogenesis. Jyoti A, Sethi P, Sharma D. Epilepsy Behav 2009;14(2):300–308.

HERBS AND SPICES: UNEXPECTED SOURCES OF ANTIEPILEPTOGENIC DRUG TREATMENTS?

According to Michael Wong, MD, PhD (1), although there’s a noticeable progress in anti-epileptic drug development, two obstacles remain unchanged for many decades.

  • The number of cases resistant to the best and newest drugs does not decrease
  • The best drugs address symptoms and not the cause of the disease, namely, they might suppress the seizures but they cannot make them disappear. As a result of such a failure, we still have no anti-epileptic therapies.

Recent studies, however, address potential neuroprotective and anti-epileptogenic actions of substances naturally occurring in plants. For example, Resveratrol (a phytoalexin) is found in plants such as peanuts and grapes, but it’s especially abundant in red wine. In plants, Resveratrol defends the cells against the consequences of injury, parasitics, and infectious diseases — hence its antiinflammatory, antioxidant, anti-tumor, and, if given to animals, its neuroprotective effects.

In the article “Protective Effect of Resveratrol Against Kainate-Induced Temporal Lobe Epilepsy in Rats” Resveratrol is described as a potent anti-epilepsy agent, which protects against epileptogenesis (not just against seizures) in animal model of temporal lobe epilepsy (2).

Another success story was told about curcumin, which is the major ingredient in the popular Indian spice, tumeric. Tumeric has been used for centuries in parts of India as an herbal therapy; including treatment of Alzheimer’s disease and epilepsy. As resveratrol, curcumin has been shown to inhibit acute seizures. The recent study (3) studied the effect of curcumin on epileptogenesis in a rat model of post-traumatic epilepsy.  Curcumin decreased the development of and seizures and improved memory and learning.

Sources

  1. M Wong. CURRENT LITERATURE IN BASIC SCIENCE. Epilepsy Currents, Vol. 10, No. 1  2010 pp. 21–23
  2. Protective Effect of Resveratrol Against Kainate-Induced Temporal Lobe Epilepsy in Rats. Wu Z, Xu Q, Zhang
  3. L, Kong D, Ma R, Wang L. Neurochem Res 2009;34(8):1393–1400.
  4. Curcumin Protects Against Electrobehavioral Progression of Seizures in the Iron-Induced Experimental Model of Epileptogenesis. Jyoti A, Sethi P, Sharma D. Epilepsy Behav 2009;14(2):300–308.

June 28, 2010

Alzheimer’s Facts

Alzheimer’s Disease Statistics

• Alzheimer’s affects approximately 4.5 million Americans and is
expected to affect up to 16 million by 2050.
• Alzheimer’s affects approximately 5 percent of men and women
ages 65–74.
• Nearly half of people 85 and older have Alzheimer’s.
• Alzheimer’s must be distinguished from mild cognitive impairment
and normal age-related memory changes.
(National Institute of Aging. Alzheimer’s Disease Information, May 9, 2006)

Physical and mental health: same strategies

Research evidence is accumulating, showing that many of the same strategies for maintaining physical health are also applicable for maintaining brain plasticity and good cognitive functioning throughout the lifespan. These studies reinforce the message that exercise—physical and mental—is an essential part of any comprehensive health program (ALTERNATIVE & COMPLEMENTARY THERAPIES—OCTOBER 2006 pp 222-227)

Exercise and balance 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 (Neuropsychologia 2006;44:1978–1983).

Meditation and cortex thickness

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 (Neuroreport 2005;16:1893–1897)

June 15, 2010

Vitamins C and E, separately or combined

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).

May 30, 2010

A theory of acupuncture, spinal cord, and endorphins

The best of the few known conventional theories on acupuncture belongs to a team of theoretical biologists working under Dr. Dmitri Chernavski, a professor at the Russian Academy of Sciences, Institute of Physics, in Moscow.  The group approached the problem from the point of view of concept of neurocomputing.
Since mid-century, using a model based on human neural structures, a whole new class of computers, possessing so called ” artificial intelligence”, has been developed  – the ones that can learn, recognize objects, and correct their own mistakes.  In somewhat of a paradox, the reverse logic has been used now, in order to explain the mechanisms of a live brain using the known electronic models.  Thus the theory of self-diagnostic function of an organism was developed.  Most of these self-diagnostic (recognizing the “image of a disease”) processes take place in the spinal cord.  In the gray matter of the spinal cord, the neurons are organized into what are called “Rexed laminae” and their functions are well-known.
The signals from the inner organs, as well as from the skin and muscles first go through the first lamina, separate from each other.  Then the signals move through the second lamina, third one, and so on, while increasingly interacting with each other and, after ten laminae, finally reach the brain in the form of one integrated set of information about the body’s state of being.  The computers that recognize objects have basically the same laminar structure and function of signal integration.  In both cases, an omitted signal from an internal organ, or one that is not strong enough, will be compensated for by the other one (e.g. from the skin), thus correcting the mistake.
According to Dr. Chernavski, skin stimulation at the point of acupuncture accomplishes the same goal.  The process of integration in the Rexed laminae increases the flow of “signals of illness” from an organ, or points out a body’s mistake in recognizing the disorder.  It is as if you wanted to send a letter to someone down the stream with little or no water using a miniature ship to carry it.  Add some water, and the ship will get there. Neither the way of adding the water nor the water itself has any effect on the content of letter sent.
Once the body has the stronger, clearer information about the injury or disease, the natural healing powers of the body take over.  What happens when the disease is recognized, the above theory does not explain, stating that the body has enough resources to battle the disease on its own.  Conventional medicine neglects that statement, while holistic medicine is based on it.
Nevertheless, conventional medicine may be missing an opportunity in dismissing this explanation too quickly.  Within the limits of the West’s strict paradigm, there has been collected a large number of facts on natural ways of fighting diseases.  We offer to discuss one of the most universal mechanisms to restore body’s balance.
It is known that a number of physical actions in excess of average intensity, including pain, stress, bleeding, acupuncture, sex, laughing, drugs and even highly palatable foods can trigger the release of endorphins (Fig. 5).  Pain reduction , in it’s turn, is the most common result associated with the release of endorphins.  It has been concluded recently, that any intense skin stimulation will cause a significant release of endorphins.
Another effect is the curious state the body falls into after the endorphin concentration has gone up: a number of other physiological regulators are released into the bloodstream such as growth hormone and insulin.  Each one of those regulators changes a number of different  body functions.  As a result, it is not surprising that many serious diseases are linked to the abnormalities in the endorphin system including may kinds of addiction, schizophrenia, epilepsy and Parkinson’s disease as well as PMS and weight problems. We believe that there may be some linkage between abnormalities in the endorphin system and various conditions such as schizophrenia, epilepsy, Parkinson’s disease, and may kinds of addiction.
Thus, skin stimulation, even not necessarily as accurate as in acupuncture, but intensive enough, does two things:
1. Provides additional information on the nature of the disorder to the body’s self-diagnostic system
2. Helps to create a new physiological state which is more adequate and favorable to the healing process

Read also Brain rewards, endorphins

The best of the few known conventional theories on acupuncture belongs to a team of theoretical biologists working under Dr. Dmitri Chernavski, an academician of Russian Academy of Sciences, Institute of Physics, in Moscow.  The group approached the problem from the point of view of concept of neurocomputing.

Since mid-century, using a model based on human neural structures, a whole new class of computers, possessing so called ” artificial intelligence”, has been developed  – the ones that can learn, recognize objects, and correct their own mistakes.  In somewhat of a paradox, the reverse logic has been used now, in order to explain the mechanisms of a live brain using the known electronic models.  Thus the theory of self-diagnostic function of an organism was developed.  Most of these self-diagnostic (recognizing the “image of a disease”) processes take place in the spinal cord.  In the gray matter of the spinal cord, the neurons are organized into what are called “Rexed laminae” and their functions are well-known.

The signals from the inner organs, as well as from the skin and muscles first go through the first lamina, separate from each other.  Then the signals move through the second lamina, third one, and so on, while increasingly interacting with each other and, after ten laminae, finally reach the brain in the form of one integrated set of information about the body’s state of being.  The computers that recognize objects have basically the same laminar structure and function of signal integration.  In both cases, an omitted signal from an internal organ, or one that is not strong enough, will be compensated for by the other one (e.g. from the skin), thus correcting the mistake.

According to Dr. Chernavski, skin stimulation at the point of acupuncture accomplishes the same goal.  The process of integration in the Rexed laminae increases the flow of “signals of illness” from an organ, or points out a body’s mistake in recognizing the disorder.  It is as if you wanted to send a letter to someone down the stream with little or no water using a miniature ship to carry it.  Add some water, and the ship will get there. Neither the way of adding the water nor the water itself has any effect on the content of letter sent.

Once the body has the stronger, clearer information about the injury or disease, the natural healing powers of the body take over.  What happens when the disease is recognized, the above theory does not explain, stating that the body has enough resources to battle the disease on its own.  Conventional medicine neglects that statement, while holistic medicine is based on it.

Nevertheless, conventional medicine may be missing an opportunity in dismissing this explanation too quickly.  Within the limits of the West’s strict paradigm, there has been collected a large number of facts on natural ways of fighting diseases.  We offer to discuss one of the most universal mechanisms to restore body’s balance.

It is known that a number of physical actions in excess of average intensity, including pain, stress, bleeding, acupuncture, sex, laughing, drugs and even highly palatable foods can trigger the release of endorphins (Fig. 5).  Pain reduction , in it’s turn, is the most common result associated with the release of endorphins.  It has been concluded recently, that any intense skin stimulation will cause a significant release of endorphins.

Another effect is the curious state the body falls into after the endorphin concentration has gone up: a number of other physiological regulators are released into the bloodstream such as growth hormone and insulin.  Each one of those regulators changes a number of different  body functions.  As a result, it is not surprising that many serious diseases are linked to the abnormalities in the endorphin system including may kinds of addiction, schizophrenia, epilepsy and Parkinson’s disease as well as PMS and weight problems. We believe that there may be some linkage between abnormalities in the endorphin system and various conditions such as schizophrenia, epilepsy, Parkinson’s disease, and may kinds of addiction.

Thus, skin stimulation, even not necessarily as accurate as in acupuncture, but intensive enough, does two things:

1. Provides additional information on the nature of the disorder to the body’s self-diagnostic system

2. Helps to create a new physiological state which is more adequate and favorable to the healing process

From the book Reflexo-therapy From Kuznetsov’s Applicator to Shakti Mat

May 28, 2010

Vitamin D and mental health – an easy solution for serious problems?

What is the problem?
Vitamin D deficiency has been linked not only to bone health, but also some types of cancer, lowered immune function, and kidney disease. Recent studies showed that vitamin D may preserve cognitive function exerting its neuroprotective effects via the vitamin D receptors abundantly expressed in regions frequently affected in cases of neurodegenerative diseases such as the hypothalamus, substantia nigra, cortex and hippocampus. An increased incidence of Alzheimer’s disease, schizophrenia and depression (including depression as a symptom of fibromyalgia and chronic fatigue syndrome, Clinical Rheumatology 1434-9949, 26, 4, April 2007) associated with vitamin D deficiency were reported (J Chem Neuroanat 2005;29:21-30.)
What are the causes?
Decreased bioavailability of vitamin D can be caused by malabsorption often present in cystic fibrosis, celiac disease, Whipple’s disease, Crohn’s disease, bypass surgery, and medications that reduce cholesterol absorption. 86,87
Obesity also educes availability of vitamin D locking it in the body fat depots.
Anticonvulsants, glucocorticoids
Inadequate sun exposure including that due to excessive sunscreen use
(N Engl J Med 2007;357:266-81)
Prevention by supplementation
Most experts agree that current recommendations for daily intake of vitamin D are in fact inadequate: without adequate sun exposure, children and adults require approximately 800 to 1000 IU per day (J Clin Invest 2006;
116:2062-72; Primer on the metabolic bone diseases and disorders of mineral metabolism. 6th ed. Washington, DC: American
Society for Bone and Mineral Research, 2006:129-37; Endocrinology. Philadelphia: W.B.Saunders, 2001:1009-28)

Related post: Both hypervitaminosis D3 and hypovitaminosis D3 cause premature aging of CNS

What is the problem?

Vitamin D deficiency has been linked not only to bone health, but also some types of cancer, lowered immune function, and kidney disease. Recent studies showed that vitamin D may preserve cognitive function exerting its neuroprotective effects via the vitamin D receptors abundantly expressed in regions frequently affected in cases of neurodegenerative diseases such as the hypothalamus, substantia nigra, cortex and hippocampus. An increased incidence of Alzheimer’s disease, schizophrenia and depression (including depression as a symptom of fibromyalgia and chronic fatigue syndrome, Clinical Rheumatology 1434-9949, 26, 4, April 2007) was proved to be associated with vitamin D deficiency  (J Chem Neuroanat 2005;29:21-30.)

What are the causes?

  • Decreased bioavailability of vitamin D can be caused by malabsorption often present in cystic fibrosis, celiac disease, Whipple’s disease, Crohn’s disease, bypass surgery, and medications that reduce cholesterol absorption.
  • Obesity also educes availability of vitamin D locking it in the body fat depots.
  • Anticonvulsants, glucocorticoids
  • Inadequate sun exposure including that due to excessive sunscreen use

(N Engl J Med 2007;357:266-81)

Prevention by supplementation

Most experts agree that current recommendations for daily intake of vitamin D are in fact inadequate: without adequate sun exposure, children and adults require approximately 800 to 1000 IU per day (J Clin Invest 2006; 116:2062-72; Primer on the metabolic bone diseases and disorders of mineral metabolism. 6th ed. Washington, DC: American  Society for Bone and Mineral Research, 2006:129-37; Endocrinology. Philadelphia: W.B.Saunders, 2001:1009-28)

May 6, 2010

Wrong foods for ADHD

The ‘few foods’ elimination diet (Arch Dis Child, 2001 84:404–409) is considered “a valuable instrument” for both testing the foods to blame for ADHD and, after eliminating these foods, for improving children’s behavior. 69.4% reduction on the ADHD assessment scale comparing with 45.3% in control group without dietary intervention (Eur Child & Adolescent Psychiatry, Volume 18, Number 1 / January, 2009).

The method

There are so called oligo-antigenic foods — foods that are unlikely to produce an adverse behavioral response: lamb, chicken, potatoes, rice, banana, apple and brassica (e.g., broccoli, Brussels sprouts, cabbage, Chinese cabbage, cauliflower, kale, kohlrabi, etc).

Additional foods were reintroduced, one by one, and if there was no adverse reaction they were retained in the diet. Foods causing adverse reactions were tested in a double-blind control setting: out of two similar meals only one contained the food causing an adverse reaction another being an analog of different chemical nature, for example, cows milk versus soya milk.

The usual suspects

Cows milk caused an adverse reaction in 64% of children; chocolate (59%), grapes (49%), wheat (49%), oranges (45%), cows cheese (40%) and hens egg (39%).

Food intolerance and behavior

• Some children with ADHD respond adversely to certain foods.
• Among the more common foods to blame are wheat, dairy products and chocolate.
• Not all children sharing diagnosis such as ADHD responded similarly to the diet intervention.

April 29, 2010

Caffeine protect against neurodegeneration in Alzheimer’s disease

Caffeine, the most widely consumed behaviourally active substance in the western world (Pharmacol Rev 51 1999: 83–133), has neuroprotective effects in cases of hypoxia and ischaemia (Brain Res Rev 33 2000: 258–274). Does caffeine protect against neurodegeneration in Alzheimer’s disease as it does in Parkinson’s? Researchers from Faculty of Medicine of Lisbon, Portugal, tested the hypothesis that average daily caffeine intake in the period of 20 years before the diagnosis could be lower than caffeine intake in age- and sex-matched healthy people and showed that indeed, people who was diagnosed with Alzheimer’s consumed an average 74 mg (less than one cup) while the controls had about 200 mg.
“These results, if confirmed with future prospective studies, may have a major impact on the prevention of AD,” concluded the researchers (Eur J Neurology, Volume 9, Issue 4, 2002: 377–382).
In a Canadian study, daily coffee intake decreased the risk of Alzheimer’s by 31% during a 5-year followup in 65-year old people [Am J Epidemiol 2002, 156, 445-453.]. The Finland, Italy and the
Netherlands Elderly (FINE) Study showed that elderly men drinking three cups of coffee daily had the least cognitive decline [Eur J Clin Nutr 2007, 61, 226-232]. Tea drinking  (Am J Epidemiol, 2004, 159, 959-967.], or flavonoid intake from tea  has not been associated with a reduced risk of dementia.
The low coffee consumers in mid-life had the highest occurrence of dementia and Alzheimer’s at late-life, and the highest scores on the depression scale (J Alzheimer’s Disease 16: 2009, 85–91).

Caffeine, the most widely consumed behaviourally active substance in the western world (Pharmacol Rev 51 1999: 83–133), has neuroprotective effects in cases of hypoxia and ischaemia (Brain Res Rev 33 2000: 258–274). Does caffeine protect against neurodegeneration in Alzheimer’s disease as it does in Parkinson’s? Researchers from Faculty of Medicine of Lisbon, Portugal, tested the hypothesis that average daily caffeine intake in the period of 20 years before the diagnosis could be lower than caffeine intake in age- and sex-matched healthy people and showed that indeed, people who was diagnosed with Alzheimer’s consumed an average 74 mg (less than one cup) while the controls had about 200 mg. ”These results, if confirmed with future prospective studies, may have a major impact on the prevention of Alzheimer’s,” concluded the researchers (Eur J Neurology, V 9, Issue 4, 2002: 377–382).

In a Canadian study, daily coffee intake decreased the risk of Alzheimer’s by 31% during a 5-year followup in 65-year old people (Am J Epidemiol 2002, 156, 445-453.). The Finland, Italy and the Netherlands Elderly (FINE) Study showed that elderly men drinking three cups of coffee daily had the least cognitive decline (Eur J Clin Nutr 2007, 61, 226-232). Tea drinking  (Am J Epidemiol, 2004, 159, 959-967.), or flavonoid intake from tea  has not been associated with a reduced risk of dementia. The low coffee consumers in mid-life had the highest occurrence of dementia and Alzheimer’s at late-life, and the highest scores on the depression scale (J Alzheimer’s Disease 16: 2009, 85–91).

One possible mechanism could involve insulin and degrading enzyme that degrades both insulin and amyloid-beta, the most suspected cause of Alzheimer’s (CNS Drugs 17, 2009, 27-45). Another mechanism is via adenosine receptors (caffein mimics effects of adenosine). It has been shown in mice that both caffeine and adenosine prevent amyloid-beta induced cognitive decline (Exp Neurol 203, 2007, 241-245).

April 28, 2010

Walking away from dementia

If we could delay the onset of dementia by 2 years, we could reduce its risks by as much as 25% — all other things being equal — and one of the most effective and simple ways is physical activity (Am J Public Health 1998;88:1337– 42). Drs Rockwood and Middleton from Dalhousie University, Halifax, Canada, analyzed 7 studies of exercise effects on risks of dementia and concluded that, without exception, 65 to 93 years old men and women who exercise the most have a lower risk of dementia relative to those who exercise the least. (Alzheimer’s & Dementia 3 2007; S38–S44)
Another, large-scale study found a significant dose-response relationship between physical activity and cognitive function was conducted as part of the Nurses’ Health Study  in 18,766 women (JAMA 2004;292:1454–61). After about 10 or more years, when the women were 70 to 81 years old, those reporting the most physical activity scored higher on several baseline tests of cognitive function. During the 2 years of additional follow up, there were again significant trends for a dose-response relationship in which those reporting the most physical activity exhibited the least decline in cognitive function (JAMA 2004;292:1454–61).
Even walking was associated with a “dose-dependent” risk reduction: those walked at an easy pace for at least 1.5 hours per week had significantly higher cognitive scores than those walking less than 40 minutes per week.
Higher activity levels might not be necessary for the benefit (Alzheimer Dis Assoc Disord 2004; 18:57– 64) – an increase of 30-minutes aerobic exercise frequency from 3 to 5 times per week did not result in a proportional decrease of cognitive decline in a group of 1146 women 65 years old or older.
However, for those in the higher-intensity exercise group, that worked out at least moderate intensity (more vigorously than walking), or for longer durations each day (Med Sci Sports Exerc 2001;33:772–7.) chances of cognitive impairment, Alzheimer’s, or all-cause dementia were lower (Arch Neurol 2001;58:498 –504).

If we could delay the onset of dementia by 2 years, we could reduce its risks by as much as 25% — all other things being equal — and one of the most effective and simple ways is physical activity (Am J Public Health 1998;88:1337– 42). Drs Rockwood and Middleton from Dalhousie University, Halifax, Canada, analyzed 7 studies of exercise effects on risks of dementia and concluded that, without exception, 65 to 93 years old men and women who exercise the most have a lower risk of dementia relative to those who exercise the least. (Alzheimer’s & Dementia 3 2007; S38–S44).

Another, large-scale study found a significant dose-response relationship between physical activity and cognitive function was conducted as part of the Nurses’ Health Study  in 18,766 women (JAMA 2004;292:1454–61). After about 10 or more years, when the women were 70 to 81 years old, those reporting the most physical activity scored higher on several baseline tests of cognitive function. During the 2 years of additional follow up, there were again significant trends for a dose-response relationship in which those reporting the most physical activity exhibited the least decline in cognitive function (JAMA 2004;292:1454–61).

Even walking was associated with a “dose-dependent” risk reduction: those walked at an easy pace for at least 1.5 hours per week had significantly higher cognitive scores than those walking less than 40 minutes per week. Higher activity levels might not be necessary for the benefit (Alzheimer Dis Assoc Disord 2004; 18:57– 64) – an increase of 30-minutes aerobic exercise frequency from 3 to 5 times per week did not result in a proportional decrease of cognitive decline in a group of 1146 women 65 years old or older.

However, for those in the higher-intensity exercise group, that worked out at least moderate intensity (more vigorously than walking), or for longer durations each day (Med Sci Sports Exerc 2001;33:772–7.) chances of cognitive impairment, Alzheimer’s, or all-cause dementia were lower (Arch Neurol 2001;58:498 –504).

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