Archive for the ‘Diseases’ Category
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
Message: Do not fear the fat
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
Message: Managing insulin resistance can help prevent mental problems
The metabolic syndrome’s area of influence seems to be growing startlingly fast. Latest research revealed its link to mental health problems. Researchers discovered that insulin resistance can be “in your head” and created a new medical term, the “type 3 diabetes” referring to the newly discovered insulin receptors in the brain.
Researchers at Rhode Island Hospital showed that insulin resistance is tied to neurodegeneration. A drop in insulin production in the hippocampus — the part of the brain responsible for memory — can contribute to early stages of Alzheimer’s disease. In the frontal cortex of the brain, a major area affected by Alzheimer’s, the levels of insulin receptors and the brain’s ability to respond to insulin decreased.
Whether or not an insulin shortage causes a breakdown in brain cell communication, which would explain another brain disease, schizophrenia, remains unknown, but people with schizophrenia are at least twice as likely to develop Type 2 diabetes. ”There’s a whole series of steps that may prevent the schizophrenic brain from responding to insulin,” said Dr Altar of the Psychiatric Genomics Center in Boston, which is now focusing on potential treatments for schizophrenia.
Sources:
- Dementia and Geriatric Cognitive Disorders, 2007;23:29-34
- JAMA. 2004; 292:2237-2242
- J Alzheimer’s Disease; March 2005
- J Alzheimer’s Disease; November 2005
Related:
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).
Message: Walk!
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 (1). 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 (2).
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 (3). 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 (3).
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 (4) – 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 (5) chances of cognitive impairment, Alzheimer’s, or all-cause dementia were lower (6).
Sources
- Am J Public Health 1998;88:1337– 42
- Alzheimer’s & Dementia 3 2007; S38–S44
- JAMA 2004;292:1454–61
- Alzheimer Dis Assoc Disord 2004; 18:57– 64
- Med Sci Sports Exerc 2001;33:772–7
- Arch Neurol 2001;58:498 –504
Related:
Message: Check your food sensitivity
The ‘few foods’ elimination diet (1) 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 (2).
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.
Sources
- Arch Dis Child, 2001 84:404–409
- Eur Child & Adolescent Psychiatry, Volume 18, Number 1 / January, 2009
Message: Know the enemy!
• 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.
Source: National Institute of Aging. Alzheimer’s Disease Information, May 9, 2006
In 1980s, 65% of all East Boston residents over the age of 65 were recruited in the study of neuroprotective effects of vitamins C and E. None of the people taking vitamin C or vitamin E developed Alzheimer’s disease when followed up in 4.5 years while among vitamin C non-users, 85% developed the disease. Among vitamin E non-users, 14% developed Alzheimer’s (1)
I was shown that supplementation with vitamin E and/or vitamin C might be useful in maintaining brain acetylcholinesterase (footnote a) activity at the normal level and serotonin (footnote b) concentration for some extent under the condition to induce experimental dementia in experimental animals (2)
High intake of vitamin E from food (tocopherol), but not from supplements (which usually contain alpha-tocopherol), is shown to reduce incidence of Alzheimer’s disease. The most common alpha-tocopherol alone may not be sufficient in the protective effects (3)
Sources
MC Morris et al, Vitamin E and Vitamin C Supplement Use and Risk of Incident Alzheimer Disease. Alzheimer Disease & Associated Disorders, 1998 – V12 – 3
LEE Lilha et al., Effect of supplementation of vitamin E and vitamin C on brain acetylcholinesterase activity and neurotransmitter levels in rats treated with scopolamine, an inducer of dementia, Journal of nutritional science and vitaminology, 2001, vol. 47, no5, pp. 323-328
MC Morris et. al., Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change. Am J Clin Nutrition, Vol. 81, No. 2, 508-514, February 2005
Footnotes
a) Acetylcholinesterase (AChE) is an enzyme that degrades the neurotransmitter acetylcholine at neuromuscular junctions and cholinergic synaptic transmission in the brain.
b) Serotonin is a neurotransmitter found in the central nervous system. It is best known as a “happiness hormone” though it’s no hormone but monoamine.
In 1980s, 65% of all East Boston residents over the age of 65 were recruited in the study of neuroprotective effects of vitamins C and E. None of the people taking vitamin C or vitamin E developed Alzheimer’s disease when followed up in 4.5 years while among vitamin C non-users, 85% developed the disease. Among vitamin E non-users, 14% developed Alzheimer’s (1)
I was shown that supplementation with vitamin E and/or vitamin C might be useful in maintaining brain acetylcholinesterase (footnote a) activity at the normal level and serotonin (footnote b) concentration for some extent under the condition to induce experimental dementia in experimental animals (2)
High intake of vitamin E from food (tocopherol), but not from supplements (which usually contain alpha-tocopherol), is shown to reduce incidence of Alzheimer’s disease. The most common alpha-tocopherol alone may not be sufficient in the protective effects (3)
Sources
- MC Morris et al, Vitamin E and Vitamin C Supplement Use and Risk of Incident Alzheimer Disease. Alzheimer Disease & Associated Disorders, 1998 – V12 – 3
- LEE Lilha et al., Effect of supplementation of vitamin E and vitamin C on brain acetylcholinesterase activity and neurotransmitter levels in rats treated with scopolamine, an inducer of dementia, Journal of nutritional science and vitaminology, 2001, vol. 47, no5, pp. 323-328
- MC Morris et. al., Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change. Am J Clin Nutrition, Vol. 81, No. 2, 508-514, February 2005
Footnotes
a) Acetylcholinesterase (AChE) is an enzyme that degrades the neurotransmitter acetylcholine at neuromuscular junctions and cholinergic synaptic transmission in the brain.
b) Serotonin is a neurotransmitter found in the central nervous system. It is best known as a “happiness hormone” though it’s no hormone but monoamine.
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
- 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
- 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
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).
Parkinson’s disease, though having some genetic forms, is thought to be largely life style-related and since no treatments exist to prevent or slow the disease down, environmental factors are of great interest to scientists. Earlier, in Germany (1) and Sweden, (2) consumption of coffee or caffeine have been shown to lower risk of Parkinson’s disease. However, there were some problems with interpretation of the results: coffee drinking was positively associated with smoking and alcohol consumption (3).
The Harvard School of Public Health followed up 183267 healthy people (free of Parkinson’s disease, cancer or stroke) during 10 years, watching their caffein intake with coffee, tee, chocolate and adjusting the results for age since and smocking since these two were strong risk factors in themselves (3). 288 cases of Parkinson’s disease were registered during this time. Women were more active coffee drinkers: the lower quintiles of caffein intake (taken as the reference point) in their population was 7 times higher than in men’s population.
Every other quintile in men had a lower risk of Parkinson’s disease, however, in women, the highest quintile was not associated with risk decrease – women consuming the largest amounts of caffein have had the same risk as those consuming the least caffein and for some of them the risk increased up to 1.8 times. The average highest caffein intake was 1.3 times higher in women than in men but the authors hesitate contributing the U-shaped of intake/risk curve to this difference and argued that “plausible biological basis for a protective effect of caffeine” should be established before making conclusions.
Read also:
Sources
- Hellenbrand W, Seidler A, Robra B-P, et al. Smoking and Parkinson’s disease: a case control study in Germany. Int J Epidemiol 1997; 26: 328-339. Links
- Fall P-A, Frederikson M, Axelson O, Granérus A-K. Nutritional and occupational factors influencing the risk of Parkinson’s disease: a case-control study in southeastern Sweden. Mov Disord 1999; 14: 28-37. Links
- Ascherio A, Zhang SM, Hernán MA, Kawachi I, Colditz GA, Speizer FE, Willett WCProspective study of caffeine consumption and risk of Parkinson’s disease in men and women. Ann Neurol. 2001 Jul;50(1):56-63.
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
