Is Q10 a fitness-enhancing or an anti-aging supplement in the long run?

When we talk about the energy level-enhancing and aging-hindering supplement, we mean Coenzyme Q or (2,3-dimethoxy-5 methyl-6-multiprenyl-1–4-benzoquinone) where Q stands for the quinone group, and 10 means the place the isoprenyl subunits occupies in the molecule. CoQ10 plays a very important role in the cellular power stations, mitochondria, participating in the electron transport chain. It’s a strong antioxidant since it is included in the oxidation-reduction cycle justifying its use for health-protecting purposes. Surprisingly, in the studies confirming that it’s good for you, low doses and short time intake protocols were used while it takes at least 14 weeks to observe increased levels of Q19 in mitochondria of heart, muscle, kidney, and brain.

A recent study published in The Journal of Nutrition (139: 1926–1932, 2009) was undertaken exactly in order to investigate the effects of long term intake of CoQ10 on the motor performance, sensory perception, and cognitive functions in doses either 0.68mg/g (low) or 2.6 mg/g (high). The high doses exacerbated, not prevented the cognitive and sensory impairments observed in old mice.

The authors conclude: “These findings do not support the notion that CoQ10 is a fitness-enhancing or an “antiaging” substance under normal physiological conditions.”

It is not clear, however, how these findings relate to human practice of using Q10 as a health-protecting supplement. The doses considered “low” in the study would mean almost 50 grams a day while only 50 to 200 mg (up to 1000 times lower) is recommended by health professionals. On the other hand, 300 mg/day effectively improved mitochondrial function in patients with ischaemic heart disease (comparing with patients receiving placebo), as shown in the study of Yuk-Ling Dai et al. (Atherosclerosis, 2011, online ahead of print)

139: 1926–1932, 2009

The authors conclude: “These findings do not support the notion that CoQ10 is a fitness-enhancing or an “antiaging” substance under normal physiological conditions.”

How can calorie restriction improve brain function?

Age-protection, Calorie restriction — Tags: aging, Calorie restriction, neuroprotectors — 8:32 am

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

4. It may prevent beta-amyloid neuropathology

5. It promotes neuronal plasticity

Source:

S. Gillette-Guyonneta, and B. VellasaCaloric restriction and brain function. Current Opinion in Clinical Nutrition and Metabolic Care 2008, 11:686–692

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

Age-protection, Alzheimer's, Exercise, Memory — Tags: aging, Alzheimr's, cognitive decline, dementia, Exercise — 8:52 am

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

Alzheimer’s Facts

Age-protection, Alzheimer's, Brain-Body-Mind — 7:06 am

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)

Walking away from dementia

Age-protection, Alzheimer's, Exercise, Prevention — Tags: Alzheimr's, dementia, Exercise, walking — 9:31 am

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).

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).

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.

Related:

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)

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.

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.

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

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