Thirty percent less calories = thirty percent better memory

Brain Aging, Calorie restriction, Memory — 6:33 am
Thirty percent less calories equals thirty percent better memory
Calorie restriction benefits for the aging brain health have been proposed and the mechanisms were suggested but a direct evidence showing that it can improve memory function in elderly humans appeared only recently. The study conducted in Munster, Germany, showed that a three months calorie intake reduction by 30% compared with habitual diet or a Mediterranean style diet rich in unsaturated fatty acids (although known to positively influence memory) resulted in a highly significant, 30% improvement in memory scores of 60 something group of relatively healthy people.
A. Witte et al., 2009. Caloric restriction improves memory in elderly humans. PNAS, vol. 106  no. 4  1255–126

Calorie restriction benefits for the aging brain health have been proposed and the mechanisms were suggested but a direct evidence showing that it can improve memory function in elderly humans appeared only recently. The study conducted in Munster, Germany, showed that a three months calorie intake reduction by 30% compared with habitual diet or a Mediterranean style diet rich in unsaturated fatty acids (although known to positively influence memory) resulted in a highly significant, 30% improvement in memory scores of 60 something group of relatively healthy people.

A. Witte et al., 2009. Caloric restriction improves memory in elderly humans. PNAS, vol. 106  no. 4  1255–126

Cutting down on sugar and adding fat to prevent Alzheimer’s disease

Alzheimer's, Carbohydrates, Fats — 6:46 am

According to this review, a simple dietary change towards lower carbohydrate intake and higher fats intake, may be efficiently protective against AD. >> read the article

Breakfast, protein, and hunger at lunch

Diet, Protein — 5:47 am
Veldhors and colleagues at Maastricht University, Netherlands, compared the effects of a high- (HP) and normal-protein (NP) breakfast on satiety and subsequent energy intake at lunch time. Casein was the only source of protein during breakfast to eliminate the influence of different amino acid composition. They reported that:
1. Taste perception, hedonic, and reward properties of the pretest brekfast did not differ for HP and NP.
2. Insulin and glucose was higher after NP in less than 1 hour. Satiety (3 and 4 hours after breakfast) and fullness (less than 1 hour) were higher after HP. Energy intake at lunch did not differ after HP versus NP.
The present study shows that a breakfast with 25% of energy from casein is rated as being more satiating than a breakfast with 10% of energy from casein at 3 and 4 h after breakfast, coinciding with prolonged elevated concentrations of plasma amino acids, but does not reduce subsequent energy intake.

Veldhors and colleagues at Maastricht University, Netherlands, compared the effects of a high- (HP) and normal-protein (NP) breakfast on satiety and subsequent energy intake at lunch time. Casein was the only source of protein during breakfast to eliminate the influence of different amino acid composition. They reported in British Journal of Nutrition (2009, 101, 295–303 ) that:

1. Taste perception, hedonic, and reward properties of the pretest brekfast did not differ for HP and NP.

2. Insulin and glucose was higher after NP in less than 1 hour.

3. Satiety (3 and 4 hours after breakfast) and fullness (less than 1 hour) were higher after HP.

4. Energy intake at lunch did not differ after HP versus NP.

“The present study shows that a breakfast with 25% of energy from casein is rated as being more satiating than a breakfast with 10% of energy from casein at 3 and 4 h after breakfast, coinciding with prolonged elevated concentrations of plasma amino acids, but does not reduce subsequent energy intake,” concluded the authors.

I calculated the ketogenic ratios of the pretest breakfasts. They both turned out to be below the ketogenic threshold, which is 1:2 according to the Wilder & Winter formula: 1:0.418 for NP and 1:0.565 for HP, which means that both breakfasts helped the carbohydrate but not fat metabolism. How the switch to the fat metabolism due to higher ketogenic ratios at breakfast influences metabolic and psychological parameters during the day, is a different story.

Q&A about dreaming and autistic-related symptoms

Brain Works, Brain-Body-Mind, Learning — Tags: — 5:28 am

Lucid dream – sleep or wakefulness?

Q&A and FAQ (archived) :: Ongoing Q&A :: Neuroscience Q&A and FAQ

QUESTION: Hello. I have a question that is somewhat difficult to categorize, but I had thought if anyone could give me a clue to an answer, someone in your field perhaps could, or come close. I was wondering if you could give me an idea about a possible explanation of something I used to experience years ago…

--> Read full Q&A

Neurobiology of autism-related conditions

Brain Diseases — Tags: — 5:38 am

Related: Mirror neurons, autism, and the theory of mind

Because of its relative inaccessibility, scientists have only recently been able to study the brain systematically. But with the emergence of new brain imaging tools—computerized tomography (CT), positron emission tomography (PET), single photon emission computed tomography (SPECT), and magnetic resonance imaging (MRI), study of the structure and the functioning of the brain can be done. With the aid of modern technology and the new availability of both normal and autism tissue samples to do postmortem studies, researchers will be able to learn much through comparative studies.

Postmortem and MRI studies have shown that many major brain structures are implicated in autism. This includes the cerebellum, cerebral cortex, limbic system, corpus callosum, basal ganglia, and brain stem (1). Other research is focusing on the role of neurotransmitters such as serotonin, dopamine, and epinephrine.

Major brain structures implicated in autism

Research into the causes of autism spectrum disorders is being fueled by other recent developments. Evidence points to genetic factors playing a prominent role in the causes for ASD. Twin and family studies have suggested an underlying genetic vulnerability to ASD (2). To further research in this field, the Autism Genetic Resource Exchange, a project initiated by the Cure Autism Now Foundation, and aided by an NIMH grant, is recruiting genetic samples from several hundred families. Each family with more than one member diagnosed with ASD is given a 2-hour, in-home screening. With a large number of DNA samples, it is hoped that the most important genes will be found. This will enable scientists to learn what the culprit genes do and how they can go wrong.

Another exciting development is the Autism Tissue Program (http://www.brainbank.org), supported by the Autism Society of America Foundation, the Medical Investigation of Neurodevelopmental Disorders (M.I.N.D.) Institute at the University of California, Davis, and the National Alliance for Autism Research. The program is aided by a grant to the Harvard Brain and Tissue Resource Center (http://www.brainbank.mclean.org), funded by the National Institute of Mental Health (NIMH) and the National Institute of Neurological Disorders and Stroke (NINDS). Studies of the postmortem brain with imaging methods will help us learn why some brains are large, how the limbic system develops, and how the brain changes as it ages. Tissue samples can be stained and will show which neurotransmitters are being made in the cells and how they are transported and released to other cells. By focusing on specific brain regions and neurotransmitters, it will become easier to identify susceptibility genes.

Recent neuroimaging studies have shown that a contributing cause for autism may be abnormal brain development beginning in the infant’s first months. This“growth dysregulation hypothesi” holds that the anatomical abnormalities seen in autism are caused by genetic defects in brain growth factors. It is possible that sudden, rapid head growth in an infant may be an early warning signal that will lead to early diagnosis and effective biological intervention or possible prevention of autism (3).

References

  1. Akshoomoff N, Pierce K, Courchesne E. The neurobiological basis of autism from a developmental perspective. Development and Psychopathology, 2002; 14: 613-634.
  2. Korvatska E, Van de Water J, Anders TF, Gershwin ME. Genetic and immunologic considerations in autism. Neurobiology of Disease, 2002; 9: 107-125.
  3. Courchesne E. Carper R, Akshoomoff N. Evidence of brain overgrowth in the first year of life in autism. JAMA, 2003; 290(3): 337-344.

Reprinted from NIHM
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Soy and the brain

Alzheimer's, Brain Metabolism — 12:48 pm

The female hormones estrogens influence not only reproductive function, but also learning and memory. In postmenopausal women, a lack of estrogen increases the incidence of Alzheimer’s disease (Mayo Clin. Proc. 75 (2000), pp. 1174–1184.). Soy has a high estrogenic potency, and if soy intake is high, this kind of diet may trigger many of the biological responses. In the brain, soy-enriched diet increased the size of sexually dimorphic nucleus of the hypothalamus of males while decreasing it in females while other hypothalamic nuclei (e.g., anteroventral periventricular) displayed opposite reaction to the soy diet (Neurotoxicology and Teratology Volume 24, Issue 1, January-February 2002, Pages 5-16).

The results published in October 2010 issue of the Phytotherapy Research journal (pages 1451–1456) showed that soy isoflavones can improve memory in the intoxicated (chronically aluminum exposed) mice, possibly by modulating the metabolism of brain neurotransmitters. However, a recent study suggested that soy phytoestrogens may improve working memory through estrogen-independent mechanisms (Nutritional Neuroscience, Volume 11, Number 6, December 2008 , pp. 251-262(12).

“Possible beneficial effects (e.g., reduction of serum lipids, increased bone mineral density, relief of hot flashes and other menopausal symptoms, mammary and prostate cancer chemoprevention) in humans have been attributed to consumption of isoflavones but evidence for potential adverse effects (e.g., stimulation of estrogen-dependent mammary tumors and aberrant perinatal development) has also been reported in experimental animal models.” — Daniel R. Doerge (Toxicology and Applied Pharmacology, Article in Press)

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

Age-protection — 12:41 pm

Related: Neuroprotective effects of Coenzyme Q10

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

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)

Why iodine is important for brain health

Brain Basics — Tags: — 12:38 pm

Severe endemic iodine deficiency such as in New Guinea, China, Indonesia, and Thailand causes the clinical picture of cretinism with dominant neurological pathologies;  that the most detrimental is the combination of iodine and selenium deficiencies. In the rat fetuses in such condition, experiments showed the developmental failure of the central nervous system…

>> Read the article

What is energy?

Brain Basics — 6:56 am

About these Q&A :: Q&A Category

Question

Is it true that if humans learned to use all of the brain, we could carry on as just energy?  What I mean is, could brains function without a body?

Read the answer >> Shall we ever use all of the brain?

Growth hormone and its releasers: a hope for Alzheimer’s?

Alzheimer's, Brain Aging, Memory, Supplements — 6:41 am
The growth hormone (GH) secretion declines as we age (by 14% per decade), the process called somatopause. Drugs like pyridostigmine (an acetylcholinesterase inhibitor) are able to enhance GH secretion, but its clinical use is limited due to the strong side effects. Rivastigmine, a drug for Alzheimer’s disease (AD), was found to enhance GH release (Gerontology. 2003;49:191–195).
Oral administration of certain amino acids (arginine, glutamine, glycine, and lysine)  increased the release of endogenous GH (Nutrition. 2002;18:657–661); the doses of arginine were 0.5 or 1 g/kg body weight increased GH level (J Clin Endocrinol Metab, 2011 ; Vol. 43 (3): 582-586) or roughly 35 to 70 g a day.
Arginine dissolved in distilled water was infused over a thirty-minute period in doses 1/12, 1/6 and 1/4 g. per pound of body weight. Only the highest dose (average 37.5 g total) was found to be effective in this administration mode. Interestingly, the responses of GH among females remain significantly higher than those among males (N Engl J Med 1967; 276:434-439).
The mixture of L-arginine, L-glutamine, L-lysine, and glycine at a ratio of 37:30:18.5:14.5) added as 5% of the daily meals total has been found to increase the release of endogenous GH. When mice were fed a diet containing GH-releasing supplements they had significantly fewer memory impairments and changes in acetylcholine level in hippocampus induced by Alzheimer’s amyloid beta 1–42  (J Pharmacol Sci; 2005, 99, 117 – 120).
Recently, a clinical target for improving the conditions of AD may be the activation not of GH alone but the entire GH/insulin-like growth factor-I (IGF-I) brain axis. IGF-I alone is also considered a physiological regulator of brain amyloid levels with therapeutic potential (Nature Medicine, 2002;  8, 1390 – 1397)

The growth hormone (GH) secretion declines as we age (by 14% per decade), the process called somatopause. Drugs like pyridostigmine (an acetylcholinesterase inhibitor) are able to enhance GH secretion, but its clinical use is limited due to the strong side effects. Rivastigmine, a drug for Alzheimer’s disease (AD), was found to enhance GH release (Gerontology. 2003;49:191–195).

Oral administration of certain amino acids (arginine, glutamine, glycine, and lysine)  increased the release of endogenous GH (Nutrition. 2002;18:657–661); the doses of arginine were 0.5 or 1 g/kg body weight increased GH level (J Clin Endocrinol Metab, 2011 ; Vol. 43 (3): 582-586) or roughly 35 to 70 g a day.

Arginine dissolved in distilled water was infused over a thirty-minute period in doses 1/12, 1/6 and 1/4 g. per pound of body weight. Only the highest dose (average 37.5 g total) was found to be effective in this administration mode. Interestingly, the responses of GH among females remain significantly higher than those among males (N Engl J Med 1967; 276:434-439).

The mixture of L-arginine, L-glutamine, L-lysine, and glycine at a ratio of 37:30:18.5:14.5) added as 5% of the daily meals total has been found to increase the release of endogenous GH. When mice were fed a diet containing GH-releasing supplements they had significantly fewer memory impairments and changes in acetylcholine level in hippocampus induced by Alzheimer’s amyloid beta 1–42  (J Pharmacol Sci; 2005, 99, 117 – 120).

Recently, a clinical target for improving the conditions of AD may be the activation not of GH alone but the entire GH/insulin-like growth factor-I (IGF-I) brain axis. IGF-I alone is also considered a physiological regulator of brain amyloid levels with therapeutic potential (Nature Medicine, 2002;  8, 1390 – 1397)

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