The last five articles by the Brain Fuels (click on titles to read)
August 30, 2010
BrainFuals.com’s articles on brain aging, neuroprotectors, and more
August 2, 2010
Carbohydrate Addict Diet – an intermittent ketosis plan?
Intermittent fasting is popular today. One of the aspects of this calorie restriction techniques is periodic ketosis, which is proved to be neuroprotective. Another aspect is periodic interruption of glycolysis, which is also good for the brain. However, the Hellers were first to empirically formulate the idea and make it very dieter-friendly: Rachael F. Heller, Richard F. Heller. The Carbohydrate Addict’s Diet: The Lifelong Solution to Yo-Yo Dieting. Signet (1993)
<– Carbohydrate Addict Diet Food Pyramid
This diet is for you if you have:
• forceful hunger
• craving for carbohydrate-rich foods
• need for starches
• desire for snack foods, junk food, or sweets?
Do you have problems:
• staying away from food between meals
• staying away from snacks at night
• stopping a meal containing starches and sweets
• eating tasty food while not being hungry
• staying alert after a large meal
• staying alert early afternoon
• keeping your weight off after losing weight due to dieting
Do you tend to overeat these foods:
• Breads
• Bagels
• Cakes
• Cereal
• Chocolate
• Cookies
• Crackers
• fruit
• juice
• ice cream
• potatoes
• pasta
• rice
• popcorn
• sodas?
Do you indulge in:
• sugar substitutes
• alcohol
• monosodium glutamate?
If you answered “yes” to at least one of the questions in each category, the CAD might be right for you.
The diet prescribes two meals, called Complementary Meals, which limit carbohydrate generally same way most low carb diets do. Most people choose breakfast and lunch for their complementary meals. The diet allows one Reward Meal not limiting carbohydrate content but limiting this meal’s duration to strictly one hour. It is believed that with this meal planning you body is tricked into releasing less insulin. Thus, it better controls blood sugar levels and therefore stores less fat.
The diet starts with the Entry Plan. You eat two complementary meals and a reward meal, no snacks, for a week, then you weigh. Your plan for the next week will depend on your weight loss and your weight loss goal. For instance, if you loss was around 2 pounds, you go to the Plan A, which is essentially same plan, but you are allowed to have a low carb snack.
If after following the Entry Plan for a week you lost 0.5 lb. To 2 lb., you go to the Plan B, which is in fact staying on the Entry Plan for one more week.
If you didn’t lose any weight on Entry Plan, you go to the Plan C and this is an interesting part. All you do differently comparing with the Entry Plan, is eating two big salads made of leafy green vegetables before both of your two daily complementary meals.
There’s also the Plan D, for the most stubborn body weight, where you add one more salad, before your Reward Meal. This planning goes on every new week.
From the book:
The Banta Diet: A diet mobilizing the fat burning biochemical pathway. 92 % success rate since 2002
Reprinted with permission
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
- 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
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).
Related:
April 20, 2010
April 17, 2010
The gut-brain-skin axis and probiotics
There are quite a few axes where the brain is involved. The most studied is hypothalamic–pituitary–adrenal axis dealing mostly with stress and the sleep/wake cycle and the hypothalamic-pituitary-gonadal axis reproduction, life cycle, and sexual dimorphism & behavior. Recently, emerging evidence supports the existence of communication axes between other organs as well, with the central role of the brain remaining. The gut-brain-skin axis is thought to be responsible also for the stress challenge that, if not managed, can cause skin inflammation and the hair growth inhibition. The good news is, there are ways to deal with the challenge by improving of the microflora of the guts by probiotics (Exp Dermatol. 2010 Jan 25).
For example, myocardial infarction (heart attack) causes the release of pro-inflammatory substances that may affect the function of other organs including various structures brain where they result in an increase in cell death (J Psychopharmacol 2009, 23, 451–459; Biol Psychiatry 2006, 59, 430–433) while the friendly probiotic bacteria Lactobacillus helveticus and Bifidobacterium longum taken in combination reduced these adverse effects (British Journal of Nutrition (2009), 102:1420-1425).
A spectacular result proving the gut-brain axis influence on the quality of life has been presented in the European Journal of Clinical Nutrition (2007, 61, 355–361). Those participants of the double blind controlled trial who reported themselves to be constipated infrequently were more clearheaded, confident and elated. When the participants prone to be depressed at the onset of the trial where treated with probiotics, they responded by reporting themselves as happy rather than depressed while these changes were not observed in the control group taking milk drinks containing no probiotics.
There are quite a few so called “axes” where the brain is involved. The most studied is hypothalamic–pituitary–adrenal axis dealing mostly with stress and the sleep/wake cycle and the hypothalamic-pituitary-gonadal axis reproduction, life cycle, and sexual dimorphism & behavior. Recently, emerging evidence supports the existence of communication axes between other organs as well, with the central role of the brain remaining. The gut-brain-skin axis is thought to be responsible also for the stress challenge that, if not managed, can cause skin inflammation and the hair growth inhibition. The good news is, there are ways to deal with the challenge by improving of the microflora of the guts by probiotics (Exp Dermatol. 2010 Jan 25).
For example, myocardial infarction (heart attack) causes the release of pro-inflammatory substances that may affect the function of other organs including various structures brain where they result in an increase in cell death (J Psychopharmacol 2009, 23, 451–459; Biol Psychiatry 2006, 59, 430–433) while the friendly probiotic bacteria Lactobacillus helveticus and Bifidobacterium longum taken in combination reduced these adverse effects (British Journal of Nutrition (2009), 102:1420-1425).
A spectacular result proving the gut-brain axis influence on the quality of life has been presented in the European Journal of Clinical Nutrition (2007, 61, 355–361). Those participants of the double blind controlled trial who reported themselves to be constipated infrequently were more clearheaded, confident and elated. When the participants prone to be depressed at the onset of the trial where treated with probiotics, they responded by reporting themselves as happy rather than depressed while these changes were not observed in the control group taking milk drinks containing no probiotics.
