Atkins diet research

Calorie restriction, Diet — 5:19 am

“The Atkins Nutritional Approach counts grams of carbohydrates instead of calories… If you are losing weight, there is no need to concern yourself with counting calories. ”

Source: atkins.com

You might be doubtful and chances are that mainstream diets are the reason. Of course you couldn’t avoid opinions like the below Q&A posted by Health Care Reality Check:

Q: Can a person eat unlimited calories, and still lose weight, as long as they severely restrict carbohydrates?

A: No, she can not. The basis of ketogenic diets, such as the Atkins Diet, is a severe restriction of carbohydrate calories, which simply causes a net reduction in total calories. Since carbohydrate calories are limited, intake of fat usually increases. This high fat diet causes ketosis (increased blood ketones from fat breakdown), which suppresses hunger, and thus contributes to caloric restriction. — Ellen Coleman, RD, MA, MPH

Is this a correct answer?

Let’s first discuss whether it’s a correct question. Or, rather, is this the real question so frequently asked by dieters. In my experience, this in fact sounds a little bit different but this makes ALL the difference.

This is what real dieters ask:

Q: Can low carb dieters eat all they want, and still lose weight as long as they only eat allowed foods?

A: Yes, they can. The basis of ketogenic diets, such as the Atkins Diet, is a restriction of carbohydrate-containing foods in favor of fat and protein containing foods, which causes the state of ketosis resulting in significant decrease in appetite. Since appetite decreases, most of low carb dieters consume significantly less calories WITHOUT INTENTIONAL CALORIE RESTRICTION.

Is there scientific evidence? There is.

Study #1 by: Bassett Research Institute in Cooperstown, NY and Durham (N.C.) Veterans Affairs Medical Center.

Reported: Proceedings of North American Association for the Study of Obesity, Oct. 29, 2000, Long Beach, CA

Who participated:

  • 18 obese men and women with 30 or more pounds to lose.
  • Average calorie intake before the study: 2,481 calories a day
  • Method:

    Dr. Atkins’ Book, the “New Diet Revolution” used as instruction for the dieters.

    Results:

    1. Calorie intake during the most restrictive induction phase (when only 20 g of carbohydrates were allowed) was 1,419 calories a day on average and weight loss was more than 8 pounds on average.

    2. Calorie intake during the ongoing weight-loss phase (when carbohydrate intake is being increased gradually, by 5 g a day) dieters ate an average of 1,500 calories a day and lost an additional 3 pounds in two weeks.

    3. The calorie reduction was attributed almost completely to carbohydrate abstaining. Intake of fat and protein remained practically the same as before the diet.

    4. After 6 months on Atkins diet, 41 overweight people lost an average of 10% of their weight. Most dieters lowered their cholesterol by 5%, but there were a few whose cholesterol increased.

    5. 20 out of 41 dieters continued the program, and kept the lost weight off for more than a year.

    Study #2 by: Harvard School of Public Health.

    Reported: American Association for the Study of Obesity, October 16, 2003

    Who participated: 21 overweight volunteers.

  • Two groups were randomly assigned to either lowfat or low-carb diets with 1,500 calories for women and 1,800 for men; a third group was also low-carb but got an extra 300 calories a day.
  • Method:

    All the food was prepared at a restaurant in Cambridge, Massachusetts. Note that most earlier studies including the above Study #1 simply gave out diet plans.

    So in this study, dieters were given dinner and a bedtime snack as well as breakfast and lunch for the next day, which made the setting a carefully controlled one. Foods were mostly fish, chicken, salads, vegetables and unsaturated oils. Red meats and saturated fats were limited (as opposed to traditional Atkins menus.)

    All meals looked similar but were cooked to different recipes. The low-carb meals were 5% carbs, 15% protein, 65% fat. The low fat group got 55% carbohydrate, 15% protein, 30% fat.

    Results:

    1. All dieters lost weight, but those on low carb diet lost more than the low fat group — even while consuming MORE calories:

    - Group on lower-cal, low-carb diet lost an average of 23 lbs.

    - Group on same-calories low-fat diet lost an average of 17 lbs.

    - Group on extra 300 calories, low-carb diet lost an average of 20 lbs.

    2. Over the course of the study, the group of low carb dieters who got an extra 300 calories a day consumed extra 25,000 calories. That should have added up to about seven pounds. But for some reason, it did not.

    Discussion:

    “It doesn’t make sense, does it?” said Barbara Rolls of Pennsylvania State University. “It violates the laws of thermodynamics. No one has ever found any miraculous metabolic effects.”

    So it violates the laws of thermodynamics, huh? Not so fast! When it comes to calorie counting, the “calorie is a calorie” concept is very deceiving.

    Let’s see what we count when we think we count calories. When you burn a piece of wood in a stove, you can directly measure how much heat energy it produces. Then you can claim that you know how many calories a piece of wood contains, right? Not exactly. You should specify what kind of wood it was, dry or wet, how you burned it, etc. Because if you spent another material to start the burning, you should subtract these calories from the total; if the wood was wet you should take into account the calories that the water evaporation took. So even with a piece of wood, it’s not that simple.

    Now look at a piece of food. You know how they tell how many calories it contains? Same way they talk about a piece of wood in a stove. It’s the calorie number that the food would produce by being burnt in a stove.

    Then in addition to the wood’s calorie estimation (that takes into account the dryness, etc.), you should add many more circumstances: how hard should one chew it before being able to swallow, how hard one’s enzyme system will have work to digest it, will it influence the hormones in charge of fat storing? What about its effect on the hormones in charge of fat burning?

    Which chain of reactions will it trigger, activity-wise or metabolism-wise? Will it make one sleepy, thus conserving the energy? Ot will it make one jumpy, thus wasting the energy?

    Study #3 by: Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto 606-8501, Japan

    Reported: J Clin Endocrinol Metab. 2003 Dec;88(12):5661-7

    Method:

    Healthy boys, aged 8-11 yr, were examined for resting energy expenditure and the thermic effect of a meal, which were measured for three hours after a same-calorie but high-fat or a high-carb meals.

    Results:

    There was no changes after high carbohydrate meals but there was an increase in resting energy expenditure after a high-fat meal.

    If the researchers in the Study #2 would have measured resting energy expenditure and the thermic effects of the meals, they would probably have registered the same changes. Then everybody would make a sigh of relief: none of the laws of thermodynamics have been violated; yes, the low-carb dieters COULD INDEED eat more calories and lose more weight than the low-fat group while violating no physical laws because — they just burnt more, all the time, even at rest. It’s that simple.

    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.

    Exercise improves IQ and cognitive scores of retarded children and adults

    Historically, the teachers, researchers and caregivers of mentally retarded children and adults paid their attention to intellectual development, while the role of physical fitness stayed uncertain. The interest in recreation activity has been increased in 1990s however, the practitioners are still reluctant to use fitness programs in their students’ curricula, although motor skills development had been emphasized.

    Researchers Drs Cabler-Halle, James W. Halle, and Barry Chung at the University of Illinois in their review tried to find causal relationships between aerobic fitness and improvements in mental, emotional, ans social scores of retarded children and adults.

    They examines (1) the effects of aerobic exercise on intellectual, behavioral, and self-conceptual changes in persons with mental retardation and comcludes that in spite of many methodical flaus and insufficiant statistical data, a clear effect of improvement was observed — often immediately — after aerovic exercising for as little as 10 minutes or as long as 2 hours. Few data have been reported positive effects of aerobic exercise on IQ scores. It’s been suggested (2) that children with developmental delays are more sensitive to the effects of interventions designed to affect mental function than individuals who are not developmentally delayed

    The authors concluded “Perhaps physical fitness programming for those with developmenral disabilities would have wider appeal and application if it were embedded in the bTOadeT contexl of psychological and behavioral change (i.e., engagement in exercise produces generalized changes beyond direct improvement in physical well-being).”

    Sources:

    1. Res Devel Disabil Vol. 14, pp. 359-386, 1993

    2. Educ Psychol Rev (2008) 20:111–131

    BrainFuels.com’s articles on brain aging, neuroprotectors, and more

    Brain Basics, Diet — 9:19 am

    The last five articles by the Brain Fuels (click on titles to read)

    1. Complex Regional Pain Syndrome (CRPS) and vegan diet
    2. MCT and beta-hydroxybutirate protect cognitive and synaptic functions
    3. Excitatory GABA: “Maybe It’s Not So Exciting After All!”
    4. Q&A: Puzzled by a poster at SFN
    5. pH, GDP, energy substrates…



    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)

    intermittent ketosis<– 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

    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

    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)

    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.

    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).

    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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