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.

    Thirty percent less calories = thirty percent better memory

    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

    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.

    Soy and the brain

    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)

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

    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)

    Vitamins C and E to prevent Alzheimer’s

    In 1980s, 65% of all East Boston residents over the age of 65 were recruited in the study of neuroprotective effects of vitamins C and E. None of the people taking vitamin C or vitamin E developed Alzheimer’s disease when followed up in 4.5 years while among vitamin C non-users, 85% developed the disease. Among vitamin E non-users, 14% developed Alzheimer’s (1)
    I was shown that supplementation with vitamin E and/or vitamin C might be useful in maintaining brain acetylcholinesterase (footnote a) activity at the normal level and serotonin (footnote b) concentration for some extent under the condition to induce experimental dementia in experimental animals (2)
    High intake of vitamin E from food (tocopherol), but not from supplements (which usually contain alpha-tocopherol), is shown to reduce incidence of Alzheimer’s disease. The most common alpha-tocopherol alone may not be sufficient in the protective effects (3)
    Sources
    MC Morris et al, Vitamin E and Vitamin C Supplement Use and Risk of Incident Alzheimer Disease. Alzheimer Disease & Associated Disorders, 1998 – V12 – 3
    LEE Lilha et al., Effect of supplementation of vitamin E and vitamin C on brain acetylcholinesterase activity and neurotransmitter levels in rats treated with scopolamine, an inducer of dementia, Journal of nutritional science and vitaminology, 2001, vol. 47, no5, pp. 323-328
    MC  Morris et. al., Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change. Am J Clin Nutrition, Vol. 81, No. 2, 508-514, February 2005
    Footnotes
    a) Acetylcholinesterase (AChE) is an enzyme that degrades  the neurotransmitter acetylcholine at neuromuscular junctions and cholinergic synaptic transmission in the brain.
    b) Serotonin is a neurotransmitter found in the central nervous system. It is best known as a “happiness hormone” though it’s no hormone but monoamine.

    In 1980s, 65% of all East Boston residents over the age of 65 were recruited in the study of neuroprotective effects of vitamins C and E. None of the people taking vitamin C or vitamin E developed Alzheimer’s disease when followed up in 4.5 years while among vitamin C non-users, 85% developed the disease. Among vitamin E non-users, 14% developed Alzheimer’s (1)

    I was shown that supplementation with vitamin E and/or vitamin C might be useful in maintaining brain acetylcholinesterase (footnote a) activity at the normal level and serotonin (footnote b) concentration for some extent under the condition to induce experimental dementia in experimental animals (2)

    High intake of vitamin E from food (tocopherol), but not from supplements (which usually contain alpha-tocopherol), is shown to reduce incidence of Alzheimer’s disease. The most common alpha-tocopherol alone may not be sufficient in the protective effects (3)

    Sources

    1. MC Morris et al, Vitamin E and Vitamin C Supplement Use and Risk of Incident Alzheimer Disease. Alzheimer Disease & Associated Disorders, 1998 – V12 – 3
    2. LEE Lilha et al., Effect of supplementation of vitamin E and vitamin C on brain acetylcholinesterase activity and neurotransmitter levels in rats treated with scopolamine, an inducer of dementia, Journal of nutritional science and vitaminology, 2001, vol. 47, no5, pp. 323-328
    3. MC  Morris et. al., Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change. Am J Clin Nutrition, Vol. 81, No. 2, 508-514, February 2005

    Footnotes

    a) Acetylcholinesterase (AChE) is an enzyme that degrades  the neurotransmitter acetylcholine at neuromuscular junctions and cholinergic synaptic transmission in the brain.

    b) Serotonin is a neurotransmitter found in the central nervous system. It is best known as a “happiness hormone” though it’s no hormone but monoamine.

    How can calorie restriction improve brain function?

    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

    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 promotes 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

    Age-related hearing loss and nutrition

    It has been suggested that nutrition may play a role in age-related hearing loss and that it may be associated with poor micronutrient status. For example, Vitamin B-12 or folate deficiencies may negatively influence blood flow to the cochlea, leading to age-related hearing loss. Australian researchers showed that people with hearing loss were more likely to be exposed to workplace noise, be a current smoker, have a doctor-diagnosed history of stroke or type 2 diabetes, and to have Vitamin B-12 (1).
    In Finland, two groups of 40-59-year olds were studied, 1) one on a diet high in saturated animal fats, 2) the other on a diet high in polyunsaturated fats. After 5 years of follow up, blood vessel condition was better in the group 2 and the participants hearing ability was also significantly better in all frequencies. After that, the diets in the two groups were reversed. Four years after the diet reversal the hearing in the now low-fat group was improved and the hearing in the now high-fat group was deteriorating. The authors concluded that a diet high in polyunsaturated fats may stop, if not reverse, hearing loss (2).
    In a recent Dutch study, 720 participants 50–70 years of age without hearing loss were tested for levels of polyunsaturated fats, very long-chain n-3 PUFA in their plasma. In high sound frequencies, there was no correlation of hearing acuity and PUFA concentrations in plasma. However, in the low frequencies, the higher PUFA levels corresponded to better hearing abilities. The authors found their results “encouraging, but requirig confirmation from future studies.” (3)
    Serum Homocysteine and Folate Concentrations Are Associated with Prevalent Age-Related Hearing Loss. Journal of Nutrition, Vol. 140, No. 8, 1469-1474, Aug, 2010
    DIETARY PREVENTION OF HEARING LOSS. Acta Otolaryng 70: 242-247, 1970
    PLASMA VERY LONG-CHAIN N-3 POLYUNSATURATED FATTY ACIDS AND AGE-RELATED HEARING LOSS IN OLDER ADULTS. THE JOURNAL OF NUTRITION, HEALTH & AGING Volume 14, Number 5, 347-351, 200

    It has been suggested that nutrition may play a role in age-related hearing loss and that it may be associated with poor micronutrient status. For example, Vitamin B-12 or folate deficiencies may negatively influence blood flow to the cochlea, leading to age-related hearing loss. Australian researchers showed that people with hearing loss were more likely to be exposed to workplace noise, be a current smoker, have a doctor-diagnosed history of stroke or type 2 diabetes, and to have Vitamin B-12 (1).

    In Finland, two groups of 40-59-year olds were studied, 1) one on a diet high in saturated animal fats, 2) the other on a diet high in polyunsaturated fats. After 5 years of follow up, blood vessel condition was better in the group 2 and the participants hearing ability was also significantly better in all frequencies. After that, the diets in the two groups were reversed. Four years after the diet reversal the hearing in the now low-fat group was improved and the hearing in the now high-fat group was deteriorating. The authors concluded that a diet high in polyunsaturated fats may stop, if not reverse, hearing loss (2).

    In a recent Dutch study, 720 participants 50–70 years of age without hearing loss were tested for levels of polyunsaturated fats, very long-chain n-3 PUFA in their plasma. In high sound frequencies, there was no correlation of hearing acuity and PUFA concentrations in plasma. However, in the low frequencies, the higher PUFA levels corresponded to better hearing abilities. The authors found their results “encouraging, but requirig confirmation from future studies.” (3)

    1. Serum Homocysteine and Folate Concentrations Are Associated with Prevalent Age-Related Hearing Loss. Journal of Nutrition, Vol. 140, No. 8, 1469-1474, Aug, 2010
    2. DIETARY PREVENTION OF HEARING LOSS. Acta Otolaryng 70: 242-247, 1970
    3. PLASMA VERY LONG-CHAIN N-3 POLYUNSATURATED FATTY ACIDS AND AGE-RELATED HEARING LOSS IN OLDER ADULTS. THE JOURNAL OF NUTRITION, HEALTH & AGING Volume 14, Number 5, 347-351, 200

    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

    Older Posts » To leave a comment or question click here