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sunnuntai 27. heinäkuuta 2008
sunnuntai 20. heinäkuuta 2008
Taubes vastaa Braylle
"Lihavuusauktoriteetti" George Bray julkaisi varsin kummallisen kirja-arvion Obesity Reviews -tiedelehdessä muutama viikko takaperin. Artikkelissa käsiteltiin Gary Taubesin Good Calories, Bad Calories -teosta. Alla Taubesin vastine.
Letter to Editor
Response to Dr George Bray's review of Good Calories, Bad Calories
G. Taubes
Dear Editor,
I would like to thank Dr Bray for recommending Good Calories, Bad Calories (GCBC) and noting that it contains important information. However, his review did not accurately reflect the contents and arguments of my book, and so may ultimately serve only to confuse the issues discussed, rather than clarify them.
Dr Bray makes several significant errors of fact that will certainly mislead readers as to the book's actual content and arguments. Bray asserts, for instance, that GCBC includes 'a number of errors of omission or commission that are important when relating diet to disease'. The first, he says, is that I make 'no mention' of low- or high-density lipoproteins in the diet-heart discussion of the book. These are indeed discussed at great length in that context, and Bray's assertion could have been easily checked by looking in the index (HDL, 139, 154, 161–3, 165, 166–8, 169, 172–3, 182, 184, 185, 187, 196, 223. LDL, 141, 154–6, 160–1, 163, 165–8, 170–6, 184, 187, 193, 196, 200–1, 205n).
Regarding obesity, Bray makes his first critical factual error in the second sentence of his abstract. He asserts that I believe 'that you can gain weight and become obese without a positive energy balance'. This statement implies that I do not believe in the first law of thermodynamics. It could not be further from the truth. In GCBC, I point out that the first law – energy conservation – tells us nothing about what causes obesity. It says that an increase (or decrease) in the energy of a closed system – fat mass, in this case – must be associated with an energy intake greater (or less) than that expended. [Tässä on ajatusvirhe. Rasvakudos ei tietenkään ole termodynaamisesti suljettu systeemi]. It says nothing about what causes that imbalance. It implies no causality. I then suggest what European researchers concluded prior to World War II: the cause of obesity – and so of the positive energy balance that must accompany increasing body mass – is not gluttony and inactivity, but a metabolic-hormonal drive to accumulate excess fat.
Because Bray's critique confuses many of the issues in GCBC, I would like to spend a few short paragraphs clarifying them. They are quite simple. The hypothesis favored by Bray and a half century of authorities on human obesity is that fat accumulation is fundamentally caused by positive energy balance, which in turn is driven, as Bray writes, by ' "environmental" agents, such as tasty, inexpensive food in large portion sizes, inactivity, viruses, toxins, and social interactions, that interact with the genetically susceptible host to produce obesity.'
The alternative hypothesis begins with the fundamental observation that obesity is a disorder of excess fat accumulation and then asks the obvious question, what regulates fat accumulation. This was elucidated by 1965 and has never been controversial. 'Insulin is the principle regulator of fat metabolism', as Solomon Berson and Rosalyn Yalow described it then, and the mobilization of fatty acids from the fat cells 'requires only the negative stimulus of insulin deficiency'(1). This is why George Cahill, a co-editor of a 1965 American Physiological Society Handbook of Physiology dedicated to this research, (2) recently summarized the relevant science as 'carbohydrate is driving insulin and insulin is driving fat' (GCBC, p. 393). Thus, the alternative hypothesis: excess fat accumulation is caused fundamentally by the effect of dietary carbohydrates on insulin and of insulin on adipocytes. In this hypothesis overeating and sedentary behavior – i.e. positive energy balance – are compensatory effects of accumulating excess fat, not causes.
To call positive energy balance the sine qua non of obesity, as Bray does, is no more meaningful than to describe a lack of energy as the sine qua non of chronic fatigue. It tells us nothing about why the person is in positive energy balance or lacks the energy to function. It provides no information about the cause of the disorder. Bray acknowledges this fact: 'I see nothing inconsistent with the truth of the idea,' he says, 'that a positive energy balance produces obesity and the idea that it does not tell us why this imbalance occurred'. But he then says, 'Let me make my position very clear. Obesity is the result of a prolonged small positive energy surplus with fat storage as the result,' yet another way of phrasing the notion that positive energy balance causes excess fat storage.
As I note in GCBC, this inference of causality is logically indefensible. Vertical growth, too, if accompanied by increasing body mass, must be associated with positive energy balance. No one, however, (not even Bray, I presume) would state that children grow because they overeat or that their growth 'is the result of prolonged small positive energy balance'. Rather children overeat because they're growing. The causality is reversed. Understanding the true causality is critical to understanding the phenomena. The underlying cause of this vertical growth and its accompanying positive energy balance is hormonal – the secretion of growth hormone. The question posed in GCBC is why we rightfully focus on hormonal regulation when discussing growth abnormalities – gigantism, for instance, or dwarfism – but insist on discussing abnormalities of fat accumulation – obesity and anorexia – as though fundamentally caused by eating behaviour without attending to the hormonal regulation of fat tissue.
Much of Bray's critique hinges on his assertion that I believe that obese individuals do not eat more than lean individuals. He quotes a line from GCBC, but by doing so out of context directs attention away from the critical observation that must be explained. 'Even if it could be established', I wrote and Bray quotes, 'that all obese individuals eat more than do the lean – which they don't – that only tells us that eating more is associated with being obese'. The keyword in the sentence, however, is 'all'. It must be the case, as discussed in GCBC, that the obese tend to eat more than the lean, because they tend to expend more energy than the lean. This does not mean, however, that all lean individuals expend less energy than all obese individuals of comparable height, sex and bone structure. The distributions of calories consumed overlap, as do the distributions of calories expended. This is the observation that requires explanation. I do not mention doubly labelled water in this context, because the necessary observations were made with calorimeters nearly a century ago (3).
In this context, Bray's statement 'that obese people eat more food energy than do lean people' is either meaningless – is he indeed claiming that it's impossible to find lean individuals who naturally expend more energy on a daily basis than obese individuals of comparable height, sex and bone structure? – or it is indefensible. The relevant point is how greatly energy expenditure and metabolic rate 'might differ between any two individuals of equal weight, or how similar [they] might be among individuals of vastly different weights' (GCBC, p. 278).
Bray also consistently confuses associations – the obese eat more than the lean; the obese are in positive energy balance as they fatten – with causes and effects. Do they get fatter because they overeat, as Bray continues to imply, or do they overeat because they're getting fatter. The goal of science is to correctly determine causality. In these two competing hypotheses, the causalities are diametrically opposed.
Bray argues that high-fat diets cause obesity, but in GCBC I note that we can find populations that achieve spectacular obesity eating very-low-fat diets – Sumo wrestlers, for instance, whose fattening diets are only 9–16% fat (4). One implication of the co-existence of malnutrition with obesity in impoverished populations – as reported in 1928 in reservation Sioux (5), in the 1960s in Trinidad (on a diet of 21% fat) (6) and Chile (7), in the 1970s in Jamaica (8), and is now a common observation (9)– is that it's possible to develop obesity in cultures that are physically active by modern standards and that subsist on diets lacking significant or 'excess' calories and certainly lacking what Bray calls 'tasty, inexpensive food in large portion sizes'.
One reason why the Atkins diet is scientifically compelling in this context is that it is a very-high-fat diet, and yet leads to weight loss, at least in the short term, not weight gain. The question is why? And if a very-high-fat diet induces weight loss, why would a merely high-fat diet lead to weight gain?
It is true that certain strains of mice and rats get fat, as Bray notes, when large amounts of hydrogenated vegetable oil are added to their chow, but this says precious little about what happens in humans (or even other strains or species of rodents), nor does it tell us whether the added fat or the carbohydrate-rich chow is the obesogenic factor. To the best of my knowledge, experiments have never been done to determine which of the two is critical.
Bray repeatedly dismisses my observation that positive energy balance tells us nothing meaningful about weight regulation by referring to it with the rhetorically loaded phrase 'calories don't count'. He then cites Kinsell's 1964 article –'Calories Do Count'– as showing 'clearly' that calories, not nutrient composition, play the critical factor in weight loss. Bray neglects to add Kinsell's own observation that carbohydrate-restricted diets inhibit hunger in a way that calorie-restricted diets do not. 'There is a good reason to believe that the satiety value of [carbohydrate-restricted] diets is superior to diets high in carbohydrate and low in fat', Kinsell wrote, 'and hence, may be associated with better dietary adherence'(10). This observation is made repeatedly in the literature, suggesting that macronutrient composition significantly affects hunger and satiety – another observation that must be explained [Todellisuudessa Kinsellin tutkimus ei osoittanut selvästi yhtikäs mitään. Bray ilmeisesti olettaa, ettei kukaan jaksa kaivaa esille näin vanhaa artikkelia kirjaston uumenista]. From GCBC, p. 347: 'Even if we could establish that weight loss on [carbohydrate-restricted diets] is universally attended by a decrease in calories consumed . . . we then have to explain why the subjects of these diets don't manifest the symptoms of semi-starvation. If they eat less on these diets, why aren't they hungry? And if they don't eat less, why do they lose weight?' Significant fat loss on carbohydrate-restricted diets, unrestricted in calories, is the kind of paradoxical observation that might actually inform our understanding of the true aetiology of the disorder itself. It should not be dismissed without careful experimentation.
One goal of GCBC is to motivate investigators in this field to take a more rigorous, strictly scientific approach to their research, rather than taking critical issues on faith because they agree with their preconceptions. The book attempts to establish that compelling evidence indeed exists for an alternative hypothesis of obesity, and that the disorder is fundamentally caused by the influence of carbohydrates on insulin and insulin on fat accumulation, not by eating too much or sedentary behaviour as has been dogma for decades. Indeed, what we have known since the 1960s about the hormonal/enzymatic regulation of adipose tissue suggests that easily digestible carbohydrate-rich foods should make us fat, and this was accompanied until the early 1970s, when Bray and a handful of his colleagues became the authority figures in this field, with more than a century of conventional wisdom that they do. 'Every woman knows that carbohydrate is fattening', as a British Journal of Nutrition article noted in 1963 (11).
Finally, I would like to identify one potential conflict of interest on Bray's part that he neglected to mention. In the 1970s, as I discuss in GCBC, the hormonal/enzymatic regulation of fat tissue was deemed irrelevant to the cause, cure and prevention of human obesity. I identify Bray as one of two individuals most responsible for this dubious accomplishment, and 'for effectively removing the [century-old] concept of the fattening carbohydrate from the nutritional canon . . .' (GCBC, p. 417). Thus, Bray's critique of GCBC may be as much a defense of his own career as it is an unbiased assessment of the book. [Boldaus minun lisäykseni.] Readers should be aware of this possibility. It would be a shame if obesity researchers based their opinions on Bray's review, rather than the book itself.
G. Taubes
References
1. Berson SA, Yalow RS. Some current controversies in diabetes research. Diabetes 1965; 14: 549–572.
2. Renold AE, Cahill GF. Jr. (eds) Handbook of Physiology. Section 5. Adipose Tissue. American Physiological Society: Washington DC, 1965.
3. Benedict FG, Emmes LE. A comparison of the basal metabolism of normal men and women. J Bio Chem 1915; 20: 253–262.
4. Nishizawa T, Akaoka I, Nishida Y, Kawaguchi Y, Hayashi E. Some factors related to obesity in the Japanese Sumo Wrestler. Am J Clin Nutr 1976; 29: 1167–1174.
5. Stene JA, Roberts IL. A nutrition study on an Indian reservation. J Am Dietet Assoc 1928; 3: 215–222.
6. McCarthy C. Dietary and activity patterns of obese women in Trinidad. J Am Diet Assoc 1966; 48: 33–37.
7. Arteaga A. The nutritional status of Latin American adults. In: Scrimshaw NS, Moises B (eds). Nutrition and Agricultural Development. Plenum Press: New York, 1974, pp. 67–76.
8. Richards R, de Casseres M. The problem of obesity in developing countries: its prevalence and morbidity. In: Burland WL, Samuel PD, Yudkin J (eds). Obesity. Churchill Livingstone: New York, 1974, pp. 74–84.
9. Caballero O. A nutrition paradox – underweight and obesity in developing countries. N Engl J Med 2005; 352: 1514–1516.
10. Kinsell LW, Gunning B, Michaels GD, Richardson J, Cox SE, Lemon C. Calories do count. Metabolism 1964; 13: 195–204.
11. Passmore R, Swindells YE. Observations on the respiratory quotients and weight gain of man after eating large quantities of carbohydrate. Br J Nutr 1963; 17: 331–339.
Letter to Editor
Response to Dr George Bray's review of Good Calories, Bad Calories
G. Taubes
Dear Editor,
I would like to thank Dr Bray for recommending Good Calories, Bad Calories (GCBC) and noting that it contains important information. However, his review did not accurately reflect the contents and arguments of my book, and so may ultimately serve only to confuse the issues discussed, rather than clarify them.
Dr Bray makes several significant errors of fact that will certainly mislead readers as to the book's actual content and arguments. Bray asserts, for instance, that GCBC includes 'a number of errors of omission or commission that are important when relating diet to disease'. The first, he says, is that I make 'no mention' of low- or high-density lipoproteins in the diet-heart discussion of the book. These are indeed discussed at great length in that context, and Bray's assertion could have been easily checked by looking in the index (HDL, 139, 154, 161–3, 165, 166–8, 169, 172–3, 182, 184, 185, 187, 196, 223. LDL, 141, 154–6, 160–1, 163, 165–8, 170–6, 184, 187, 193, 196, 200–1, 205n).
Regarding obesity, Bray makes his first critical factual error in the second sentence of his abstract. He asserts that I believe 'that you can gain weight and become obese without a positive energy balance'. This statement implies that I do not believe in the first law of thermodynamics. It could not be further from the truth. In GCBC, I point out that the first law – energy conservation – tells us nothing about what causes obesity. It says that an increase (or decrease) in the energy of a closed system – fat mass, in this case – must be associated with an energy intake greater (or less) than that expended. [Tässä on ajatusvirhe. Rasvakudos ei tietenkään ole termodynaamisesti suljettu systeemi]. It says nothing about what causes that imbalance. It implies no causality. I then suggest what European researchers concluded prior to World War II: the cause of obesity – and so of the positive energy balance that must accompany increasing body mass – is not gluttony and inactivity, but a metabolic-hormonal drive to accumulate excess fat.
Because Bray's critique confuses many of the issues in GCBC, I would like to spend a few short paragraphs clarifying them. They are quite simple. The hypothesis favored by Bray and a half century of authorities on human obesity is that fat accumulation is fundamentally caused by positive energy balance, which in turn is driven, as Bray writes, by ' "environmental" agents, such as tasty, inexpensive food in large portion sizes, inactivity, viruses, toxins, and social interactions, that interact with the genetically susceptible host to produce obesity.'
The alternative hypothesis begins with the fundamental observation that obesity is a disorder of excess fat accumulation and then asks the obvious question, what regulates fat accumulation. This was elucidated by 1965 and has never been controversial. 'Insulin is the principle regulator of fat metabolism', as Solomon Berson and Rosalyn Yalow described it then, and the mobilization of fatty acids from the fat cells 'requires only the negative stimulus of insulin deficiency'(1). This is why George Cahill, a co-editor of a 1965 American Physiological Society Handbook of Physiology dedicated to this research, (2) recently summarized the relevant science as 'carbohydrate is driving insulin and insulin is driving fat' (GCBC, p. 393). Thus, the alternative hypothesis: excess fat accumulation is caused fundamentally by the effect of dietary carbohydrates on insulin and of insulin on adipocytes. In this hypothesis overeating and sedentary behavior – i.e. positive energy balance – are compensatory effects of accumulating excess fat, not causes.
To call positive energy balance the sine qua non of obesity, as Bray does, is no more meaningful than to describe a lack of energy as the sine qua non of chronic fatigue. It tells us nothing about why the person is in positive energy balance or lacks the energy to function. It provides no information about the cause of the disorder. Bray acknowledges this fact: 'I see nothing inconsistent with the truth of the idea,' he says, 'that a positive energy balance produces obesity and the idea that it does not tell us why this imbalance occurred'. But he then says, 'Let me make my position very clear. Obesity is the result of a prolonged small positive energy surplus with fat storage as the result,' yet another way of phrasing the notion that positive energy balance causes excess fat storage.
As I note in GCBC, this inference of causality is logically indefensible. Vertical growth, too, if accompanied by increasing body mass, must be associated with positive energy balance. No one, however, (not even Bray, I presume) would state that children grow because they overeat or that their growth 'is the result of prolonged small positive energy balance'. Rather children overeat because they're growing. The causality is reversed. Understanding the true causality is critical to understanding the phenomena. The underlying cause of this vertical growth and its accompanying positive energy balance is hormonal – the secretion of growth hormone. The question posed in GCBC is why we rightfully focus on hormonal regulation when discussing growth abnormalities – gigantism, for instance, or dwarfism – but insist on discussing abnormalities of fat accumulation – obesity and anorexia – as though fundamentally caused by eating behaviour without attending to the hormonal regulation of fat tissue.
Much of Bray's critique hinges on his assertion that I believe that obese individuals do not eat more than lean individuals. He quotes a line from GCBC, but by doing so out of context directs attention away from the critical observation that must be explained. 'Even if it could be established', I wrote and Bray quotes, 'that all obese individuals eat more than do the lean – which they don't – that only tells us that eating more is associated with being obese'. The keyword in the sentence, however, is 'all'. It must be the case, as discussed in GCBC, that the obese tend to eat more than the lean, because they tend to expend more energy than the lean. This does not mean, however, that all lean individuals expend less energy than all obese individuals of comparable height, sex and bone structure. The distributions of calories consumed overlap, as do the distributions of calories expended. This is the observation that requires explanation. I do not mention doubly labelled water in this context, because the necessary observations were made with calorimeters nearly a century ago (3).
In this context, Bray's statement 'that obese people eat more food energy than do lean people' is either meaningless – is he indeed claiming that it's impossible to find lean individuals who naturally expend more energy on a daily basis than obese individuals of comparable height, sex and bone structure? – or it is indefensible. The relevant point is how greatly energy expenditure and metabolic rate 'might differ between any two individuals of equal weight, or how similar [they] might be among individuals of vastly different weights' (GCBC, p. 278).
Bray also consistently confuses associations – the obese eat more than the lean; the obese are in positive energy balance as they fatten – with causes and effects. Do they get fatter because they overeat, as Bray continues to imply, or do they overeat because they're getting fatter. The goal of science is to correctly determine causality. In these two competing hypotheses, the causalities are diametrically opposed.
Bray argues that high-fat diets cause obesity, but in GCBC I note that we can find populations that achieve spectacular obesity eating very-low-fat diets – Sumo wrestlers, for instance, whose fattening diets are only 9–16% fat (4). One implication of the co-existence of malnutrition with obesity in impoverished populations – as reported in 1928 in reservation Sioux (5), in the 1960s in Trinidad (on a diet of 21% fat) (6) and Chile (7), in the 1970s in Jamaica (8), and is now a common observation (9)– is that it's possible to develop obesity in cultures that are physically active by modern standards and that subsist on diets lacking significant or 'excess' calories and certainly lacking what Bray calls 'tasty, inexpensive food in large portion sizes'.
One reason why the Atkins diet is scientifically compelling in this context is that it is a very-high-fat diet, and yet leads to weight loss, at least in the short term, not weight gain. The question is why? And if a very-high-fat diet induces weight loss, why would a merely high-fat diet lead to weight gain?
It is true that certain strains of mice and rats get fat, as Bray notes, when large amounts of hydrogenated vegetable oil are added to their chow, but this says precious little about what happens in humans (or even other strains or species of rodents), nor does it tell us whether the added fat or the carbohydrate-rich chow is the obesogenic factor. To the best of my knowledge, experiments have never been done to determine which of the two is critical.
Bray repeatedly dismisses my observation that positive energy balance tells us nothing meaningful about weight regulation by referring to it with the rhetorically loaded phrase 'calories don't count'. He then cites Kinsell's 1964 article –'Calories Do Count'– as showing 'clearly' that calories, not nutrient composition, play the critical factor in weight loss. Bray neglects to add Kinsell's own observation that carbohydrate-restricted diets inhibit hunger in a way that calorie-restricted diets do not. 'There is a good reason to believe that the satiety value of [carbohydrate-restricted] diets is superior to diets high in carbohydrate and low in fat', Kinsell wrote, 'and hence, may be associated with better dietary adherence'(10). This observation is made repeatedly in the literature, suggesting that macronutrient composition significantly affects hunger and satiety – another observation that must be explained [Todellisuudessa Kinsellin tutkimus ei osoittanut selvästi yhtikäs mitään. Bray ilmeisesti olettaa, ettei kukaan jaksa kaivaa esille näin vanhaa artikkelia kirjaston uumenista]. From GCBC, p. 347: 'Even if we could establish that weight loss on [carbohydrate-restricted diets] is universally attended by a decrease in calories consumed . . . we then have to explain why the subjects of these diets don't manifest the symptoms of semi-starvation. If they eat less on these diets, why aren't they hungry? And if they don't eat less, why do they lose weight?' Significant fat loss on carbohydrate-restricted diets, unrestricted in calories, is the kind of paradoxical observation that might actually inform our understanding of the true aetiology of the disorder itself. It should not be dismissed without careful experimentation.
One goal of GCBC is to motivate investigators in this field to take a more rigorous, strictly scientific approach to their research, rather than taking critical issues on faith because they agree with their preconceptions. The book attempts to establish that compelling evidence indeed exists for an alternative hypothesis of obesity, and that the disorder is fundamentally caused by the influence of carbohydrates on insulin and insulin on fat accumulation, not by eating too much or sedentary behaviour as has been dogma for decades. Indeed, what we have known since the 1960s about the hormonal/enzymatic regulation of adipose tissue suggests that easily digestible carbohydrate-rich foods should make us fat, and this was accompanied until the early 1970s, when Bray and a handful of his colleagues became the authority figures in this field, with more than a century of conventional wisdom that they do. 'Every woman knows that carbohydrate is fattening', as a British Journal of Nutrition article noted in 1963 (11).
Finally, I would like to identify one potential conflict of interest on Bray's part that he neglected to mention. In the 1970s, as I discuss in GCBC, the hormonal/enzymatic regulation of fat tissue was deemed irrelevant to the cause, cure and prevention of human obesity. I identify Bray as one of two individuals most responsible for this dubious accomplishment, and 'for effectively removing the [century-old] concept of the fattening carbohydrate from the nutritional canon . . .' (GCBC, p. 417). Thus, Bray's critique of GCBC may be as much a defense of his own career as it is an unbiased assessment of the book. [Boldaus minun lisäykseni.] Readers should be aware of this possibility. It would be a shame if obesity researchers based their opinions on Bray's review, rather than the book itself.
G. Taubes
References
1. Berson SA, Yalow RS. Some current controversies in diabetes research. Diabetes 1965; 14: 549–572.
2. Renold AE, Cahill GF. Jr. (eds) Handbook of Physiology. Section 5. Adipose Tissue. American Physiological Society: Washington DC, 1965.
3. Benedict FG, Emmes LE. A comparison of the basal metabolism of normal men and women. J Bio Chem 1915; 20: 253–262.
4. Nishizawa T, Akaoka I, Nishida Y, Kawaguchi Y, Hayashi E. Some factors related to obesity in the Japanese Sumo Wrestler. Am J Clin Nutr 1976; 29: 1167–1174.
5. Stene JA, Roberts IL. A nutrition study on an Indian reservation. J Am Dietet Assoc 1928; 3: 215–222.
6. McCarthy C. Dietary and activity patterns of obese women in Trinidad. J Am Diet Assoc 1966; 48: 33–37.
7. Arteaga A. The nutritional status of Latin American adults. In: Scrimshaw NS, Moises B (eds). Nutrition and Agricultural Development. Plenum Press: New York, 1974, pp. 67–76.
8. Richards R, de Casseres M. The problem of obesity in developing countries: its prevalence and morbidity. In: Burland WL, Samuel PD, Yudkin J (eds). Obesity. Churchill Livingstone: New York, 1974, pp. 74–84.
9. Caballero O. A nutrition paradox – underweight and obesity in developing countries. N Engl J Med 2005; 352: 1514–1516.
10. Kinsell LW, Gunning B, Michaels GD, Richardson J, Cox SE, Lemon C. Calories do count. Metabolism 1964; 13: 195–204.
11. Passmore R, Swindells YE. Observations on the respiratory quotients and weight gain of man after eating large quantities of carbohydrate. Br J Nutr 1963; 17: 331–339.
lauantai 19. heinäkuuta 2008
Mitä Atkins-ryhmä söi?
Internetissä porukka ihmettelee mitä em. dieettitutkimuksen Atkins-ryhmäläiset söivät, sillä eräissä tiedotusvälineissä on höpisty kasvipainoitteisesta Atkins-dieetistä. Tässä vastaus suoraan pääkallopaikalta:
This is kind of funny that some could think of a "vegetarian low-carb"
diet. Is it a new suggested strategy? Could be interesting idea but this
wasn't the case here. Our low-carb diet was based on Atkins, the
participants read the book and the recipes were more or less comparable
to what you know in the states. Beef is the main red meat. What could be
different? People here would not mix in the same meal meat and butter, a
salad is considered a very rich one and not a lettuce based, and the
main dressing is olive oil. As for beverages, same industry that makes
money everywhere.
For example, a plate could include: fish or fried/not bread coated
chicken/or red meet, broccoli and mushrooms coated with eggs, roasted
eggplants, vegetable salad (peppers, cucumber, green leaves, not
lettuce) with olive oil dressing. I understand that some of the
low-fat people find it hard to believe that such a low-carb diet was
tremendously favorable within 2 years in a well designed study, but
these are the facts and the science of tomorrow, with the next long term
studies in the pipeline, may confirm or not these findings.
Best regards, Iris
This is kind of funny that some could think of a "vegetarian low-carb"
diet. Is it a new suggested strategy? Could be interesting idea but this
wasn't the case here. Our low-carb diet was based on Atkins, the
participants read the book and the recipes were more or less comparable
to what you know in the states. Beef is the main red meat. What could be
different? People here would not mix in the same meal meat and butter, a
salad is considered a very rich one and not a lettuce based, and the
main dressing is olive oil. As for beverages, same industry that makes
money everywhere.
For example, a plate could include: fish or fried/not bread coated
chicken/or red meet, broccoli and mushrooms coated with eggs, roasted
eggplants, vegetable salad (peppers, cucumber, green leaves, not
lettuce) with olive oil dressing. I understand that some of the
low-fat people find it hard to believe that such a low-carb diet was
tremendously favorable within 2 years in a well designed study, but
these are the facts and the science of tomorrow, with the next long term
studies in the pipeline, may confirm or not these findings.
Best regards, Iris
perjantai 18. heinäkuuta 2008
Paula-täti varoittaa Atkins-dieetistä
New England Journal of Medicine -tiedelehdessä julkaistu dieettitutkimus on aiheuttanut ihan syystäkin paljon keskustelua myös kotimaisissa lehdissä, radiossa ja TV:ssä. Kyseessä oli siis suurella koehenkilöjoukolla suoritettu, kontrolloitu kliininen tutkimus, ei siis mikään epidemiologinen hömppätutkimus. Niinpä jokainen itseään kunnioittava ravitsemusasiantuntija on varmasti tutustunut ko. tiedelehden nettisivuilla ilmaiseksi luettavissa olevaan kokotekstiartikkeliin. Paprun voi löytää esim. google-hauan kautta noin kymmenessä sekunnissa.
Tekniikan lisensiaatti, ravitsemusasiantuntija (?) Paula Heinonen ei nähtävästi ole vielä oppinut käyttämään internettiä tai sitten hän on asunut viime päivät jossain luolassa. Hän oli nimittäin juuri Radio Voimassa "asiantuntijakommentaattorina" kyseisen tutkimuksen tiimoilta. Muuten ihan hyvä, mutta Paula-tätä ei ollut edes lukenut ko. julkaisua. Olen uhrannut lähes viisi minuuttia Paula-tädin ravitsemusläpysköiden lukemiseen, ja ne tarjoavat ihan pätevää tietoa maha-suolikanavan terveyden ja ravitsemuksen välisistä yhteyksistä. Lienee kuitenkin selvää, että Paula-täti ei ole oikea henkilö kommentoimaan mitään kliinisiä dieettitutkimuksia (erityisesti jos ei ole niitä edes lukenut!).
Tulee mieleen kolmisen vuotta takaperin käyty keskustelu allekirjoittaneen, NY:n valtionyliopiston lääkiksen biokemian professorin ja amerikkalaisen kansanterveystieteilijän välillä. Viimeksi mainittu ilkkui "vaihtoehtoisten dieettien" fysiologis-biokemiallista perustaa, joskin ihan väärin perustein. Ihmettelin biokemian profalle, että "Mitä hemmettiä toi äijä höpisee? Eihän toi ymmärrä edes ihmisen metabolian alkeita." (tietysti lontoon kielellä). Biokemian proffa närkästyi kansanterveystietelijän keljuiluista ja tokaisi varsin vihaisena: "You have no credentials [kritisoida kenenkään fysiologis-biokemiallista tietämystä]". Totesin kansanterveystieteilijälle, että eihän hän ymmärrä edes ihmisen metabolian peruskonsepteja, joten hänen olisi parempi olla höpisemättä mitään näistä asioista. Vastaus oli, että lähiaikoina julkaistavat tutkimukset tulevat osoittamaan, että kumpi se ei oikeasti ymmärrä. Niin ne osoittivatkin.
Keskustelu alkoi saada tulenkatkuisia piirteitä, joten Jeff Volek diplomaattisena miehenä rupesi hieromaan sovintoa "koulukuntien" välille todeten, että "Sun jutuissa on järkeä, mutta niin on myös toisen leirin jutuissa [insuliinitasojen vaikutukset veren lipoproteiineihin, varastorasvojen mobilisaatioon yms.]". Muuten, kyseisen kansanterveystietelijän alkuperäisiin "neronleimauksiin" kuuluu myös KTL:n pääjohtajan Pekka Puskan käyttämä "kyllä rotanmyrkylläkin laihtuu" -argumentti (sic).
Paula-täti, you have no credentials either.
Tekniikan lisensiaatti, ravitsemusasiantuntija (?) Paula Heinonen ei nähtävästi ole vielä oppinut käyttämään internettiä tai sitten hän on asunut viime päivät jossain luolassa. Hän oli nimittäin juuri Radio Voimassa "asiantuntijakommentaattorina" kyseisen tutkimuksen tiimoilta. Muuten ihan hyvä, mutta Paula-tätä ei ollut edes lukenut ko. julkaisua. Olen uhrannut lähes viisi minuuttia Paula-tädin ravitsemusläpysköiden lukemiseen, ja ne tarjoavat ihan pätevää tietoa maha-suolikanavan terveyden ja ravitsemuksen välisistä yhteyksistä. Lienee kuitenkin selvää, että Paula-täti ei ole oikea henkilö kommentoimaan mitään kliinisiä dieettitutkimuksia (erityisesti jos ei ole niitä edes lukenut!).
Tulee mieleen kolmisen vuotta takaperin käyty keskustelu allekirjoittaneen, NY:n valtionyliopiston lääkiksen biokemian professorin ja amerikkalaisen kansanterveystieteilijän välillä. Viimeksi mainittu ilkkui "vaihtoehtoisten dieettien" fysiologis-biokemiallista perustaa, joskin ihan väärin perustein. Ihmettelin biokemian profalle, että "Mitä hemmettiä toi äijä höpisee? Eihän toi ymmärrä edes ihmisen metabolian alkeita." (tietysti lontoon kielellä). Biokemian proffa närkästyi kansanterveystietelijän keljuiluista ja tokaisi varsin vihaisena: "You have no credentials [kritisoida kenenkään fysiologis-biokemiallista tietämystä]". Totesin kansanterveystieteilijälle, että eihän hän ymmärrä edes ihmisen metabolian peruskonsepteja, joten hänen olisi parempi olla höpisemättä mitään näistä asioista. Vastaus oli, että lähiaikoina julkaistavat tutkimukset tulevat osoittamaan, että kumpi se ei oikeasti ymmärrä. Niin ne osoittivatkin.
Keskustelu alkoi saada tulenkatkuisia piirteitä, joten Jeff Volek diplomaattisena miehenä rupesi hieromaan sovintoa "koulukuntien" välille todeten, että "Sun jutuissa on järkeä, mutta niin on myös toisen leirin jutuissa [insuliinitasojen vaikutukset veren lipoproteiineihin, varastorasvojen mobilisaatioon yms.]". Muuten, kyseisen kansanterveystietelijän alkuperäisiin "neronleimauksiin" kuuluu myös KTL:n pääjohtajan Pekka Puskan käyttämä "kyllä rotanmyrkylläkin laihtuu" -argumentti (sic).
Paula-täti, you have no credentials either.
Leusiinin antikataboliset ominaisuudet
Nutrition & Metabolism -tiedelehdessä ilmestyi juuri varsin hyvä katsausartikkeli leusiinin antikatabolisista vaikutuksista luustolihaksissa. Leusiini on siis haaraketjuinen aminohappo, jonka tiedetään stimuloivan tehokkaasti lihasproteiinianaboliaa. Kyseinen katsaus kuitenkin pureutui leusiinin lihasproteiinien hajoamista estäviin vaikutuksiin.
Lyhyt yhteenveto:
1. Leusiini vähentää selvästi luustolihasproteiinien hajoamista (kataboliaa).
2. Leusiinin proteiinisynteesiä (anaboliaa) lisäävä vaikutus saadaan aikaiseksi suhteellisen pienellä annoksella, mutta antikatabolisen vaikutuksen puolella annos-vastesuhde säilyy, vaikka annos nostettaisiin n. 10-20-kertaiseksi verrattuna proteiinisynteesin maksimoivaan annokseen.
3. Leusiinista voi olla hyötyä erityisesti tilanteissa, joissa lihasproteiinien katabolia on lisääntynyt. Terveiden urheilijoiden ja kuntoilijoiden tapauksessa antikatabolisesta vaikutuksesta lienee hyötyä ainakin tiukan dieetin aikana.
Lyhyt yhteenveto:
1. Leusiini vähentää selvästi luustolihasproteiinien hajoamista (kataboliaa).
2. Leusiinin proteiinisynteesiä (anaboliaa) lisäävä vaikutus saadaan aikaiseksi suhteellisen pienellä annoksella, mutta antikatabolisen vaikutuksen puolella annos-vastesuhde säilyy, vaikka annos nostettaisiin n. 10-20-kertaiseksi verrattuna proteiinisynteesin maksimoivaan annokseen.
3. Leusiinista voi olla hyötyä erityisesti tilanteissa, joissa lihasproteiinien katabolia on lisääntynyt. Terveiden urheilijoiden ja kuntoilijoiden tapauksessa antikatabolisesta vaikutuksesta lienee hyötyä ainakin tiukan dieetin aikana.
torstai 17. heinäkuuta 2008
Uusi, merkittävä dieettitutkimus
New England Journal of Medicine -tiedelehti julkaisi juuri uuden dieettitutkimuksen. Onneksi Christer ehti jo asiasta kirjoittaa suomenkielisen yhteenvedon, joten minun ei tarvitse vaivautua.
lauantai 12. heinäkuuta 2008
Tieteellisen kirjallisuuden lukeminen - Osa I
[Juttu jäi keskeneräiseksi, sillä blogi taas temppuilee. Jatkan myöhemmin]
Uffen foorumilla oli puhetta tieteellisten tutkimusten tulkinnasta ynnä muusta sellaisesta. Maallikoilla on taipumusta tulkita väärin tiettyjä engl.kielisiä termejä, joten päätin pitää lyhykäisen "luennon" asian tiimoilta.
Ensimmäisessa esimerkkitutkimuksessa Joy Frested ja kumppanit selvittivät heraproteiinivalmisteen vaikutuksia kehonkoostumukseen laihdutuksen aikana.
Tutkimustiivistelmä:
Background
This study evaluated a specialized whey fraction (Prolibra™, high in leucine, bioactive peptides and milk calcium) for use as a dietary supplement to enhance weight loss.
Methods
This was a randomized, double-blind, parallel-arm, 12-week study. Caloric intake was reduced 500 calories per day. Subjects consumed Prolibra or an isocaloric ready-to-mix beverage 20 minutes before breakfast and 20 minutes before dinner. Body fat and lean muscle tissue were measured by dual-energy x-ray absorptiometry (DEXA). Body weight and anthropometric measurements were recorded every 4 weeks. Blood samples were taken at the beginning and end of the study. Statistical analyses were performed on all subjects that completed (completer analysis) and all subjects that lost at least 2.25 kg of body weight (responder analysis). Within group significance was determined at P <>
Results
Both groups lost a significant amount of weight and the Prolibra group tended to lose more weight than the control group; however the amount of weight loss was not significantly different between groups after 12 weeks. Prolibra subjects lost significantly more body fat compared to control subjects for both the completer (2.81 vs. 1.62 kg P = 0.03) and responder (3.63 vs. 2.11 kg, P = 0.01) groups. Prolibra subjects lost significantly less lean muscle mass in the responder group (1.07 vs. 2.41 kg, P = 0.02). The ratio of fat to lean loss (kg fat lost/kg lean lost) was much larger for Prolibra subjects for both completer (3.75 vs. 1.05) and responder (3.39 vs. 0.88) groups.
Conclusion
Subjects in both the control and treatment group lost a significant amount of weight with a 500 calorie reduced diet. Subjects taking Prolibra lost significantly more body fat and showed a greater preservation of lean muscle compared to subjects consuming the control beverage. Because subjects taking Prolibra lost 6.1% of their body fat mass, and because a 5% reduction of body fat mass has been shown to reduce the risk of obesity related disease, the results have practical significance.
Tiivistelmästä ilmenevät keskisimmät asiat. Kyseessä oli siis 12 viikon kestoinen, satunnaistettu (koehenkilöt heitettiin kahteen ryhmään sattumanvaraisesti) kaksoissokkotutkimus (tutkijat ja koehenkilöt eivät tienneet vielä tutkimuksen aikana kuka sai mitäkin valmistetta). Lumetuotteena oli samanmakuista ja -näköistä hiilihydraattijauhetta. Ruokavalion kalorimäärää vähennettiin 500 kcal/vrk.
Termi "paraller-arm" ei tietenkään viittaa anatomiseen käsivarteen, vaan kahteen "tutkimuskäsivarteen" (isompi ryhmä jakautui siis kahteen käsivarteen eli tutkimusryhmään). Pääasiallinen muuttuja tutkimuksessa oli kehonkoostumus, joka mitattiin ns. DEXA:lla. Kyseessä on tarkka, muttei kuitenkaan täydellinen menetelmä. (Tiivistelmässä on pieni epätarkkuus; pitäisi lukea "lean body mass", ei lean muscle mass", joskin tässä tapauksessa nämä käsitteet ovat lähes synonyymejä.)
Kehonkoostumuksen osalta tulokset olivat seuraavanlaisia:
No baseline differences were found between groups for any body composition parameters (Table 1). After 12 weeks there were significant differences (Table 5). Weight loss was consistently higher in the Prolibra subjects and DEXA analyses showed that the weight loss in the Prolibra group was primarily the result of losing body fat. Prolibra subjects lost significantly more body fat compared to control subjects in both the completer (2.81 kg vs. 1.62 kg P = 0.03) and responder (3.63 kg vs. 2.11 kg, P = 0.01) analysis. The Prolibra subjects lost significantly less lean muscle mass compared to control subjects in the responder analysis (2.41 kg vs. 1.07 kg, P = 0.02); however the completer analysis did not show a significant difference between Prolibra and control subjects (1.55 kg vs. 0.75 kg, P = 0.11). Fat loss to lean loss ratio (kg fat loss/kg of lean loss) for Prolibra subjects was higher compared to the control in both the completer (3.75 vs. 1.05) and responder (3.39 vs. 0.88) analysis.
Eli tutkimuksen alussa ryhmien välillä ei ollut eroja. Tutkimuksen lopussa heraproteiinivalmistetta saanut ryhmä vähensi kehon rasvoja merkitsevästi enemmän kuin plaseboryhmä. Heraproteiiniryhmä myöskin menetti merkitsevästi vähemmän rasvatonta massaa kuin plaseboryhmä, joskin tilastolliseti merkitsevä tulos saavutettiin vain ns. responder-henkilöillä (nämä henkilöt tiputtivat painoa väh. 2,25 kg). On syytä huomata, että "significantly" tarkoittaa tieteellisessä kirjallisuudessa tilastollista merkitsevyyttä, ei välttämättä käytännön merkittävyyttä. Tässä tapauksessa tutkijat kuitenkin totesivat, että "the results have practical significance". Allekirjoittanut yhtyy tähän tulkintaan.
On myös huomattava, että termit "lean body mass" tai "fat free mass" eivät tarkoita lihasmassaa. Fat free mass tarkoittaa nimensä mukaisesti kehon massaa ilman rasvoja. Lean body mass tarkoittaa melkein samaa asiaa, mutta siihen sisältyy myös ns. essentielli rasva, joka sijaitsee mm. luuytimessä, maksassa, pernassa ja munuaisissa (n. 3 % painosta). Tässä tutkimuksessa DEXA:lla määritetty lean body mass kuvastaa hyvin lihasmassassa taphtuneita muutoksia, mutta urheiluravinnekuluttajien on syytä tietää, että aikuisella rasvattoman kehonosan vesipitoisuus on noin 73 %. Näin ollen väitteet, että esim. "tuote X lisää lihasmassaa kaksi kiloa 6 viikossa" ovat hölynpölyä.
Uffen foorumilla oli puhetta tieteellisten tutkimusten tulkinnasta ynnä muusta sellaisesta. Maallikoilla on taipumusta tulkita väärin tiettyjä engl.kielisiä termejä, joten päätin pitää lyhykäisen "luennon" asian tiimoilta.
Ensimmäisessa esimerkkitutkimuksessa Joy Frested ja kumppanit selvittivät heraproteiinivalmisteen vaikutuksia kehonkoostumukseen laihdutuksen aikana.
Tutkimustiivistelmä:
Background
This study evaluated a specialized whey fraction (Prolibra™, high in leucine, bioactive peptides and milk calcium) for use as a dietary supplement to enhance weight loss.
Methods
This was a randomized, double-blind, parallel-arm, 12-week study. Caloric intake was reduced 500 calories per day. Subjects consumed Prolibra or an isocaloric ready-to-mix beverage 20 minutes before breakfast and 20 minutes before dinner. Body fat and lean muscle tissue were measured by dual-energy x-ray absorptiometry (DEXA). Body weight and anthropometric measurements were recorded every 4 weeks. Blood samples were taken at the beginning and end of the study. Statistical analyses were performed on all subjects that completed (completer analysis) and all subjects that lost at least 2.25 kg of body weight (responder analysis). Within group significance was determined at P <>
Results
Both groups lost a significant amount of weight and the Prolibra group tended to lose more weight than the control group; however the amount of weight loss was not significantly different between groups after 12 weeks. Prolibra subjects lost significantly more body fat compared to control subjects for both the completer (2.81 vs. 1.62 kg P = 0.03) and responder (3.63 vs. 2.11 kg, P = 0.01) groups. Prolibra subjects lost significantly less lean muscle mass in the responder group (1.07 vs. 2.41 kg, P = 0.02). The ratio of fat to lean loss (kg fat lost/kg lean lost) was much larger for Prolibra subjects for both completer (3.75 vs. 1.05) and responder (3.39 vs. 0.88) groups.
Conclusion
Subjects in both the control and treatment group lost a significant amount of weight with a 500 calorie reduced diet. Subjects taking Prolibra lost significantly more body fat and showed a greater preservation of lean muscle compared to subjects consuming the control beverage. Because subjects taking Prolibra lost 6.1% of their body fat mass, and because a 5% reduction of body fat mass has been shown to reduce the risk of obesity related disease, the results have practical significance.
Tiivistelmästä ilmenevät keskisimmät asiat. Kyseessä oli siis 12 viikon kestoinen, satunnaistettu (koehenkilöt heitettiin kahteen ryhmään sattumanvaraisesti) kaksoissokkotutkimus (tutkijat ja koehenkilöt eivät tienneet vielä tutkimuksen aikana kuka sai mitäkin valmistetta). Lumetuotteena oli samanmakuista ja -näköistä hiilihydraattijauhetta. Ruokavalion kalorimäärää vähennettiin 500 kcal/vrk.
Termi "paraller-arm" ei tietenkään viittaa anatomiseen käsivarteen, vaan kahteen "tutkimuskäsivarteen" (isompi ryhmä jakautui siis kahteen käsivarteen eli tutkimusryhmään). Pääasiallinen muuttuja tutkimuksessa oli kehonkoostumus, joka mitattiin ns. DEXA:lla. Kyseessä on tarkka, muttei kuitenkaan täydellinen menetelmä. (Tiivistelmässä on pieni epätarkkuus; pitäisi lukea "lean body mass", ei lean muscle mass", joskin tässä tapauksessa nämä käsitteet ovat lähes synonyymejä.)
Kehonkoostumuksen osalta tulokset olivat seuraavanlaisia:
No baseline differences were found between groups for any body composition parameters (Table 1). After 12 weeks there were significant differences (Table 5). Weight loss was consistently higher in the Prolibra subjects and DEXA analyses showed that the weight loss in the Prolibra group was primarily the result of losing body fat. Prolibra subjects lost significantly more body fat compared to control subjects in both the completer (2.81 kg vs. 1.62 kg P = 0.03) and responder (3.63 kg vs. 2.11 kg, P = 0.01) analysis. The Prolibra subjects lost significantly less lean muscle mass compared to control subjects in the responder analysis (2.41 kg vs. 1.07 kg, P = 0.02); however the completer analysis did not show a significant difference between Prolibra and control subjects (1.55 kg vs. 0.75 kg, P = 0.11). Fat loss to lean loss ratio (kg fat loss/kg of lean loss) for Prolibra subjects was higher compared to the control in both the completer (3.75 vs. 1.05) and responder (3.39 vs. 0.88) analysis.
Eli tutkimuksen alussa ryhmien välillä ei ollut eroja. Tutkimuksen lopussa heraproteiinivalmistetta saanut ryhmä vähensi kehon rasvoja merkitsevästi enemmän kuin plaseboryhmä. Heraproteiiniryhmä myöskin menetti merkitsevästi vähemmän rasvatonta massaa kuin plaseboryhmä, joskin tilastolliseti merkitsevä tulos saavutettiin vain ns. responder-henkilöillä (nämä henkilöt tiputtivat painoa väh. 2,25 kg). On syytä huomata, että "significantly" tarkoittaa tieteellisessä kirjallisuudessa tilastollista merkitsevyyttä, ei välttämättä käytännön merkittävyyttä. Tässä tapauksessa tutkijat kuitenkin totesivat, että "the results have practical significance". Allekirjoittanut yhtyy tähän tulkintaan.
On myös huomattava, että termit "lean body mass" tai "fat free mass" eivät tarkoita lihasmassaa. Fat free mass tarkoittaa nimensä mukaisesti kehon massaa ilman rasvoja. Lean body mass tarkoittaa melkein samaa asiaa, mutta siihen sisältyy myös ns. essentielli rasva, joka sijaitsee mm. luuytimessä, maksassa, pernassa ja munuaisissa (n. 3 % painosta). Tässä tutkimuksessa DEXA:lla määritetty lean body mass kuvastaa hyvin lihasmassassa taphtuneita muutoksia, mutta urheiluravinnekuluttajien on syytä tietää, että aikuisella rasvattoman kehonosan vesipitoisuus on noin 73 %. Näin ollen väitteet, että esim. "tuote X lisää lihasmassaa kaksi kiloa 6 viikossa" ovat hölynpölyä.
torstai 10. heinäkuuta 2008
Voimailu ja alakarppaus
Jenkktutkijat selvittivät vastikään alakarppaamisen yhdistämistä voimailuun. Tutkimusta ei ole vielä julkaistu, mutta Jeff Volek lähetti minulle juuri tutkimustiivistelmän.
Effects of diets restricted in fat and carbohydrate with and without resistance training on body composition and cardiovascular risk
Kevin D. Ballard, Erin E. Quann, Michael J. Puglisi, Cassandra E. Forsythe, Brittanie M. Volk, Cherise C. Labonte, Maria-Luz L. Fernandez, William J. Kraemer, Timothy P. Scheett, Jeff S. Volek.
PURPOSE: We examined the effects of low-carbohydrate and low-fat diets alone and in combination with resistance training on body composition and cardiovascular risk.
METHODS: Forty-seven overweight (BMI 31.26±3.78) men (age 33.7±1.5y) were assigned to a low-fat diet (LFD) (25% of energy) or a carbohydrate restricted diet (CRD) (15% of energy). Two additional groups performed a whole-body, nonlinear periodized resistance training (RT) program 3 d/wk while consuming either the LFD or the CRD diet. Body composition (via DXA), fasting blood lipids and exercise performance were determined before and after the 12-wk intervention.
RESULTS: Reductions in body mass, fat mass, percent body fat and abdominal fat were greater in the CRD than the LFD (p<0.001). The addition of RT to the CRD resulted in greater improvements in percent body fat than diet alone (-4.8 vs. -5.5% for CRD and CRD-RT, respectively). Gains in lean body mass were demonstrated in the training groups only (p=0.004). CRD resulted in greater reductions in plasma triglycerides (TG) (p=0.023) and TG/HDL-C ratio (p=0.035), while increasing LDL peak particle size (p<0.001). Maximum bench press and back squat strength were greater (p≤0.002) in the RT groups, with no diet effect detected.
CONCLUSION: Resistance exercise is an effective strategy to combat diet-induced losses of lean body mass. The combination of CRD and RT resulted in the greatest improvements in body composition and cardiovascular health.
Effects of diets restricted in fat and carbohydrate with and without resistance training on body composition and cardiovascular risk
Kevin D. Ballard, Erin E. Quann, Michael J. Puglisi, Cassandra E. Forsythe, Brittanie M. Volk, Cherise C. Labonte, Maria-Luz L. Fernandez, William J. Kraemer, Timothy P. Scheett, Jeff S. Volek.
PURPOSE: We examined the effects of low-carbohydrate and low-fat diets alone and in combination with resistance training on body composition and cardiovascular risk.
METHODS: Forty-seven overweight (BMI 31.26±3.78) men (age 33.7±1.5y) were assigned to a low-fat diet (LFD) (25% of energy) or a carbohydrate restricted diet (CRD) (15% of energy). Two additional groups performed a whole-body, nonlinear periodized resistance training (RT) program 3 d/wk while consuming either the LFD or the CRD diet. Body composition (via DXA), fasting blood lipids and exercise performance were determined before and after the 12-wk intervention.
RESULTS: Reductions in body mass, fat mass, percent body fat and abdominal fat were greater in the CRD than the LFD (p<0.001). The addition of RT to the CRD resulted in greater improvements in percent body fat than diet alone (-4.8 vs. -5.5% for CRD and CRD-RT, respectively). Gains in lean body mass were demonstrated in the training groups only (p=0.004). CRD resulted in greater reductions in plasma triglycerides (TG) (p=0.023) and TG/HDL-C ratio (p=0.035), while increasing LDL peak particle size (p<0.001). Maximum bench press and back squat strength were greater (p≤0.002) in the RT groups, with no diet effect detected.
CONCLUSION: Resistance exercise is an effective strategy to combat diet-induced losses of lean body mass. The combination of CRD and RT resulted in the greatest improvements in body composition and cardiovascular health.
perjantai 4. heinäkuuta 2008
EnergyTube - Energiaporetabletti
Manninen Nutraceuticals Oy tuo lähitulevaisuudessa markkinoille herkullisen energiaporetabletin. Tuotteen nimi on EnergyTube. Yhdessä putkilossa on 20 poretablettia ja yksi poretabletti sisältää energiaa 7,5 kcal, 64 mg kofeiinia, 400 mg tauriinia, 6 mg niasiinia, 2 mg pantoteenihappoa jne. Näillä näkymin EnergyTube-valmistetta tullaan myymään kymmenen putkilon laatikoissa.
Korkea kofeiinipitoisuus (32 mg/100 ml valmista juomaa). Korkeintaan kolme tablettia päivässä. Ei suositella lapsille, raskaana oleville tai kofeiiniherkille henkilöille. Älä käytä tuotetta jos sinulla on joku sydänsairaus, kohonnut verenpaine, aivoverenkiertohäiriö, kilpirauhasen liika- tai vajaatoiminta, virtsaamisvaikeuksia, diabetes, mahahaava tai sairaaloisesti ylipainoa. Älä käytä tuotetta jos kärsit unettomuudesta, ahdistuksesta tai hermostuneisuudesta. Käyttäessäsi tätä tuotetta vähennä selvästi muiden kofeiinipitoisten tuotteiden, kuten kahvin, teen ja energiajuomien, käyttöä. Tätä tuotetta ei saa käyttää yhdessä alkoholin kanssa. Jos tuotteen käyttö aiheuttaa haittavaikutuksia, kuten päänsärkyä, sydämentykytystä tai unettomuutta, lopeta käyttö välittömästi ja ota yhteyttä lääkäriisi sekä tuotteen markkinoijaan tuotepalautuksen sopimiseksi. Tuotetta ei tule käyttää monipuolisen ruokavalion korvikkeena. Tuotetta ei ole tarkoitettu minkään sairauden hoitoon, parantamiseen, ehkäisyyn tai diagnosointiin. EnergyTube säilytetään huoneenlämmössä poissa lasten ulottuvilta. Viimeinen käyttöpäivä on merkitty pakkaukseen.
Korkea kofeiinipitoisuus (32 mg/100 ml valmista juomaa). Korkeintaan kolme tablettia päivässä. Ei suositella lapsille, raskaana oleville tai kofeiiniherkille henkilöille. Älä käytä tuotetta jos sinulla on joku sydänsairaus, kohonnut verenpaine, aivoverenkiertohäiriö, kilpirauhasen liika- tai vajaatoiminta, virtsaamisvaikeuksia, diabetes, mahahaava tai sairaaloisesti ylipainoa. Älä käytä tuotetta jos kärsit unettomuudesta, ahdistuksesta tai hermostuneisuudesta. Käyttäessäsi tätä tuotetta vähennä selvästi muiden kofeiinipitoisten tuotteiden, kuten kahvin, teen ja energiajuomien, käyttöä. Tätä tuotetta ei saa käyttää yhdessä alkoholin kanssa. Jos tuotteen käyttö aiheuttaa haittavaikutuksia, kuten päänsärkyä, sydämentykytystä tai unettomuutta, lopeta käyttö välittömästi ja ota yhteyttä lääkäriisi sekä tuotteen markkinoijaan tuotepalautuksen sopimiseksi. Tuotetta ei tule käyttää monipuolisen ruokavalion korvikkeena. Tuotetta ei ole tarkoitettu minkään sairauden hoitoon, parantamiseen, ehkäisyyn tai diagnosointiin. EnergyTube säilytetään huoneenlämmössä poissa lasten ulottuvilta. Viimeinen käyttöpäivä on merkitty pakkaukseen.
keskiviikko 2. heinäkuuta 2008
Kofeiini ja glykogeenin resynteesi
Journal of Applied Physiology -tiedeläpyskässä ilmestyi juuri mielenkiintoinen tutkimus, jonka mukaan kofeiini tehostaa selvästi luustolihasten glykogeeniresynteesiä eli hiilihydraatin varastomuodon uudelleen muodostumista harjoittelun jälkeen. Koehenkilöt saivat joko 1) hiilihydraatteja 4 grammaa per painokilo + 8 milligrammaa kofeiinia per painokilo tai 2) pelkästään hiilareita 4 grammaa per painokilo. Tulokset osoittivat, että hiilareita pakkautui lihaksiin hiilari+kofeiini -ryhmässä n. 66 prosenttia enemmän 4 tunnin aikana kuin hiilariryhmässä. Samainen tutkimusryhmä aikoo tutkia pienemmän kofeiiniannoksen vaikutuksia lähitulevaisuudessa. Senioritutkija John Hawleyn haastattelun voit tsekata täältä.
tiistai 1. heinäkuuta 2008
MyoReco-kuvat
Jälleenmyyjillemme tiedoksi, että MyoReco-kuvat ovat vihdoin kuvagalleriassa. Tuotetiedot löytyvät täältä. MyoRecon tukkumyyntierä on 4 x 3000 g.
PS. Blogissa jotain vikaa, kun parina viime päivänä tekstinasettelut eivät ole toimineet, joten sanat katkeilevat mistä kohtaa sattuu toiselle riville. Myöskään kappalejako ei jostain syystä onnistu. Yritän fiksata probleeman.
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