Just came across THIS paper, entitled "Low-Total-Fat Diet Did Not Reduce the Risk of Cardiovascular Events".
The Women's Health Initiative Dietary Modification Trial (WHI DMT) was the largest single randomized trial to date examining the effects of a lowfat diet on health outcomes, including the incidence of cardiovascular events over 8 years in 48,835 women. WHI DMT compared the effect of intensive dietary counseling designed to reduce the intake of total fat to < 20% of daily caloric intake against conventional diet.
Conclusions. Intensive dietary counseling to promote a low-total-fat diet did not reduce cardiovascular events in healthy adults.
That won't stop the 'experts' doling out the same old wrong and pointless advice, though.
Friday, 13 November 2009
UK Trends in Fat Consumption
Here's a bit of data from the university course in nutrition I did recently. It is from a course text, but no origin of the data is specified.
The average total fat intake per person per day in the UK was apparently 121 grams in 1970, 106 grams in 1980, 86 grams in 1990 and 74 grams in 2000.
We can see that, according to these figures, total fat intake has dropped considerably, by about 40% in fact.
Average intake of saturated fats per person per day was 19.3% in 1970, 18.9% in 1980, 16.7% in 1990 and 15% in 2000. Unfortunately, the text doesn't specify what the percentage was exactly. Percentage of total calories? Percentage of fat calories? Percentage of weight of food eaten?? Anyways, let's assume from these figures that saturated fat consumption has been going down.
Similarly, monounsaturated fat consumption decreased between 1970 and 2000, from 16% to 13.5%. (Again, % of what??)
However, polyunsaturated fat consumption nearly doubled during that period, from about 4% to about 7%.
So, total fat consumption has decreased over the last 30 years. Saturated fat consumption has decreased. Monounsaturated fat consumption has decreased. Only consumption of polyunsaturates has increased.
Interesting.
So, what is the conclusion of the people who offered this data?
...rises in obesity over the past 50 years do correlate with increasing fat intake and decreasing carbohydrate intake.
Hmmm... Obesity increasing.... fat consumption decreasing...
I am still looking for the correlation.
The average total fat intake per person per day in the UK was apparently 121 grams in 1970, 106 grams in 1980, 86 grams in 1990 and 74 grams in 2000.
We can see that, according to these figures, total fat intake has dropped considerably, by about 40% in fact.
Average intake of saturated fats per person per day was 19.3% in 1970, 18.9% in 1980, 16.7% in 1990 and 15% in 2000. Unfortunately, the text doesn't specify what the percentage was exactly. Percentage of total calories? Percentage of fat calories? Percentage of weight of food eaten?? Anyways, let's assume from these figures that saturated fat consumption has been going down.
Similarly, monounsaturated fat consumption decreased between 1970 and 2000, from 16% to 13.5%. (Again, % of what??)
However, polyunsaturated fat consumption nearly doubled during that period, from about 4% to about 7%.
So, total fat consumption has decreased over the last 30 years. Saturated fat consumption has decreased. Monounsaturated fat consumption has decreased. Only consumption of polyunsaturates has increased.
Interesting.
So, what is the conclusion of the people who offered this data?
...rises in obesity over the past 50 years do correlate with increasing fat intake and decreasing carbohydrate intake.
Hmmm... Obesity increasing.... fat consumption decreasing...
I am still looking for the correlation.
Wednesday, 11 November 2009
Neuroprotective and disease-modifying effects of the ketogenic diet
I just came across THIS paper on the benefits of a ketogenic diet for neurological problems.
I have read about these before, as I have a personal interest in dietary treatments for epilepsy, and I know that a ketogenic diet is also being studied as a means of improving Alzheimer's and Parkinson's diseases.
This is the abstract:
The ketogenic diet has been in clinical use for over 80 years, primarily for the symptomatic treatment of epilepsy. A recent clinical study has raised the possibility that exposure to the ketogenic diet may confer long-lasting therapeutic benefits for patients with epilepsy. Moreover, there is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer’s disease and Parkinson’s disease, and may also be protective in traumatic brain injury and stroke. These observations are supported by studies in animal models and isolated cells that show that ketone bodies, especially β-hydroxybutyrate, confer neuroprotection against diverse types of cellular injury. This review summarizes the experimental, epidemiological and clinical evidence indicating that the ketogenic diet could have beneficial effects in a broad range of brain disorders characterized by the death of neurons. Although the mechanisms are not yet well defined, it is plausible that neuroprotection results from enhanced neuronal energy reserves, which improve the ability of neurons to resist metabolic challenges, and possibly through other actions including antioxidant and anti-inflammatory effects. As the underlying mechanisms become better understood, it will be possible to develop alternative strategies that produce similar or even improved therapeutic effects without the need for exposure to an unpalatable and unhealthy, high-fat diet.
It's an awful shame that the authors feel that a diet with such amazing potential is unhealthy and unpalatable. But I guess there's no money in advising a diet.. the money is in a drug-related solution.
I have read about these before, as I have a personal interest in dietary treatments for epilepsy, and I know that a ketogenic diet is also being studied as a means of improving Alzheimer's and Parkinson's diseases.
This is the abstract:
The ketogenic diet has been in clinical use for over 80 years, primarily for the symptomatic treatment of epilepsy. A recent clinical study has raised the possibility that exposure to the ketogenic diet may confer long-lasting therapeutic benefits for patients with epilepsy. Moreover, there is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer’s disease and Parkinson’s disease, and may also be protective in traumatic brain injury and stroke. These observations are supported by studies in animal models and isolated cells that show that ketone bodies, especially β-hydroxybutyrate, confer neuroprotection against diverse types of cellular injury. This review summarizes the experimental, epidemiological and clinical evidence indicating that the ketogenic diet could have beneficial effects in a broad range of brain disorders characterized by the death of neurons. Although the mechanisms are not yet well defined, it is plausible that neuroprotection results from enhanced neuronal energy reserves, which improve the ability of neurons to resist metabolic challenges, and possibly through other actions including antioxidant and anti-inflammatory effects. As the underlying mechanisms become better understood, it will be possible to develop alternative strategies that produce similar or even improved therapeutic effects without the need for exposure to an unpalatable and unhealthy, high-fat diet.
It's an awful shame that the authors feel that a diet with such amazing potential is unhealthy and unpalatable. But I guess there's no money in advising a diet.. the money is in a drug-related solution.
Saturated Fat Snippets
I just came across these snippets of information on the website of The European Food Information Council (EUFIC).
Emerging research suggests that individual saturated fatty acids have their own important biological functions in the body:
Butyric acid regulates the expression of several genes and may play a role in cancer prevention by stopping the development of cancer cells;
Palmitic acid is involved in the regulation of hormones;
Palmitic and myristic acids are involved in cell messaging and immune function.
Other roles of saturated fatty acids that still require further evidence in humans include:
Myristic acid may regulate the availability of polyunsaturated fatty acids like docosahexaenoic acid (DHA)
Lauric acid may be the raw material for producing omega-3 fatty acids (when omega-3 fatty acids are unavailable in the diet).
They then go on to say that saturated fats must, of course, be avoided.
Emerging research suggests that individual saturated fatty acids have their own important biological functions in the body:
Butyric acid regulates the expression of several genes and may play a role in cancer prevention by stopping the development of cancer cells;
Palmitic acid is involved in the regulation of hormones;
Palmitic and myristic acids are involved in cell messaging and immune function.
Other roles of saturated fatty acids that still require further evidence in humans include:
Myristic acid may regulate the availability of polyunsaturated fatty acids like docosahexaenoic acid (DHA)
Lauric acid may be the raw material for producing omega-3 fatty acids (when omega-3 fatty acids are unavailable in the diet).
They then go on to say that saturated fats must, of course, be avoided.
Omega-6
Well, HERE is a paper that was published in 1999 in Carcinogenesis journal.
Studies in animal models and recent observations in humans, however, have provided evidence that a high intake of omega-6 polyunsaturated fatty acids (PUFAs), stimulates several stages in the development of mammary and colon cancer, from an increase in oxidative DNA damage to effects on cell proliferation, free estrogen levels to hormonal catabolism.
Current evidence from experimental and human studies is summarized that implicates a high intake of omega-6 PUFAs in cancer of the breast, colon and, possibly, prostate.
If you do a search, you'll find many, many studies that say the same thing.. omega-6 PUFA, also called linoleic acid, is associated with increased incidence of various types of cancer.
What about heart disease? Surely sunflower oil is best for that?
HERE's another paper.
Can linoleic acid contribute to coronary artery disease?
JM Hodgson, ML Wahlqvist, JA Boxall and ND Balazs
Department of Medicine, Monash Medical Centre, Melbourne, Australia.
The adipose tissue concentration of linoleic acid was positively associated with the degree of coronary artery disease (CAD) in a cross- sectional study of 226 patients undergoing coronary angiography. Linoleic acid concentration in adipose tissue is known to reflect the intake of this fatty acid. These results are therefore indicative of a positive relationship between linoleic acid intake and CAD. The platelet linoleic acid concentration was also positively associated with CAD.
So, that sunflower oil, which is stuffed full of linoleic acid, doesn't seem so healthy after all.
Tuesday, 10 November 2009
More on Protein and Bones
I've just been reading about protein and bone health in one of the courses I am doing... The text mentions a study that was done to investigate whether protein supplements helped recovery of elderly patients who had suffered a fractured neck of femur. It states 'The supplemented group spent, on average, less time in the hospital than did the control group.'
So, the protein supplementation improved recovery from a nasty break.
The course text doesn't identify the exact study, but Googling 'protein supplementation femur' gives a few positive studies, including this one:
Dietary Protein Supplementation and Recovery from Femoral Fracture
Kimberly H. Porter M.S. Mary Ann Johnson Ph.D.
Department of Foods and Nutrition, University of Georgia, Athens, GA 30602.
A recent randomized, double-blind, placebo-controlled trial found that protein supplementation improved recovery from femoral fractures in an elderly population. A 6-month course of protein supplementation (20 g/day, 5 days/week) improved serum prealbumin and insulin-like growth factor I (IGF-I) concentrations, minimized bone loss, and decreased length of stay in rehabilitation facilities.
While I was Googling, I also found this interesting article:
Protein intake and bone health: the influence of belief systems on the conduct of nutritional science
Robert P Heaney
It was first shown nearly 80 years ago, and has been confirmed many times since, that ingestion of protein increases urinary calcium excretion. Most such work involved isolated protein feedings, and questions arose as to whether protein-containing foods would exert the same effect. Spencer et al showed that hamburger did not induce a rise in urinary calcium, noting that the phosphorus that commonly accompanies animal protein would tend to offset the protein-related calciuria. However, Spencer et al did not measure endogenous fecal calcium loss, which we showed increases with phosphorus intake; hence, a negative effect of meat on calcium balance still could not be excluded. Indeed, my colleagues at Creighton University and I showed, in free-living middle-aged women who were studied in a metabolic ward and ingested diets matched to their home intakes of protein and phosphorus, that urinary calcium was significantly positively correlated with protein intake and that, accordingly, calcium balance was significantly negatively correlated. This study, cited extensively since its publication, contributed to the widespread impression that protein is harmful to bone. It is therefore appropriate that I take this opportunity to revisit our original observations in the context of what is now known about the calcium economy.
A sometimes ignored feature of our study’s findings was a positive correlation between calcium intake and calcium balance, ie, higher calcium intakes offset the calciuric effects of protein. The mean calcium intake of the women in our study was 16.5 mmol/d, substantially below intakes now understood to be necessary for bone health. The aggregate effect of protein on calcium balance at such intakes does, indeed, tend to be negative because, at low calcium intakes, the efficiency of intestinal absorption cannot be increased sufficiently to offset an increase in obligatory calcium loss. In brief, if protein exerts a negative effect, it is only under conditions of low calcium intake.
Since our study was reported, an impressive body of literature has proven that protein tends to have a positive effect on bone overall. Two randomized controlled trials showed that increased protein intake dramatically improved outcomes after hip fracture, and subsequent work showed that protein supplements reduce bone loss at the contralateral hip in patients with upper femoral fracture. The most likely explanation is a protein induced increase in insulin-like growth factor I, which is known to be osteotrophic.
In parallel with this more or less normal advance of the science, a ferment in the larger society has arisen out of opposition to the use of animal products. Although only a tiny proportion of the general public or the nutritional science community holds this view, the zeal of these groups and their eagerness to exploit any evidence that suggests harmful effects of animal products have had a disproportionate effect both on public consciousness and on the agenda of nutritional science itself.
Sellmeyer et al, in this issue of the Journal, report that individuals consuming diets with high ratios of animal to vegetable protein lost bone more rapidly than did those with lower ratios and had a greater risk of hip fracture. It would be surprising this study had not been influenced to some extent by currents in the larger society. Although the study was well done and interpreted cautiously, it is virtually certain that it will be used by animal activists to “prove” that animal protein is positively harmful. It may contribute to the dialog to point out here that, on entry into the Sellmeyer study, subjects with the highest ratios of animal to vegetable protein intake had marginally higher bone mineral densities (BMDs) at the hip, not lower BMDs as the hypothesis suggests; after multiple adjustments, there was still not a significantly lower baseline BMD in subjects with high ratios of animal to vegetable protein intake compared with subjects with lower ratios. Moreover, because BMD can be estimated with substantially greater accuracy than can change in BMD, one might have expected, if anything, the opposite, ie, a significant difference at baseline but not an association with bone change. This inconsistency therefore raises significant questions about the generalizability of the findings of this study.
On precisely this same point, Hannan et al, using a larger cohort of individuals, this time from the Framingham Study, reported effects opposite those of Sellmeyer et al. Bone loss over a 4-y period was greatest in individuals with the lowest protein intakes and the relation showed a stepwise, inverse gradient of loss as a function of protein intake. Additionally, Hannan et al, also undoubtedly influenced by animal-rights activists, looked at animal protein intakes in their subjects but found no deleterious effect. Indeed, because most of the protein in their subjects’ diets was of animal origin, the apparent beneficial effect of total protein intake had to have been due to its animal component.
Further evidence of the influence of external pressures on the way nutritional science is conducted is found in the discussion by Sellmeyer et al of the metabolism of sulfur-containing amino acids to sulfuric acid, often cited as an explanation of the “harmful” effects of animal protein. Yet a vegan diet with protein derived equally from grains and legumes would deliver at least as many millimoles of sulfur per gram of protein as would a purely meat-based diet, so the discussion by Sellmeyer et al of this point is at the very least a red herring.
Finally, recent sophisticated analyses of the primitive diet, based on ethnographic studies, analysis of the diets of huntergatherer societies, and nitrogen isotope ratios of fossil bone collagen, indicate that human physiology evolved in the context of diets with high amounts of animal protein. Although caution has been urged in the interpretation of such analyses, it remains true that there is certainly no evidence that primitive humans had low intakes of either total protein or animal protein. That, coupled with the generally very robust skeletons of our hominid forbears, makes it difficult to sustain a case, either evidential or deductive, for overall skeletal harm related either to protein intake or to animal protein. Indeed, the balance of the evidence seems to indicate the opposite.
The full article is here:
http://www.ajcn.org/cgi/reprint/73/1/5.pdf
The important point that this chap is making is that nutritional science is being used to support political beliefs rather than to get at the truth. This doesn't do anyone any good.
What's also refreshing is that this person had the sense to 'revisit' his findings and revise his conclusions based on further evidence. That is what real science is about.
Here's another good article:
http://www.jacn.org/cgi/content/full/24/suppl_6/526S
So, the protein supplementation improved recovery from a nasty break.
The course text doesn't identify the exact study, but Googling 'protein supplementation femur' gives a few positive studies, including this one:
Dietary Protein Supplementation and Recovery from Femoral Fracture
Kimberly H. Porter M.S. Mary Ann Johnson Ph.D.
Department of Foods and Nutrition, University of Georgia, Athens, GA 30602.
A recent randomized, double-blind, placebo-controlled trial found that protein supplementation improved recovery from femoral fractures in an elderly population. A 6-month course of protein supplementation (20 g/day, 5 days/week) improved serum prealbumin and insulin-like growth factor I (IGF-I) concentrations, minimized bone loss, and decreased length of stay in rehabilitation facilities.
While I was Googling, I also found this interesting article:
Protein intake and bone health: the influence of belief systems on the conduct of nutritional science
Robert P Heaney
It was first shown nearly 80 years ago, and has been confirmed many times since, that ingestion of protein increases urinary calcium excretion. Most such work involved isolated protein feedings, and questions arose as to whether protein-containing foods would exert the same effect. Spencer et al showed that hamburger did not induce a rise in urinary calcium, noting that the phosphorus that commonly accompanies animal protein would tend to offset the protein-related calciuria. However, Spencer et al did not measure endogenous fecal calcium loss, which we showed increases with phosphorus intake; hence, a negative effect of meat on calcium balance still could not be excluded. Indeed, my colleagues at Creighton University and I showed, in free-living middle-aged women who were studied in a metabolic ward and ingested diets matched to their home intakes of protein and phosphorus, that urinary calcium was significantly positively correlated with protein intake and that, accordingly, calcium balance was significantly negatively correlated. This study, cited extensively since its publication, contributed to the widespread impression that protein is harmful to bone. It is therefore appropriate that I take this opportunity to revisit our original observations in the context of what is now known about the calcium economy.
A sometimes ignored feature of our study’s findings was a positive correlation between calcium intake and calcium balance, ie, higher calcium intakes offset the calciuric effects of protein. The mean calcium intake of the women in our study was 16.5 mmol/d, substantially below intakes now understood to be necessary for bone health. The aggregate effect of protein on calcium balance at such intakes does, indeed, tend to be negative because, at low calcium intakes, the efficiency of intestinal absorption cannot be increased sufficiently to offset an increase in obligatory calcium loss. In brief, if protein exerts a negative effect, it is only under conditions of low calcium intake.
Since our study was reported, an impressive body of literature has proven that protein tends to have a positive effect on bone overall. Two randomized controlled trials showed that increased protein intake dramatically improved outcomes after hip fracture, and subsequent work showed that protein supplements reduce bone loss at the contralateral hip in patients with upper femoral fracture. The most likely explanation is a protein induced increase in insulin-like growth factor I, which is known to be osteotrophic.
In parallel with this more or less normal advance of the science, a ferment in the larger society has arisen out of opposition to the use of animal products. Although only a tiny proportion of the general public or the nutritional science community holds this view, the zeal of these groups and their eagerness to exploit any evidence that suggests harmful effects of animal products have had a disproportionate effect both on public consciousness and on the agenda of nutritional science itself.
Sellmeyer et al, in this issue of the Journal, report that individuals consuming diets with high ratios of animal to vegetable protein lost bone more rapidly than did those with lower ratios and had a greater risk of hip fracture. It would be surprising this study had not been influenced to some extent by currents in the larger society. Although the study was well done and interpreted cautiously, it is virtually certain that it will be used by animal activists to “prove” that animal protein is positively harmful. It may contribute to the dialog to point out here that, on entry into the Sellmeyer study, subjects with the highest ratios of animal to vegetable protein intake had marginally higher bone mineral densities (BMDs) at the hip, not lower BMDs as the hypothesis suggests; after multiple adjustments, there was still not a significantly lower baseline BMD in subjects with high ratios of animal to vegetable protein intake compared with subjects with lower ratios. Moreover, because BMD can be estimated with substantially greater accuracy than can change in BMD, one might have expected, if anything, the opposite, ie, a significant difference at baseline but not an association with bone change. This inconsistency therefore raises significant questions about the generalizability of the findings of this study.
On precisely this same point, Hannan et al, using a larger cohort of individuals, this time from the Framingham Study, reported effects opposite those of Sellmeyer et al. Bone loss over a 4-y period was greatest in individuals with the lowest protein intakes and the relation showed a stepwise, inverse gradient of loss as a function of protein intake. Additionally, Hannan et al, also undoubtedly influenced by animal-rights activists, looked at animal protein intakes in their subjects but found no deleterious effect. Indeed, because most of the protein in their subjects’ diets was of animal origin, the apparent beneficial effect of total protein intake had to have been due to its animal component.
Further evidence of the influence of external pressures on the way nutritional science is conducted is found in the discussion by Sellmeyer et al of the metabolism of sulfur-containing amino acids to sulfuric acid, often cited as an explanation of the “harmful” effects of animal protein. Yet a vegan diet with protein derived equally from grains and legumes would deliver at least as many millimoles of sulfur per gram of protein as would a purely meat-based diet, so the discussion by Sellmeyer et al of this point is at the very least a red herring.
Finally, recent sophisticated analyses of the primitive diet, based on ethnographic studies, analysis of the diets of huntergatherer societies, and nitrogen isotope ratios of fossil bone collagen, indicate that human physiology evolved in the context of diets with high amounts of animal protein. Although caution has been urged in the interpretation of such analyses, it remains true that there is certainly no evidence that primitive humans had low intakes of either total protein or animal protein. That, coupled with the generally very robust skeletons of our hominid forbears, makes it difficult to sustain a case, either evidential or deductive, for overall skeletal harm related either to protein intake or to animal protein. Indeed, the balance of the evidence seems to indicate the opposite.
The full article is here:
http://www.ajcn.org/cgi/reprint/73/1/5.pdf
The important point that this chap is making is that nutritional science is being used to support political beliefs rather than to get at the truth. This doesn't do anyone any good.
What's also refreshing is that this person had the sense to 'revisit' his findings and revise his conclusions based on further evidence. That is what real science is about.
Here's another good article:
http://www.jacn.org/cgi/content/full/24/suppl_6/526S
Monday, 9 November 2009
The Matrix
No, this has nothing at all to do with The Matrix films, but it's a good excuse to put a pic of Keanu up.....
I spend a lot of time fretting about why nutritionists say what they say and give the advice that they give. Over the ten years or so that I have been a low-carber, (and taking account of the previous unmentionable number of decades that I was a low-fat dieter) my experience has been that low-carb eating is superior in just about every way... for satisfaction, for satiety and for health. My years of study of the science behind low-carb has also convinced me that it is blatantly and obviously the best way to go to solve a whole shed-load of health problems.
So WHY do the 'experts' insist on talking such a load of tosh?
The following matrix is one of the reasons I came up with, and I put a page about it on the Livable Low Carb website, but here is a version..
Let's consider 4 types of diet:
The values in the matrix represent some sort of fictitious 'health value'. These are numbers I've just made up to illustrate my point.
A problem is that 'experts' assume up-front that carbs are good, so they only look at the column on the right, the high-carb column. They then compare the high-carb + low-fat diet with the high-carb + high-fat diet and, of course, the high-fat one appears to be less healthy. So they don't look any further. Fat is evil, carbs are good, full stop.
BUT, carbs make people hungry and if one eats fat with the carbs, then one WILL eat more calories. Carbs cause any excess calories to be packed away as fat, and a high carb + high-fat diet WILL make you fatter and sicker. But that isn't the whole story.
If people doing studies would look at the whole picture, including the column on the left for the low-carb option, then a whole new situation will be seen.
Cutting carbs means less hunger, and therefore means that less calories are eaten, even if most of them are coming from natural fats. Cutting carbs means that stored fat can be turned into energy. Carbs means insulin means fat storage instead of fat use for energy. With Diet C, you'll be able to eat less because you won't be so hungry. You'll be able to exercise more because you'll have more energy. It really isn't rocket science. They just need to take the blinkers off.
If we look at the whole picture and study the 'low-carb' column on the left, we see that the 'health value' for Diet C is higher by a significant factor. The value I have added is a conservative guess for illustration of my point. But the factor could be far higher, when you consider the effects of years of advice to eat 60% of our calories as sugar.. rampant diabetes leading to many other truly horrible health problems.
This is just a thought I had.. if the 'experts' would stop being so blinkered by the results in the righthand column and consider the lefthand column too, they might learn something.
- Diet A = low-carb + low-fat
- Diet B = high-carb + low-fat
- Diet C = low-carb + high-fat
- Diet D = high-carb + high-fat
| Low Carb | High Carb | |
| Low Fat | A(ignore) | B(10) |
| High Fat | C(ignore) | D(9) |
The values in the matrix represent some sort of fictitious 'health value'. These are numbers I've just made up to illustrate my point.
A problem is that 'experts' assume up-front that carbs are good, so they only look at the column on the right, the high-carb column. They then compare the high-carb + low-fat diet with the high-carb + high-fat diet and, of course, the high-fat one appears to be less healthy. So they don't look any further. Fat is evil, carbs are good, full stop.
BUT, carbs make people hungry and if one eats fat with the carbs, then one WILL eat more calories. Carbs cause any excess calories to be packed away as fat, and a high carb + high-fat diet WILL make you fatter and sicker. But that isn't the whole story.
If people doing studies would look at the whole picture, including the column on the left for the low-carb option, then a whole new situation will be seen.
Cutting carbs means less hunger, and therefore means that less calories are eaten, even if most of them are coming from natural fats. Cutting carbs means that stored fat can be turned into energy. Carbs means insulin means fat storage instead of fat use for energy. With Diet C, you'll be able to eat less because you won't be so hungry. You'll be able to exercise more because you'll have more energy. It really isn't rocket science. They just need to take the blinkers off.
Low Carb | High Carb | |
Low Fat | A(12) | B(10) |
High Fat | C(20) | D(9) |
This is just a thought I had.. if the 'experts' would stop being so blinkered by the results in the righthand column and consider the lefthand column too, they might learn something.
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