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Recommended articles foods and diet |
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A
very readable account of the history behind the ‘mass murder’ resulting from
the low fat, and thus high carb diet. It
isn’t bad science that got us in the obesity epidemic, but business funding
tobacco science to prove that fats are bad, and carbs are better, and our corporatist state http://www.bmj.com/content/349/bmj.g7654 12/15/14
http://healthfully.org/h-b/id3.html
Are some diets “mass murder”? BMJ
2014; 349 doi: http://dx.doi.org/10.1136/bmj.g7654 (Published 15 December 2014) |
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Forty
years after he first put them forward, John Yudkin’s warnings on sugar are
finally being recognised. Geoff Watts reports “Diets high in added
sugar raise heart disease risk”; “One soft drink a day raises heart attack
danger”; “Added sugars increase heart disease risk.” Few things are more prey
to fad and fashion than alleged dietary influences on health. So the word
“sugar” in headlines where, for 30 years, we’ve been accustomed to expect the
word “fat” may be little more than a caprice. Alternatively it may indicate a
more substantial change. Which is perhaps why Penguin Books is reissuing Pure,
White
and Deadly, John Yudkin’s
valiant, 40 year old attempt to warn us against our lust for sucrose.1 Born in 1910, Yudkin
studied physiology and biochemistry at Cambridge University, embarked on a
career in microbiology, but then switched to medicine and nutrition. In 1945 he
was appointed professor of physiology at Queen Elizabeth College, London, and
set about creating a department with an international reputation in nutrition.
He died in July 1995. His book Pure, White
and Deadly is about the uses of
sugar, who consumes it, in what amounts, and how it’s handled by the body. But
most of all it’s about what he saw as sugar’s deleterious effects on health. As
he points out, carbohydrates have always been part of our diet and, until 50
years ago, the general view was that the form in which you consumed them was
neither here nor there. But the more he thought and read, the more doubtful he
became—about this, and also about the role of fat in heart disease. Back in 1957,
commenting that much had been said on the role of diet in coronary thrombosis,
he wrote: “In particular, many believe that the disease is related to the
amount of dietary fat, or of a particular sort of fat. In support of these
beliefs, we are presented with evidence of an epidemiological nature . . . From
time to time, however, it becomes evident that some of the epidemiological data
do not fit . . . As more and more of these awkward facts turn up, one begins to
have the uneasy feeling that both the proponents and opponents of a dietary
hypothesis are quoting only those data which support their view.”2 One of the earliest
exponents of the hypothesis that fat is the principal culprit was the American
biologist Ancel Keys. Following epidemiological work that began in the 1950s
and led eventually to the Seven Countries Study,3 Keys suggested that a diet high in animal fats
led to heart disease while one low in animal fat—a Mediterranean diet—offered
protection against it. Although considerably refined since then, it’s this view
that remains broadly prevalent. In 1957 Yudkin tried
his own hand at analysing the available statistics on heart disease and diet.
He found a “moderate but my no means excellent relationship between fat
consumption and coronary mortality.” Moreover he noted that the relationship
with sugar consumption was actually closer. Typically, he also pointed to an
even better one between coronary mortality and the possession of radio and
television sets. “He could be a bit of a tease,” says Tom Sanders of King’s
College London, the man who now occupies what was Yudkin’s chair in nutrition
and dietetics. From reading and
thinking Yudkin moved to experiments: “not always very well organised,”
according to Sanders. But his findings, initially on animals and later on
humans, reinforced a growing conviction that fat was not the only or even the
main culprit. By the time he published the second (1986) edition of Pure,
White
and Deadly he was even more
certain that sugar was the guilty substance. In his first chapter he wrote, “If
only a small fraction of what we already know about the effects of sugar were
to be revealed in relation to any other material used as a food additive, that
material would promptly be banned.” Industry
dismissal The sugar industry
responded to Yudkin and his views with a mixture of public rebuttal and private
subversion. Jobs and research grants that might predictably have come Yudkin’s
way did not always materialise. He comments in the second edition of the book
that while the sugar industry’s product is pure and white it would be difficult
to use these adjectives to describe the behaviour of some of its supporters.
And in the end, thinks Yudkin’s son Michael, sometime professor of biochemistry
at Oxford, the focus on fat rather than sugar as the prime culprit had as
much—or more—to do with commercial pressures as with science. In the final chapter of the second edition of
his book Yudkin itemises some of the responses of the industry to his views.
These include the abrupt cancellation of conferences suspected of promulgating
anti-sugar findings; attacks on Pure, White and Deadlyas a work
of fiction; and the application of
pressure to other food industries that were drawing attention to the harmful
effects of sugar. This all left the field clear for fat to assume the role of
chief culprit. Sanders dismisses any
suggestion that Yudkin was devastated by the unenthusiastic reception for his
ideas. “He had a sense of proportion,” says Sanders, adding that he wasn’t a
“conviction scientist” like Denis Burkitt or Hugh Trowell, the pair who
campaigned so vigorously in favour of dietary fibre. However, Michael Yudkin
says that his father did feel a sense of personal disappointment. “He was
disappointed not so much for himself as for the implications for public health.
Public health was something he’d worked on since he was a young man.” Medical interest in
the sugar hypothesis faded. The only lively discussion focused on its generally
accepted role in dental caries. The book went out of print—but in Britain at
least never entirely out of mind, partly on account of its clever title. The
phrase “pure, white, and deadly” is memorable for the way in which the upbeat
confidence of the first two adjectives is so swiftly contradicted by the
damning verdict of the third. New evidence In recent years, and
slowly, the sugar hypothesis has been making a comeback, driven in part by the
emerging perception of heart disease as a consequence of what’s now described
as the metabolic syndrome: obesity, dyslipidaemia, raised blood pressure, and
insulin resistance. Although there is still no consensus about the causes of
the syndrome, an excess of fat in the liver—a response to dietary sugar—is one
of the acknowledged possibilities.4 5 Fructose,
found in large quantities in nearly all added sugars, is known to increase
lipogenesis in the liver and the synthesis of hepatic triglyceride. Endocrinologist Robert
Lustig, professor of
paediatrics in the University of California at San Francisco, has contributed
an enthusiastic introduction to the reissue of Yudkin’s book. He does not deny
that fats—trans fats and omega-6 fatty acids in particular—have a role in the
genesis of heart disease, but he does think sugar has been neglected until
recently. “There’s been
a lot of
research that’s come out lately showing that fructose, because of the way it’s
metabolised, is different from glucose,” he says. “It contributes
specifically to the emergence of the metabolic syndrome.” This, more than anything else, is what has
started the ball rolling once again in a sweet direction. Fructose does things
that other carbohydrates don’t, Lustig adds. “Because it’s metabolised in the liver it gets converted
to liver
fat, and this causes insulin resistance, which drives the metabolic syndrome.” In the US, in parallel
with awareness of the food industry’s increasing use of high fructose corn
syrup, more researchers do seem to be giving sugars serious consideration. Last year
a group at Emory University,
Atlanta, found a statistically significant correlation between dietary added
sugars and blood lipid levels in adults.6 More
recently a New England
Journal of Medicine editorial commenting on dietary fructose
and
the development of insulin resistance said: “An emerging association between
the increased consumption of sugar-sweetened beverages and chronic diseases
such as type 2 diabetes, hypertension, and coronary heart disease is a major
concern.”7 In similar vein, a
prospective cohort study of more than 40 000 men by Lawrence de Koning and
colleagues at Harvard School of Public Health has shown that consuming sugar sweetened
drinks is
associated with an increased risk of coronary heart disease, while consuming
artificially sweetened drinks is not.8 As Yudkin recalled in Pure,
White
and Deadly, as a child when he
was thirsty he had a glass of water. “Nowadays when children are thirsty,” he
went on, “it seems almost obligatory that they quench their thirst with some
sugar-laden cola or other drink. And this is true for adults too.” Three
decades later, he would have argued, we are witnessing the consequence. Not surprisingly, the
sugar lobby maintains its opposition to Yudkin’s views. In an email to the BMJ Dr
Richard Cottrell, director of the World
Sugar Research Organisation (WSRO), dismissed his theories as “based on flawed
experiments in rats, whose metabolism of carbohydrate differs from that in
humans.” Invited to comment on the de Koning study he said it will not “lead to
any revision of the WSRO position statement, since the nature of this study is
inherently unable to attribute causality to any associations observed. In
addition, the relative risks quoted in this study are below the threshold for
credibility normally set by epidemiologists for this kind of study.” Since 1986 when Yudkin
revised his book, much has been learnt about the metabolism of the
carbohydrates, and its consequences. But the bones of the “new” view of sugar
are already there. As Yudkin writes on page 105, “If the cells have become
insensitive to insulin, the pancreas produces more and more insulin in order to
counteract the insensitivity.” He also writes extensively of the links between
heart disease, diabetes, obesity, and high blood pressure. The metabolic
syndrome is there in all but name. Where this debate on
the role of sugar will lead is hard to predict. Michael Yudkin draws an analogy
with smoking. “As time went on the denials that smoking tobacco had adverse
effects became less and less tenable . . . I think we’re seeing the beginning
of a similar shift in public opinion.” Right now, beyond
reiterating sugar’s obvious importance as a source of calories, even the
British Heart Foundation feels that present uncertainties prevent it taking a
position on other effects it might have. But Lustig remains confident that
things will continue to move in his (and Yudkin’s) direction. We have causation
as well as correlation, he says. “These shifts occur slowly. I think we’re in
the middle of a shift. We will see where it goes.” Notes Cite
this as: BMJ 2013;346:e7800 Footnotes Competing interests:
The author has completed the ICMJE unified disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding
author) and declares no support from any organisation for the submitted work;
no financial relationships with any organisation that might have an interest in
the submitted work in the previous three years; and no other relationships or
activities that could appear to have influenced the submitted work. Provenance and peer
review: Commissioned; not externally peer reviewed. References 1. ↵ Yudkin J. Pure, white and deadly. Penguin
Books, 2012. 2. ↵ Yudkin J. Diet and coronary thrombosis:
hypothesis and fact. Lancet1957;270:155-62. 3. ↵ Keys A,
ed. Seven countries: a multivariate analysis of death
and coronary heart disease. Harvard University Press, 1980. 4. ↵ Lutsey PL, Steffen LM, Stevens J. Dietary
intake and the development of the metabolic syndrome: The atherosclerosis risk
in communities study. Circulation2008;117:754-61. 5. ↵ Johnson RK, Appel LJ, Brands M, Howard BV,
Lefevre M, Lustig RH, et al. Dietary sugars intake and cardiovascular health: a
scientific statement from the American Heart
Association. Circulation2009;120:1011-20. 6. ↵ Welsh JA, Sharma A, Abramson JL, Vaccarino V,
Gillespie C, Vos MB. Caloric sweetener consumption and dyslipidemia among US
adults. JAMA2010;303:1490-7. 7. ↵ Caprio S. Calories from soft drinks—do they
matter? N Engl J Med2012;367:1462-3. 8. ↵ De Koning L, Malik VS, Kellogg MD, Rimm EB,
Willett WC, Hu FB. Sweetened beverage consumption, incident coronary heart
disease, and biomarkers of risk in men/clinical
perspective. Circulation2012;125:1735-41. |
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For an outline of what of the association of fructose
to
insulin resistance and fatty liver, and obesity, and endothelial dysfunction, and
age related chronic condition start with Why We Get Fat, then click on
more links. Lustig endocrinologist, UC system on sugar, saw
it with
Janice last year The issue is very complex, and the decisive studies have not
been done. Are sugars the cause of
higher cholesterol levels, rising blood pressure, falling
testosterone—possible. But
there are
other choices. I favor estrogen
mimics,
especially the bisphenols and like compounds.
Possible they are additive. You
will find this article challenging. http://www.youtube.com/watch?v=dBnniua6-oM
Article concludes that fructose causes fatty deposits to develop
in the liver: ”Fructose, found in large quantities in nearly
all added sugars, is known to increase lipogenesis in the liver and the
synthesis of hepatic triglyceride…. It contributes specifically to the
emergence of the metabolic syndrome…. Because it’s metabolised
in the liver it gets converted to liver fat, and this causes insulin
resistance, which drives the metabolic syndrome… consuming sugar
sweetened drinks is associated with an increased risk of coronary heart
disease, while consuming artificially sweetened drinks is not.”
http://www.bmj.com/content/346/bmj.e7800?etoc=
BMJ 2013; 346 doi:
http://dx.doi.org/10.1136/bmj.e7800 (Published 15 January 2013) Cite this as: BMJ 2013;346:e7800 FEATURE British Medical Journal 15 January
2013 Public
Health Sugar and the heart: old ideas revisited 1. Geoff Watts,
freelance journalist, BMJ Author Affiliations geoff@scileg.freeserve.co.uk Forty
years after he first put them forward, John Yudkin’s warnings on sugar are
finally being recognised. Geoff Watts reports “Diets high in added
sugar raise heart disease risk”; “One soft drink a day raises heart attack
danger”; “Added sugars increase heart disease risk.” Few things are more prey
to fad and fashion than alleged dietary influences on health. So the word
“sugar” in headlines where, for 30 years, we’ve been accustomed to expect the
word “fat” may be little more than a caprice. Alternatively it may indicate a
more substantial change. Which is perhaps why Penguin Books is reissuing Pure,
White
and Deadly, John Yudkin’s
valiant, 40 year old attempt to warn us against our lust for sucrose.1 Born in 1910, Yudkin
studied physiology and biochemistry at Cambridge University, embarked on a
career in microbiology, but then switched to medicine and nutrition. In 1945 he
was appointed professor of physiology at Queen Elizabeth College, London, and
set about creating a department with an international reputation in nutrition.
He died in July 1995. His book Pure, White
and Deadly is about the uses of
sugar, who consumes it, in what amounts, and how it’s handled by the body. But
most of all it’s about what he saw as sugar’s deleterious effects on health. As
he points out, carbohydrates have always been part of our diet and, until 50
years ago, the general view was that the form in which you consumed them was
neither here nor there. But the more he thought and read, the more doubtful he
became—about this, and also about the role of fat in heart disease. Back in 1957,
commenting that much had been said on the role of diet in coronary thrombosis,
he wrote: “In particular, many believe that the disease is related to the
amount of dietary fat, or of a particular sort of fat. In support of these
beliefs, we are presented with evidence of an epidemiological nature . . . From
time to time, however, it becomes evident that some of the epidemiological data
do not fit . . . As more and more of these awkward facts turn up, one begins to
have the uneasy feeling that both the proponents and opponents of a dietary
hypothesis are quoting only those data which support their view.”2 One of the earliest
exponents of the hypothesis that fat is the principal culprit was the American
biologist Ancel Keys. Following epidemiological work that began in the 1950s
and led eventually to the Seven Countries Study,3 Keys suggested that a diet high in animal fats
led to heart disease while one low in animal fat—a Mediterranean diet—offered
protection against it. Although considerably refined since then, it’s this view
that remains broadly prevalent. In 1957 Yudkin tried
his own hand at analysing the available statistics on heart disease and diet.
He found a “moderate but my no means excellent relationship between fat
consumption and coronary mortality.” Moreover he noted that the relationship
with sugar consumption was actually closer. Typically, he also pointed to an
even better one between coronary mortality and the possession of radio and
television sets. “He could be a bit of a tease,” says Tom Sanders of King’s
College London, the man who now occupies what was Yudkin’s chair in nutrition
and dietetics. From reading and
thinking Yudkin moved to experiments: “not always very well organised,”
according to Sanders. But his findings, initially on animals and later on
humans, reinforced a growing conviction that fat was not the only or even the
main culprit. By the time he published the second (1986) edition of Pure,
White
and Deadly he was even more
certain that sugar was the guilty substance. In his first chapter he wrote, “If
only a small fraction of what we already know about the effects of sugar were
to be revealed in relation to any other material used as a food additive, that
material would promptly be banned.” Industry
dismissal The sugar industry
responded to Yudkin and his views with a mixture of public rebuttal and private
subversion. Jobs and research grants that might predictably have come Yudkin’s
way did not always materialise. He comments in the second edition of the book
that while the sugar industry’s product is pure and white it would be difficult
to use these adjectives to describe the behaviour of some of its supporters.
And in the end, thinks Yudkin’s son Michael, sometime professor of biochemistry
at Oxford, the focus on fat rather than sugar as the prime culprit had as
much—or more—to do with commercial pressures as with science. In the final chapter of the second edition of
his book Yudkin itemises some of the responses of the industry to his views.
These include the abrupt cancellation of conferences suspected of promulgating
anti-sugar findings; attacks on Pure, White and Deadlyas a work
of fiction; and the application of
pressure to other food industries that were drawing attention to the harmful
effects of sugar. This all left the field clear for fat to assume the role of
chief culprit. Sanders dismisses any
suggestion that Yudkin was devastated by the unenthusiastic reception for his
ideas. “He had a sense of proportion,” says Sanders, adding that he wasn’t a
“conviction scientist” like Denis Burkitt or Hugh Trowell, the pair who
campaigned so vigorously in favour of dietary fibre. However, Michael Yudkin
says that his father did feel a sense of personal disappointment. “He was
disappointed not so much for himself as for the implications for public health.
Public health was something he’d worked on since he was a young man.” Medical interest in
the sugar hypothesis faded. The only lively discussion focused on its generally
accepted role in dental caries. The book went out of print—but in Britain at
least never entirely out of mind, partly on account of its clever title. The
phrase “pure, white, and deadly” is memorable for the way in which the upbeat
confidence of the first two adjectives is so swiftly contradicted by the
damning verdict of the third. New evidence In recent years, and
slowly, the sugar hypothesis has been making a comeback, driven in part by the
emerging perception of heart disease as a consequence of what’s now described
as the metabolic syndrome: obesity, dyslipidaemia, raised blood pressure, and
insulin resistance. Although there is still no consensus about the causes of
the syndrome, an excess of fat in the liver—a response to dietary sugar—is one
of the acknowledged possibilities.4 5 Fructose,
found in large quantities in nearly all added sugars, is known to increase
lipogenesis in the liver and the synthesis of hepatic triglyceride. Endocrinologist Robert
Lustig, professor of
paediatrics in the University of California at San Francisco, has contributed
an enthusiastic introduction to the reissue of Yudkin’s book. He does not deny
that fats—trans fats and omega-6 fatty acids in particular—have a role in the
genesis of heart disease, but he does think sugar has been neglected until
recently. “There’s been
a lot of
research that’s come out lately showing that fructose, because of the way it’s
metabolised, is different from glucose,” he says. “It contributes
specifically to the emergence of the metabolic syndrome.” This, more than anything else, is what has
started the ball rolling once again in a sweet direction. Fructose does things
that other carbohydrates don’t, Lustig adds. “Because it’s metabolised in the liver it gets converted
to liver
fat, and this causes insulin resistance, which drives the metabolic syndrome.” In the US, in parallel
with awareness of the food industry’s increasing use of high fructose corn
syrup, more researchers do seem to be giving sugars serious consideration. Last year
a group at Emory University,
Atlanta, found a statistically significant correlation between dietary added
sugars and blood lipid levels in adults.6 More
recently a New England
Journal of Medicine editorial commenting on dietary fructose
and
the development of insulin resistance said: “An emerging association between
the increased consumption of sugar-sweetened beverages and chronic diseases
such as type 2 diabetes, hypertension, and coronary heart disease is a major
concern.”7 In similar vein, a
prospective cohort study of more than 40 000 men by Lawrence de Koning and
colleagues at Harvard School of Public Health has shown that consuming sugar sweetened
drinks is
associated with an increased risk of coronary heart disease, while consuming
artificially sweetened drinks is not.8 As Yudkin recalled in Pure,
White
and Deadly, as a child when he
was thirsty he had a glass of water. “Nowadays when children are thirsty,” he
went on, “it seems almost obligatory that they quench their thirst with some
sugar-laden cola or other drink. And this is true for adults too.” Three
decades later, he would have argued, we are witnessing the consequence. Not surprisingly, the
sugar lobby maintains its opposition to Yudkin’s views. In an email to the BMJ Dr
Richard Cottrell, director of the World
Sugar Research Organisation (WSRO), dismissed his theories as “based on flawed
experiments in rats, whose metabolism of carbohydrate differs from that in
humans.” Invited to comment on the de Koning study he said it will not “lead to
any revision of the WSRO position statement, since the nature of this study is
inherently unable to attribute causality to any associations observed. In
addition, the relative risks quoted in this study are below the threshold for
credibility normally set by epidemiologists for this kind of study.” Since 1986 when Yudkin
revised his book, much has been learnt about the metabolism of the
carbohydrates, and its consequences. But the bones of the “new” view of sugar
are already there. As Yudkin writes on page 105, “If the cells have become
insensitive to insulin, the pancreas produces more and more insulin in order to
counteract the insensitivity.” He also writes extensively of the links between
heart disease, diabetes, obesity, and high blood pressure. The metabolic
syndrome is there in all but name. Where this debate on
the role of sugar will lead is hard to predict. Michael Yudkin draws an analogy
with smoking. “As time went on the denials that smoking tobacco had adverse
effects became less and less tenable . . . I think we’re seeing the beginning
of a similar shift in public opinion.” Right now, beyond
reiterating sugar’s obvious importance as a source of calories, even the
British Heart Foundation feels that present uncertainties prevent it taking a
position on other effects it might have. But Lustig remains confident that
things will continue to move in his (and Yudkin’s) direction. We have causation
as well as correlation, he says. “These shifts occur slowly. I think we’re in
the middle of a shift. We will see where it goes.” Notes Cite
this as: BMJ 2013;346:e7800 Footnotes Competing interests:
The author has completed the ICMJE unified disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding
author) and declares no support from any organisation for the submitted work;
no financial relationships with any organisation that might have an interest in
the submitted work in the previous three years; and no other relationships or
activities that could appear to have influenced the submitted work. Provenance and peer
review: Commissioned; not externally peer reviewed. References 1. ↵ Yudkin J. Pure, white and deadly. Penguin
Books, 2012. 2. ↵ Yudkin J. Diet and coronary thrombosis:
hypothesis and fact. Lancet1957;270:155-62. 3. ↵ Keys A,
ed. Seven countries: a multivariate analysis of death
and coronary heart disease. Harvard University Press, 1980. 4. ↵ Lutsey PL, Steffen LM, Stevens J. Dietary
intake and the development of the metabolic syndrome: The atherosclerosis risk
in communities study. Circulation2008;117:754-61. 5. ↵ Johnson RK, Appel LJ, Brands M, Howard BV,
Lefevre M, Lustig RH, et al. Dietary sugars intake and cardiovascular health: a
scientific statement from the American Heart
Association. Circulation2009;120:1011-20. 6. ↵ Welsh JA, Sharma A, Abramson JL, Vaccarino V,
Gillespie C, Vos MB. Caloric sweetener consumption and dyslipidemia among US
adults. JAMA2010;303:1490-7. 7. ↵ Caprio S. Calories from soft drinks—do they
matter? N Engl J Med2012;367:1462-3. 8. ↵ De Koning L, Malik VS, Kellogg MD, Rimm EB,
Willett WC, Hu FB. Sweetened beverage consumption, incident coronary heart
disease, and biomarkers of risk in men/clinical
perspective. Circulation2012;125:1735-41.
Fructose
is converted to fat only in the liver and insulin causes this fat to be stored
in the liver. Fatty liver >>>> IR in liver >>>> IR
in muscle and fat tissues >>>> IR
causes abnormal high insulin >>>> excess fat storage
Carbs
raises the insulin level in the body, and insulin causes body to burn glucose
and store fat ^^^^^^^^^^^^^^^^^^^^^^^^^^^^
For Dr.
Fung, one important, obvious suggestion:
Everyone believes that if one burns more calories than one consumes that
weight will be lost. So instead of
arguing that this is false, simply point out that there is one more step in the
process to losing weight and keeping it off, that of going into the metabolic
fat-burning mode and staying one it--a very low carbs diet with fasting.
The eat
less exercise advice is not wrong, just incomplete. The common advice of “eat
less and exercise more”; this should also include “stay in the fat-burning
mode with a very
low carb diet”, and “this will work
quicker with the addition of fasting”.
This addition piece leads into
the explanation of the role of insulin resistance and how this diet cures it. Insulin
resistance is caused by the Western
diet which is low in fats and thus high in carbs including the sugar fructose
which starts the path to insulin resistance.
On my health website (http://healthfully.org/rh/id8.html) I have a
recommendation very similar to yours, only I suggest a short-term fast as many
days and hours as the dieter feels comfortable with (for higher compliance). In
your video Richard’s
Story, his did this and lost 40 lbs.
Your comment on the short-term fast would be appreciated. Dr. Michael Mosley of the BBC
also recommends a
short-term fast.
One last bit of interest, the US Dietary Guidelines issued in
2015 continue with “more turds in the punch bowl (from your blog’s title) and
this has resulted in an article
in the BMJ (British Medical Journal Sept 23, 2015) on the stench coming
from those guidelines. This leads to one
more comment, follow the bucks. Bad
advice is a result of corporate political influence. To blame a person (David
Kurtz) instead of
the corporation behind the curtain is a partial truth. You have an article up
on food industry funding
dietary conferences. A current article
in In
These Times lists
the donations made by Coca Cola.
REPLY: Dr. Jason Fung: Both short term fasts and
longer
ones have their place. We use both extensively.
Looking for a topic, use Google Internal Search Engine
INTERNAL SITE SEARCH ENGINE by Google
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