safe-carb's Dr.Lustig

7.26: health/zone/safe-carb's Dr.Lustig

reincarnation of saint Atkins found!

. the spirit of Dr.atkins
was the same as Jesus Christ:
going against the established culture
to make big improvements for even the least of us .
. his particular achievement was to reveal
that, contrary to conventional medical advice,
a high fat diet was actually
safer for your heart than a
low-fat, normal-carb diet;
-- at least when you were
obese and insulin resistant --
because, among the insulin resistant
there is carb intolerance,
so that what seems like normal carb intake
is actually perpetuating
insulin resistance and high insulin
-- by far the highest risk factors
for heart disease;
he also revealed that for those who were
highly insulin resistant,
a zero-carb diet was essential to
getting back your insulin sensitivity,
and getting back into fat-burning mode .


[7.29:
. the spirit of Saint Atkins
appears to have first been embodied
by the europeans, but later
usa contributed significant theory .

. the first popular high-fat reducing diet
was invented by the French,
and popularized by the British:

1864 William Banting`Letter on Corpulence

. Banting's diet was introduced to him by his doctor
Dr. William Harvey, who learned of it from
physiologist Claude Bernard,
lecturing on the evils of sugars
and on controlling diabetes with a no-sugar diet .

1951 Alfred W. Pennington, M.D. (usa):

. the obese-prone are not simply gluttons;
rather, they have a defect in their metabolism
whereby they are carb intolerant,
and are storing too much of whatever they eat .
. low-Calorie diets only serve to starve them,
rather than address this calorie storage defect .

1961 Herman Taller`Calories Don't Count (usa):

obstetrician-gynecologist treats his own obesity
and emphasizes the use of polyunsaturates
to promote lipo-equilibrium (using vs storing fats).
. he is convicted of mail fraud for using his book
to sell safflower oil supplements .
. he discovered the stimulating effects of poly'fats
when his doctor put him on a low-cholesterol diet;
ironically,
while he was convicted for an Atkins theory,
his actual disservice was pushing poly'fats
which can promote aging and cancer
all while happily lowering cholesterol that
could have been controlled safely with
a diet of egg yolks, beans, and no sugar .]
. Atkins said
"(in a sense I adapted Taller's approach
... This is 13 years later.
A lot of scientific evidence has linked
insulin and heart disease
and hammered down the case against carbohydrates.
I believe the evidence overwhelmingly
implicates sugar as a major epidemiological culprit.).

1963 JAMA`A New Concept in the Treatment of Obesity

. this would inspire Dr.Atkins' anti-obesity strategy .
[Atkins for Life", 2003, page xii]

1971 Vogue mag`Super Diet:

. the publication that made Dr.Atkins famous
and started a book invitation .
[Vogue#1971 October 15 Page 148]

1972 Dr.John Yudkin:

. he was not sympathetic to Atkin's tactic of
adding high-fat to the esteemed zero-sugar diet
but true to the Saint Atkins spirit,
he battled valiantly with the medical mainstream
to protect the public from assuming
dietary fats rather than sugars
were the primary cause of rising heart disease .

2003.4 Dr.Atkins' spirit is released again:

. the Saint Atkins spirit transitions to
Healthy Weight Kids Coalition
which got its funding from
# CATCH (Coordinated Approach to Child Health) grant
# Foundation for a Healthy Kentucky grant .

. eventually the Saint Atkins' spirit
would be blazing in Dr. Robert H. Lustig,
expert in neuroendocrinology,
bravely challenging established culture
to defend the health of children by
# expertly vilifying sugar,
# promoting beans (safe-carb's with high fiber) .

table of contents

• 7.13: 7.27: summary:
  
  • Taubes:
    
    • opposition:
  • Lustig:
    
    • 7.28: opposition to coaches:
    • 7.28: opposition to industry:
    • my own reservations:
• 7.14: Lustig's youtube lecture:
  
  • Jeffrey Norris on June 25, 2009:
    
    • Lustig's controversial ideas:
    • Lustig’s own groundbreaking studies:
    • Lustig's Guidelines for heavy kids:
• 7.16: other report's of Lustig's video lecture:
  
  • 2010.5 Sean Croxton’s interviewwith Dr. Lustig
    
    • is it a medical addiction?
    • Lustig's definition ofmetabolic disorder:
    • a rash of obese 6mo old's ?:
      
      • # envirotoxins:
      • # diet changes:
    • how do computer programmer's replace soda?:
  • 7.16: lifeasrx.com's intro:
  • 7.16: Lustig at thelivinlowcarbshow.com:
    
    • The Livin’ La Vida Low-Carb Show with Jimmy Moore!:
    • 2010 dietary guidelines:
    • safe carb vs low carb:
    • is it the sugar or the carbs?:
    • anything he'd change in hislecture?:
    •  speaking of athletics,
    • comments of the thelivinlowcarbshow with Lustig:
  • 7.18: Gary Taubes April 13,
    2011/review's Lustig:
    
    • 1924, Haven Emerson:
    • [1957 John Yudkin
    • John Yudkin 1978`Sweet and Dangerous
    • 1970, Ancel Keys`SevenCountries Study.
    • 2004 cancer linked to metabolic syndrome
    • 2007 high insulin linked tocancer:
    • guide to cheap insulin monitoring:
• 7.29: events that inspired Lustig
  
  • 7.16: Lustig et al, 1999`somatostatin agonist
  • 7.16: Lustig RH (2001)`childhood obesity
  • 7.16: Lustig RH et al. (2003)Octreotide therapy
  • 7.16: Lustig RH (2003) pathogenesis of obesity
  • 7.16: Lustig RH et al. (2003)obesity from brain tumors
  • 7.16: Lustig 2006` First Law of Thermodynamics:
  • 7.16: Lustig RH et al. (2006)octreotide dose
  • 7.17: Lustig 2007 with Norman Swan:
  • Lustig (2008)`Limbic Triangle
  • March 2008: How Bad Is Fructose: Pure White and Deadly
    
    • good science: bad sodas
    • Framingham Study,
• 7.28: fan's of Lustig's message:
  
  • 180degreehealth:
  • 7.15: thatpaleoguy.blogspot.com:
    
    • about Jamie Scott:
    • June 2010: Fructose: Making Your Kids Fatter
    • Scott July 2010: David Gillespie vs sugar
    • Scott October 2010 Fructose Intolerance:
      
      • Eating too much fructose can induce leptin resistance:
• 7.15: other fans of low-fructose for childhood obesity:
  
  • Dr. Redmond, Metametrix Clinical Laboratories:
  • Melania Manco, MD Ph.D:
  • Zivkovic AM, German JB, Sanyal AJ:
  • ucsf.edu`Jeffrey Norris June 25, 2009:
  • Kirsten Bibbins-Domingo, PhD, MD:

7.13: 7.27: summary:

. I was recently introduced to more giants
in the field of [hormones in the zone] dieting:
Gary Taubes and Robert Lustig .
they are great resources for fructose pathology
and how there are good calories and bad calories .
. they reconfirm the conclusions of Dr.Atkins,
and they are just as controversial!

Taubes:

. a calorie of fat is much less fattening
than a calorie of sugar.
. and more recently (with Vogue.mag):
. we’re storing too much energy because
of chronically elevated insulin levels
because we’re eating too many simple carbs.
. he recommends unlimited quantities of
meat, fish, poultry, and eggs, plus vegetables daily.
He embraces fat but is skeptical of
whole grains and milk .

opposition:

"( Taubes ignores what diabetes researchers say is
a body of published papers documenting
a complex system of metabolic controls
that, in the end, assure that
a calorie is a calorie is a calorie )
--
. that opponent also wrote a feel-good book
about genetic set-points controlling your weight,
yet gives an example of a guy who
can lose weight at Jenny Craig's
and then quits as if his only problem
was losing weight
(you think that's about his set-point?
his instinctual diet is obviously
less sensible than Jenny Craig's!)
[7.29:
. oh, but why fight a set-point, right?
why fight a beans, greens, and raw yolk diet?
can't lose the weight you already have?
zero-carb zero-med zero-stress diet is
scientifically proven to start fat-burning mode;
still hungry? help yourself to monounsaturates
liberally freshened with rosemary herb .
. where's your set-point now? ]

Lustig:

. people concerned about their obesity
need to avoid unfibered sugars;
because these can destroy your will power
by causing leptin resistance .
. a high-fat, zero-carb diet
is at least trivially a safe-carb diet:
no unfibered combinations of
fructose and glucose .
. keep in mind the endocrinological
basis of will power:
the people with the most powerful wills
don't tempt the devil with combinations of
high-dose insulin provokers (glucose)
and insulin resistors (fructose),
or anything else that is a leptin resistor
(choices that contribute to high insulin states).

7.28: opposition to Lustig from coaches:

(basically just counter-alarmist sneerings
citing Lustig for making a public statement
about something that concerns only food addicts):
"(The evidence that HFCS consumption uniquely increases
the risk of weight gain is very weak)
. but Lustig's point was that added sugars
do uniquely contribute to
eroded will power;
and, his opponent clearly wasn't understanding
Lustig's description of leptin-based will power:
Aragon misquotes Lustig:
"(A point he hammers throughout his talk
is that unlike glucose,
fructose does not elicit an insulin (& leptin) response,
and thus does not blunt appetite. )
. here's Lustig's endocrinology on
how both fructose and glucose affect leptin:
. high insulin causes leptin resistance;
and, both fructose and glucose
can cause high insulin levels;
because:
# glucose spiking causes insulin spikes
and these spiked levels of insulin
make the body deaf to low levels insulin,
so then high levels are used all the time .
# fructose can result in a rise in triglycerides*
which contributes to insulin resistance
so that insulin levels are higher
even when glucose is properly managed .
. that is how fructose hammers leptin .
*
"(Plasma triglyceride levels are increased
by the ingestion of large amounts of sugar)

7.28: opposition to Lustig from industry:

7.14: Lustig's abc news/nightline interview:
. they contrasted his view with another doctor
(a consultant to the corn refiners association)
who said: "(every time they've tried to
blame obesity on any one thing,
they've been wrong ).
. but Lustig claims 2 things are causing it:
# using much more fructose than is
found naturally in unprocessed foods,
# using much less fiber than is
normally found with natural sources of fructose .

. it has been pointed out by the Corn industry
that obesity and diabetes trends
are rising despite a fall in added sugars .
. here's how Lustig still has a solid case:
his arguments promote the theory that
our hormone responses have been
maltrained by sugar in such a way that
its lasting effects are causing us to eat
much more of what is fattening us:
the non-sugar but still high-glycemic carb's;
in other words,
rather than help the sugar industry,
their own data shows that
sugar causes a vicious addiction
where trying to cut back from large doses
causes overcompensation of other calories .

my own reservations:

. looking back at my lean college days
despite all the sugar I ate in
(I amassed dozens of 25lb bags,
along with 12eggs/day,
powdered milk, and cabbage),
I wondered if the actual source of obesity
is mostly from increased stress due to
sea changes in modern overpopulated culture .
. this fructose invasion coincides with
nixon's war on poverty,
and blazing changes in the levels of risk
from new sexual norms, casual use of drugs,
and competition from both automation and
exponentially increasing population growth .
. then there was a war on drugs,
and all sorts of new social behaviors
similar to road rage .
. relax, have another soda,
and then get some real energy
with sugar-injected meats
sugar-mixed breads,
and of course your favorite unprocessed foods
should be great natural sources of sugar
(fructose + glucose):
oranges, apples, honey ...
[7.29:
. also, if you have any big ideas about
removing just the fructose
(say, by sweetening glucose with citric acid)
keep in mind that use of unfibered glucose
can easily spike blood glucose levels,
causing insulin spikes that rebound
causing low glucose levels
which provoke the overuse of cortisol:
our body's natural insulin resistor
that keeps the brain's supply
from going to other cells .
-- again, as with fructose,
there is the risk of insulin resistance,
from from high insulin and cortisol,
that may feed cancers, and promote diabetes .]

7.14: Lustig's youtube lecture:

"(Sugar: The Bitter Truth) is on youtube
as part of a series,
current controversies in nutrition,
. it can also be found here:
UCSF Mini Medical School for the Public
(here's a direct link).
. it's introduced by his university's
news service:

Jeffrey Norris on June 25, 2009:

. Lustig presented his case against fructose
in a recent UCSF Mini Medical School course on
diet and nutrition,
part of a series sponsored by the
Osher Lifelong Learning Institute.
Audience members may have been surprised to hear
such unequivocally strong statements
from a researcher.
Lustig framed the obesity epidemic
as a societal issue
that pits the profit-centric agenda of
federal agencies and major corporations
against public health needs.
. yet he's not here to take on Big Corn:
“High-fructose corn syrup and sucrose
are exactly the same, equally bad.
They’re both poison in high doses.”

Americans have increased their fructose consumption
from 15 grams per day
to 75 grams per day or more, Lustig explains.
The trend accelerated beginning about three decades ago,
when cheap, high-fructose corn syrup
became widely available.
Much of processed food labeled “reduced fat”
instead has sugar added to make it more palatable,
But when it comes to harmful health effects,
sugar is worse than fat .

Lustig's controversial ideas:

# “You are not what you eat;
you are what you do with what you eat,
And what you do with fructose
is particularly dangerous.”
#
A Calorie Is Not Just a Calorie:
. not all food calories have the same impact
on fat storage and energy expenditure .
. calorie for calorie,
sugar causes more insulin resistance in the liver
than other edibles.
The pancreas then has to release more insulin
to satisfy the liver’s needs.
High insulin levels, in turn,
interfere with a hormone called leptin,
secreted by fat cells .
. fructose calories, therefore,
fail to blunt appetite
in the same way as other foods.
#
Higher Insulin does not Curb Appetite:
. the conventional view holds that
insulin, like leptin,
provides feedback to limit food intake.
. chronically elevated insulin
blocks leptin’s negative feedback signal:
“Most people think insulin
does the same thing as leptin:
it does just the opposite.”
#
Exercise is a Hormone not a Calorie burner:
. the main benefit of exercise
is not burning off calories:
it improves insulin sensitivity in skeletal muscle,
lowering insulin levels in the bloodstream.
Exercise reduces stress and, therefore,
reduces stress-induced eating,
and, exercise increases metabolic rate.
#
Fructose is a Poison:
. fructose is just as bad as alcohol
in causing fat storage in the liver
— and in causing fatty liver disease.

Lustig’s own groundbreaking studies:

In the 1990s, Lustig worked with
children diagnosed with hypothalamic obesity,
a disorder that can occur after surgery
[when tumor removal damages the hypothalamus] .
The children [had high insulin],
and Lustig [hypothesized that they had
leptin resistance from high insulin].
Lustig administered a drug to lower insulin;
and, the children ate less, lost weight,
spontaneously became more active
and improved their quality of life.
. a subset of obese adults also responded
to same treatment .

Lustig's Guidelines for heavy kids:

# Get rid of every sugared liquid in the house.
Kids should drink only water and milk.
use only high-fiber carbohydrates:
. we should think twice before drinking juice
or feeding it to our kids.
The fiber in whole fruit contributes to
a sense of fullness.
. it is rare to see a child eat
more than one orange,
but it is common for kids to consume
much more sugar and calories as orange juice.
Eating fiber also results in
less carbohydrate being absorbed in the gut,
and allows the brain to receive a satiety signal
sooner than it would otherwise .
# Wait 20 minutes before serving second portions.
# Have kids buy their [office time]
minute-for-minute with physical activity.
. The [halved-office time] directive
is the most difficult one to comply with,
But failure to limit sugar intake
is the most predictive of
poor weight control in children .

7.16: other report's of Lustig's video lecture:

2010.5 Sean Croxton’s interview with Dr. Lustig

7.29: my notes of the Croxton podcast:
. the mid 90's was when Lustig
got involved with the obesity issue .
Leptin had just been discovered
when he was seeing Hypothalmic obesity
and having these facts in place
helped him solve the obesity riddle .

not just "(calories in calories out):
. the high insulin generated by hypothalmic obesity
was a brilliant example of what
high insulin can do to that equation:
. they had these kids on 500 calories/day,
and they were still gaining weight!

. when insulin-lowering worked on some adults
but not others, the question arose:
what is causing their insulin to be high?
. since introducing hfcs in everything
the food industry has quintupled its profits:
it used to grow with the population growth: 1%
but now it grows 5% per year .
. not only are there more people;
they are now all eating more .
[. now you could attribute that to
hfcs making the food 5 times cheaper to produce;
but he's estimated somehow that]
usa gets hundreds more calories per day
than before the hfcs in everything invasion .
. engineering the food for palatibility
should be seen as code for addictibility .
. it's not that they are trying to poison us
but when you sugar it, people buy more:
you've found a legal addiction !

is it a medical addiction?

it does meet the 4 criteria in animal models:
binging, withdrawal, craving,
and cross-sentization with other drugs of abuse .
[zombie alert:]
. hfcs is more addicting than sucrose;
a very new study from utah in animals
suggests hfcs might be assimilated quicker .

. Lustig was intro'd to Yudkin just 2 years ago,
"(he's a real reanassance man,
very impressed by his predictions:
he wrote them in 1972 and they are all true).
. Lustig is pen-pal's with his son,
a prof at oxford .

. Yudkin was debating Keys' 7 country study:
the way Key's 1971 paper discredited Yudkin
as having no substantial evidence
showed he was really wanting
fat to be the cause of our problems .
[. recalling Keys authored a book about beans
The Benevolent Bean (Doubleday, 1967)
I wondered if he had a vegetarian agenda
and wanted a fat scare
to discourage meat use .]
. in his own words Keys admitted
he did not do the multi-variate analysis
needed to show that sat'fat
was still the culprit even when
sucrose was taken out of the equation .

. we've based a lot of dietician policy
on that research by Keys
and that's an on-going problem .

. we know from familial hyper.cholesterol.emia
that LDL is bad, but some think that the
large buoyant variety is not so bad;
whereas there is universal agreement
that the small dense LDL
is a major predictor of heart disease .

. dietary fat increases the large buoyant LDL
but sugar raises the small dense, worst LDL .

. TG/HDL ratio is a measure for
the extent of insulin resistance,
and how well your liver is working .
. TG/HDL is driven by sugar and glycemic load;
it is not driven by fat .

. we've based a lot of dietician policy
on "(fat is worse than sugar)
and that's an on-going problem .

Lustig's definition of metabolic disorder:

fatty liver, kidney failure,
thyroid dysfunction,
dementia,
... name your degenerative disease .
--[ this is our man ! he's on to the dementia link .]
. the classic definition of metabolic syndrome
is from what we knew in 1988
. we now think all the mitochondria are sickened;
and this can result in any number of
degenerative diseases .

. they already have human adult studies
showing that a fructose-free diet
reduces liver fat by 30% in 10 days .

. a caller craving sugar after giving it up,
wondered how long the cravings endure:
5 years is typical !
--[ here's the problem with caf'addiction:
it helps with all other addictions
so you wonder what people are talking about! ]

. one of the callers is a low-carb blogger
wondering how he could get an interview
--[that blogger's interview is next].
. he says he's not interested in low-carb
because any gains it makes
is likely to be only from
the sugar restriction .
[. he will later be asked this question again
during the low-carb interview;
where he will clarify the role on insulin
and glycemic load .]

. no one has yet done a study on
the low-carb vs low sugar /sensation/
[. the very meaning of that question
would depend on context:
is the diet concerned with weight reduction
or optimal health?
how low is low-carb?
are we prefering whey&eggs to beans ?
. anyway, he's had a bagel for breakfast;
what do you say to a low-carb guy
after that?! ]

a rash of obese 6mo old's ?:

. this is a good example of
a calorie is not just a calorie:
. babies shouldn't need will power
just to stay healthy around here .
. causes of infant obesity could be:

# envirotoxins:

BPA in plastics like baby bottles,
phthalates(plastisizers) in baby toys,
there are other estrogens as well,
[(Xenoestrogens, endocrine disruptors)]
a big one is the Genistein in soy .

# diet changes:

. the usa poverty program
gives kids free juice
which contains a lot of glucose+fructose
(whether any is added or not).
. soy formula also uses sucrose
as its lactose replacement .

how do computer programmer's replace soda?:

. sweet potatoes? [high fructose]
sure, that has a good dose of fiber!
but also remember your roots:
the men were hunters,
and didn't get a lot carb's;
it's not like you need them to think .
trivia:
agave healthier? no:
. it's mostly fructose .
[ Agave nectar (or agave syrup)
is trumpeted as “Better Than Sugar”]
martinez project:
. the whole town is going sugar free!
. sunrise cafe is already doing it .

7.16: lifeasrx.com's intro:

. in Lustig's “Sugar: The Bitter Truth,”
over-consumption of fructose
is effectively poisoning the liver.
He postulates that anything over
50 grams of fructose per day
is like 50 grams of alcohol per day:
a hepatoxin (liver toxin).

. application of a drug to lower insulin
then the obese feel like being more active
and there is weight loss.
Thus, we have another expert pointing out
that the arrow of causation is reversed:
instead of gluttony and laziness causing obesity,
high insulin is giving your energy to fat stores,
which leaves you starved, and of course,
hungry and lethargic.
Paradoxically,
the one who appears to be getting too much
can actually be getting too little .

7.16: Lustig at thelivinlowcarbshow.com:

The Livin’ La Vida Low-Carb Show with Jimmy Moore!:

Today’s guest is Dr. Robert Lustig,
the viral YouTube Internet sensation
for his neuroendocrinologist evangelism in
“Sugar: The Bitter Truth”.
. he originally declined to be interviewed
because he said he didn’t believe in
the low-carb lifestyle.
. he finally agreed to be interviewed
on the subject of fructose
as it relates to health and obesity
and why he thinks a total “low-carb” approach
misses the boat.
You’ll also discover
why the vagus (or pneumogastric) nerve
and insulin metabolism are forcing us to
bank energy as fat and be less active.
Furthermore, his studies show that fructose is
metabolized more like alcohol than glucose,
and therefore contributes to liver damage.
[my notes from listening:]
. this is a good explanation of how
the food that causes high insulin
is stealing energy
and causing hunger and laziness .
. the problem is our environment:
it's contaminated with fructose .

. although an insulin-reducing drug
sounds like a great tool,
it is very expensive
and comes with many sideaffects .
[7.17: moreover,
Lustig(ABC radio`Health Report`Norman Swan):
. 80% of obese adults are insulin-resistant
and an insulin antagonist does not work
in them at all.
Metformin will work in them
but only to a certain point
-- because it’s not the perfect drug either --
and it has other side effects .]
. fructose causes dysfunction of mitochondria;
and is a main source of the insulin resistance
that is causing leptin resistance .
. fructose increases the uric acid load
that can drive a hypertension condition .

. Lustig was a proofreader for
Gary Taubes`good calories bad calories
[. this book is another perspective on
hormones-in-the-zone dieting,
arguing that what appears to be
a problem of excess calorie consumption
may instead be simply an excess of
low-fiber high-glycemic carbohydrates .
. he reviews the poor track record of
low-fat, calorie-controlled diets.]

2010 dietary guidelines:

. Lustig was a candidate for that panel
but was specifically not allowed
because he's not here to sell
the food they find cheapest to produce !
in fact, there's not one proponent
of low-carb or high-fiber
on that entire committee .
. the usda controls the food pyramid;
why? they sell food; not health:
they are the fox in charge of the hen house .

safe carb vs low carb:

. Lustig's problem with being associated
with the "(low-carb diet), is that
[... (drum roll), ...
he's another legume fan!
. as Dr.Atkins showed,
a low carb [ketogenic] diet may act as
an insulin-lowering agent,
but even Atkins does that for only 2 weeks,
and under medical supervision .
. a low carb level is essential for
high fat diets
because carb's require insulin sensitivity
whereas fats cause insulin resistance .
. a diet-for-life can include
plenty of safe carb's, as found in legumes .]

. is a low-carb diet working because of its
carb' restriction?
or for its fructose restriction?
. fructose makes the liver insulin resistant;
the insulin rises until the liver responds,
and this exposes the entire body
to higher insulin .
[7.17: web: here's how that works:
. tissues that do not require insulin
for efficient uptake of glucose
include the brain and the liver;
however,
the liver needs insulin sensitivity
in order to its job of converting
between glucose and glycogen .
. glucose raises insulin,
then if the liver is sensing the insulin
it converts most of a meal's glucose
into glycogen
-- "(most of) is the keyword here,
because if the blood sugar keeps rising
it's primarily the liver's fault .
. if the liver is insulin resistant
that makes for very slow glucose control .
. after glycogen stores are full(5% of liver),
further glucose processing produces lipoproteins.
which become a source of free fatty acids
for use in other tissues, including
adipocytes,[fat cells]
which use them to synthesize triglyceride.
. insulin drives most cells to use
glucose instead of fatty acids .
. as levels of glucose and then insulin fall,
the insulin-sensitive liver then begins to
turn glycogen back into glucose .
. states of hypoglycemia cause a rise in glucagon,
another activator of glucose generation .
. glucagon also converts amino acids into glucose
and may assist in releasing fatty acids
to conserve glucose for the brain .
. a high protein meal raises glucagon and insulin .
Insulin inhibits the intracellular lipase
[inside-the-cell fat disolver]
that hydrolyzes [breaks apart] triglycerides
to release fatty acids.
Insulin facilitates entry of glucose into adipocytes,
and within those [fat]cells,
glucose can be used to synthesize glycerol.
for combining with the liver's fatty acids
to then synthesize triglyceride .]

is it the sugar or the carbs?:

. we do know that insulin is the bad guy;
when we lowered high insulin
the obese lost their appetite for carbohydrates .
[. from a practical perspective,]
a safe diet is about glycemic index,
and glycemic load (index * portion size):
[7.29:
. the glycemic load may explain why
a diet rich in high-glycemic rice
would not increase the diabetes rate:
the culture in that case
may simply be using smaller portions .]

. safe-carb'ing is about
how fast the glucose is being assimiliated;
and, there are 2 classes of carb's
most relevant to glycemic index:
# amylose: eg, legumes, slow and safe;
# amylopectin: eg, grains: quick .
-- these quick carb's are a problem
even though they have no fructose,
because they spike insulin too much .

. another dimension of carbohydrate
that determines its healthiness,
is high-fiber vs low-fiber .
. a lack of fiber increases glycemic load;
and, fiber fermentation may produce
heart protectives .

. the low-carb audience is repeatedly reminded
that the problem with grains
is not that they're carb's,
but that they're high-glycemic carb's .
. Lustig redefines other low-carb questions
in terms of glycemic index and load
-- we're restricting ourselves to safe carb's
not from carb's .

. he does note that those who
the Dr.Atkins's diet is targetting
(the insulin resistant)
will do well on an Atkins diet!
. conversely,
those who are not insulin resistant
may do better with a low fat diet .
[7.29:
-- a non-ketogenic slow-carb vs low-carb style]

anything he'd change in his lecture?:

. Lustig regrets not emphasizing more
how the toxicity of fructose is
dose dependent (and context dependent):
. in exhausted athletes,
a low dose of fructose does better than glucose
at quickly rebuilding glycogen stores .
--[. he did say that during the lecture,
and handily identified both dose and context;
but he got a lot of flack for
psychologically poisoning
a lot of proud athletic juice users
who do not have an obesity problem .]

 speaking of athletics,

the sodas got banned from school
but those same companies can still sell
the same sugar in sports drinks and juices!
. people around the world are getting fatter
and it is happening on cheap sugars .
. he didn't so much deny there were
other reasons for global obesity
as to scoff at the notion that
obesity was a lack of will power:
. we as a society need to recognize
that not everyone is carb tolerant;
and for the sake of the less fortunate,
society should make sure that
the cheapest food is safe carb's:
low-glycemic and high-fiber .

comments of the thelivinlowcarbshow with Lustig:

commenter"Ned Kock, Ph.D, July 6, 2010
 The extra fructose, not used for glycogen replenishment,
is converted into fat by the liver.
That fat is packaged in the form of triglycerides,
which are then quickly secreted by the liver
as small VLDL particles.
The VLDL particles contribute to body fat.
After delivering their cargo,
small VLDL particles eventually become
small-dense LDL particles;
the ones that can potentially cause atherosclerosis.
. see  The huge gap between glycemic loads of
refined and unrefined carbohydrate-rich foods .

7.18: Gary Taubes April 13, 2011/review's Lustig:

Gary Taubes, author of “Why We Get Fat”
. independent investigator in health policy
for the Robert Wood Johnson Foundation .
. he's spent much of the last decade
doing journalistic research on
diet and chronic disease
and has come to conclusions similar to
Lustig's May 26, 2009 lecture,
“Sugar: The Bitter Truth” :
[7.28:
. he also clarifies some of Lustig's language,
eg, explaining the context of a
"(Japanese Diet) .]

. an adviser to the Corn Refiners Association,
reminds us that sugar might be toxic,
but so might any substance consumed in
unnatural ways or quantities .
. Lustig wants to remind us
that when we use sugar "(in moderation)
it should be the same sort of moderation
we would reserve for alcohol and tobacco:
 sugar is a “toxin” or a “poison”;
it's danger has nothing to do with
[empty] calories.

1924, Haven Emerson:

a rise in diabetes deaths coincided with
a rise in sugar consumption
— almost doubling from 1890 to the early 1920s .
Elliott Joslin counters Emerson:
The Japanese eat lots of rice,
and Japanese diabetics are few and far between;
[ rice's main sugar is glucose
whereas diabetics were occurring from
the combination of glucose and fructose
7.29:
. the Japanese at that time may have had
a Zone Diet, affectively lowering
both the glycemic index (mixing it with other food)
and the glycemic load of their rice (small portions).]

[1957 John Yudkin

. he showed that the consumption of sugar
and refined sweeteners is closely associated with
coronary heart disease and type 2 diabetes.
He became internationally famous with his book
Pure, White and Deadly (published in 1972)]

John Yudkin 1978`Sweet and Dangerous

. sugar raises blood levels of triglycerides
and insulin levels .
. like Atkins he was fighting official dogma:
he asserted that all the blame that is
now being put on dietary fats
should instead be put on dietary sugars;
and,
no academic would try that again until Lustig .

1970, Ancel Keys`Seven Countries Study.

[ he also co.authored a cook book:
The Benevolent Bean (Doubleday, 1967)]
. saturated-fat and sugar consumption
were almost equally predictive of heart disease;
but Keys and others in the usa
interpreted this as ok'ing sugar;
whereas European clinicians and Yudkin
interpreted it as further villifying sugar .
[7.18:
. it's the combination:
most cultures use both sugar to
provoke an insulin response,
and they use sat'fat to cause
an insulin resistance .
. this combination powerfully raises insulin .]

2004 cancer linked to metabolic syndrome

World Health Organization’s
International Agency for Research on Cancer:
. more likely to get cancer if you’re
obese or diabetic or have metabolic syndrome .

. metabolic syndrome is seen as the #1 risk factor
for heart disease and diabetes;
. insulin-resistance is very strongly related
to processes that deposit fat in the liver .
[. Lustig has pointed out animal studies
showing that high-dosing fructose+glucose
will cause fatty liver .]
. as to whether our typical use of sugar
causes fatty liver,
the science is still not complete;
because were missing human-subject
sucrose intervention studies
in which high-fructose consumers
have their useage level randomly changed .

. however there is general agreement
that cancer has much to do with our diet .
. elevated insulin signaling
appears to be a necessary step in many human cancers,
particularly cancers like breast and colon cancer.
. perhaps 80 % of human cancers are driven by
either mutations or environmental factors
that work to enhance or mimic the effect of insulin
on the incipient tumor cells.
[7.28:
. from the context,
I think he was trying to suggest this:
. when you cause chronic insulin resistance
(as with diet of a high-glycemics and sat'fats)
then cells are encouraged to evolve ways to
get more energy without insulin's help;
these changes then facilitate unchecked growth
as well as higher metabolisms .]

2007 high insulin linked to cancer:

 World Cancer Research Fund
American Institute for Cancer Research
“Food, Nutrition, Physical Activity and the Prevention of Cancer.”
. higher levels of insulin and igf
(insulin-like growth factor)
are promoting tumor growth .
[7.28:
. so that is your sugar vilifying clincher:
unless you can refute that finding;
sugar or any other lifestyle choice
that is raising your insulin
should be considered to be a risk for
unnecessary costs, pain, and disability

guide to cheap insulin monitoring:

. you can test the health of your diet
 by watching it`s effect upon insulin levels,
which are mirrored by
 the ratio of triglycerides (TG)
to HDL (helpful) cholesterol
. when my diet was high in eggs and olive-oil,
while having no sugar, flour, or starchy vegetables,
I had a perfect TG/HDL ratio of around 1/1 !
( a typically horrible ratio is 4/1 ) .]

7.29: events that inspired Lustig

7.16: Lustig et al, 1999`somatostatin agonist

Hypothalamic obesity caused by cranial insult in children:
altered glucose and insulin dynamics
and reversal by a somatostatin agonist.
J Pediatr. 1999 Aug;135(2 Pt 1):162-8.
Patients with hypothalamic obesity
demonstrate excessive insulin secretion.
Octreotide administration promoted weight loss,
which correlated with reduction in insulin secretion
on OGTT and with reduction in leptin levels.
Pre-study biochemical glucose tolerance
improved in several patients
while they were receiving octreotide.
These results suggest that
normalization of insulin secretion
may be an effective therapeutic strategy
in this syndrome.

7.16: Lustig RH (2001)`childhood obesity

The neuroendocrinology of childhood obesity.
Pediatr Clin North Am 48: 909–930
The regulation of energy balance is enormously complex,
with numerous genetic, hormonal, neural and behavioral,
and societal influences.
Although the current epidemic of obesity
clearly has its underpinnings in the changes in culture
during the past half-century
(see other articles in this issue),
the role of the neuroendocrine system in the genesis of
obesity, as described in this article,
is physiologically and therapeutically unavoidable.
The Centers for Disease Control and Prevention
now supplies BMI charts for boys and girls .
www.cdc.gov/growthcharts
 Plotting of the BMI versus age allows pediatricians
 to determine the age at which the BMI starts to increase
(mean, 5.5 years). The earlier the adiposity rebound,
the more likely the child will be obese as an adult,
and the more likely that an organic cause can be determined.
In such patients, thyroid levels and fasting
insulin and leptin levels should be measured.
An initial attempt at diet and exercise is essential;
patients who do not respond with BMI stabilization
should be investigated for a more ominous cause
of their obesity.
As the nosology of obesity improves,
pediatricians will be able to increase the
diagnostic efficiency and therapeutic success
of this unfortunate, debilitating, and expensive epidemic.

7.16: Lustig RH et al. (2003) Octreotide therapy

Octreotide therapy of pediatric hypothalamic obesity:
a double-blind, placebo-controlled trial.
J Clin Endocrinol Metab. 2003 Jun;88(6):2586-92.

7.16: Lustig RH (2003) pathogenesis of obesity

Autonomic dysfunction of the beta-cell
and the pathogenesis of obesity.
Rev Endocr Metab Disord 4: 23–32

7.16: Lustig RH et al. (2003) obesity from brain tumors

Risk factors for the development of
obesity in children surviving brain tumors.
J Clin Endocrinol Metab 88: 611–616
. the hypothalamus is vital to energy balance;
damage to it is a primary cause of obesity
in those treated for brain tumors .

7.16: Lustig 2006` First Law of Thermodynamics:

Childhood Obesity: Behavioral Aberration or Biochemical Drive?
Reinterpreting the First Law of Thermodynamics
Nature Clinical Practice Endocrinology & Metabolism 2(8):447-458 (2006)
Robert H Lustig 
Division of Pediatric Endocrinology,
University of California San Francisco,

Childhood obesity has become epidemic
over the past 30 years.
The First Law of Thermodynamics is routinely interpreted
to imply that weight gain is secondary to
increased caloric intake and/or
decreased energy expenditure,
two behaviors that have been documented
during this interval;
nonetheless,
lifestyle interventions are notoriously ineffective
at promoting weight loss.
Obesity is characterized by hyperinsulinemia.
Although it is usually thought that
hyperinsulinemia is secondary to obesity,
it can instead be primary, due to autonomic dysfunction.

Obesity is also a state of leptin resistance,
in which defective leptin signal transduction
promotes excess energy intake,
to maintain normal energy expenditure.
Insulin and leptin share a common
central signaling pathway,
and it seems that insulin functions as an
endogenous leptin antagonist.
Suppressing insulin ameliorates leptin resistance,
with ensuing reduction of caloric intake,
increased spontaneous activity,
and improved quality of life.

Hyperinsulinemia also interferes with
dopamine clearance in the ventral tegmental area
and nucleus accumbens,
promoting increased food reward.

Accordingly,
the First Law of Thermodynamics can be reinterpreted,
such that the behaviors of increased caloric intake
and decreased energy expenditure
are secondary to obligate weight gain.
This weight gain is driven by [high insulin]
through three mechanisms:
# energy partitioning into adipose tissue;
# interference with leptin signal transduction;
# interference with extinction of the
hedonic response to food.

. our current Western diet is very insulinogenic,
[promoting chronic high insulin]
as demonstrated by its
# increased energy density,
(high fat, low fiber, high glycemic index)
# increased fructose composition,
# decreased dairy content .

the CNS mechanisms underlying weight gain:
. Within the afferent arm of
the homeostatic pathway of energy balance,
leptin and insulin are often equated
[by those who are measuring only the]
short-term effects of these hormones;
however,
the hyperinsulinemic [chronic high insulin] state
interferes with leptin signal transduction,
as insulin acts as an endogenous leptin antagonist.
This interference promotes leptin resistance,
which should decrease SNS activity
to reduce REE,
and increase vagal activity
to promote energy storage;
except that, of course,
the obese subject—of necessity—
increases caloric intake,
which raises their leptin concentration
above the level at which leptin resistance occurs,
so as to maintain normal energy expenditure
and quality of life.
The insulin resistance that is a
characteristic of the obese state
promotes further leptin resistance.
Hyperinsulinemia also decreases dopamine clearance
and uptake in the hedonic pathway,
which promotes an increased reward of food
that causes increased food intake.
This effect also maintains the hyperinsulinemic state .

The phenomenon of hyperinsulinemia
turns two neuroendocrine negative feedback systems
into feed-forward systems (or 'vicious cycle',
in which the product stimulates further
substrate production or action,
rather than inhibiting it).
Hyperinsulinemia promotes increased energy intake
and decreased energy expenditure (Figure 4).
Externally, this manifests as 'gluttony and sloth',
but it is biochemically driven.
In this paradigm, the First Law of Thermodynamics
can be expressed so that the weight gain is primary,
and the resulting behaviors are secondary:
"If you store it (obligate weight gain
occurs in response to hyperinsulinemia),
and you expect to burn it
(to maintain normal REE and quality of life),
then you must eat the difference
(add the calories that lipogenesis stole)".

Although there are numerous contributors
to hyperinsulinemia,
our current food and activity environment
is the most important,
and the most amenable to change;
however, to make a difference in the lives of children.
it will take acknowledgment of
the concepts of biological susceptibility
and societal accountability,
and de-emphasis of the concept of
personal responsibility .

7.16: Lustig RH et al. (2006) octreotide dose

A multicenter, randomized, double-blind, placebo-controlled,
dose-finding trial of a long-acting formulation of octreotide
in promoting weight loss in obese adults
with insulin hypersecretion
International Journal of Obesity (2006) 30, 331–341.
Obesity is a dysregulation of the
negative feedback energy balance pathway.
Insulin is a component of the efferent pathway,
promoting storage of energy substrate in adipose tissue.
Although obesity is routinely associated with
insulin resistance,
it has previously been shown that a subset of
children who develop intractable obesity
after treatment for brain tumors, termed 'hypothalamic obesity',
exhibit insulin hypersecretion in response to
oral glucose tolerance test (OGTT)
due to excessive vagal stimulation of the beta-cell.
The vagus nerve increases insulin secretion by
three mechanisms:
opening of a sodium channel,
which increases beta-cell depolarization
and widens the voltage-gated calcium channel
resulting in greater calcium influx;
stimulation of phospholipase C,
which increases insulin exocytosis;
and stimulation of intestinal glucagon-like peptide-1 (GLP-1),
which binds to the beta-cell membrane,
stimulates adenyl cyclase,
and increases insulin secretion.
Insulin secretion can be assessed from an OGTT
using the index variable corrected insulin response
at the glucose peak (CIRgp).

Octreotide is a synthetic analogue of the
natural hormone somatostatin.
Like somatostatin, octreotide limits
beta-cell insulin secretion by
inhibiting the G0 protein associated with the
widening of the voltage-gated calcium channel.
Octreotide also inhibits secretion of gastric acid,
pancreatic enzymes, and bile,
prolongs intestinal transit time,
and decreases gallbladder contractility.
Both somatostatin and octreotide inhibit the release of
pituitary and gastroenteropancreatic hormones
such as growth hormone (GH),
thyroid stimulating hormone (TSH),
glucagon, cholecystokinin (CCK),
vasoactive intestinal peptide (VIP),
gastrin, and ghrelin.
Octreotide acetate (Sandostatin®; Novartis)
is normally administered subcutaneously,
three times per day.

7.17: Lustig 2007 with Norman Swan:

9 July 2007 ABC radio's/Norman Swan's Health Report
. transcribed on nourishedmagazine interview,
and at healthyweightkids.org .
. Asians have been traditionally thin
and for centuries they've eaten processed rice?
. the Atkins diet was no-carb, high-fat,
and it worked.
We look at the [traditional] Japanese diet,
the high-carb, no-fat also worked.
When you put them together
you get something called McDonalds
and clearly that doesn't work.
So the question is
what is it about the Japanese diet,
even though they eat all of this white rice,
that still allows this phenomenon to be OK?
And the answer is very simple
-- it's the [low dose of] fructose,
because fructose is really not a carbohydrate.
If you look at the metabolism,
it is just like a fat,
it doesn't stimulate insulin, just like fat.
it causes deposition of fat within the liver,
it's actually like alcohol
and alcohol is like a fat.
So in fact
a low fat diet with sugar
is not really a low fat diet,
it is really a high-fat high-carb diet
and that explains what's going on.

So a [traditional] Japanese diet
is not getting any fructose from processed rice,
and is still getting fiber from other veg's .
but in the last ten years,
[the modern Japanese diet does include fructose]
and childhood obesity has doubled in Japan
whereas adult obesity hasn't moved.

. a non drug that (helps obesity) is
resistance exercise building up your muscles.
. it increases skeletal muscle insulin sensitivity,
. it’s the single best way to
lower cortisol levels,
it’s the hormone that basically causes
visceral(bad) fat deposition
and it has been tied to the metabolic syndrome.
So by getting your cortisol down
you’re actually reducing the amount of fat deposited
. it reduces food intake.
. it actually helps detoxify the sugar fructose.
(a hepato-toxin in unnatural doses);

Glucose, the standard sugar, can be taken up by
every organ in the body,
only 20% of glucose load ends up at your liver.

two slices of white bread:
120 calories of glucose,
only 24 of those 120 calories
will be metabolised by the liver,
the rest of it will be metabolised by
by other cells .

Now let’s take the same 120 calories
but from orange juice:
60 of those calories are going to be fructose
(sucrose is half fructose);
your liver has much more to process:
60 calories of fructose
plus 20% of the glucose,
-- three times the substrate
as when it was just glucose alone.

That extra substrate to your liver
does some very bad things to it:
#
. high-dose fructose is damaging your liver
the same way alcohol is.
it’s the exact same pathway, in fact,
fructose is alcohol without the buzz.
#
. fructose increases the phosphate depletion
of the hepatocyte [liver cells]
which ultimately causes an increase in
uric acid:
an inhibitor of nitric oxide,
-- that keeps your blood pressure normal;
and so fructose is famous for
causing hypertension [high blood pressure]
#
. large doses of fructose promote
de novo lipogenesis [liver produces fat]
which raises VLDL (very low density lipoproteins)
and results in dyslipidaemia
in a way that glucose does not .
#
. fructose has been bandied about [by dieticians]
because, it doesn’t raise your insulin directly
but it does do so indirectly
since fructose contributes to insulin resistance;
because, it initiates the enzyme [JNK-1]
Insulin levels all over your body have to rise
interfering with normal brain response to insulin
thereby causing the leptin dysfunction,
[and prolonged hunger signals] .
. your liver is not responding to insulin
because of ... serum phosphorylation
of the insulin receptor.
[7.28: web(JNK?, phosphorylation?):
A central role for JNK in obesity and insulin resistance
(September 2002; doi:10.1038/nature01137) (pdf)
The JNK's (c-Jun amino-terminal kinases)
can interfere with insulin action
and are activated by inflammatory cytokines
and free fatty acids, [from fructose or...]
. JNK activity is abnormally elevated in obesity.
Furthermore, an absence of JNK-1 results in
# decreased adiposity,
# significantly improved insulin sensitivity
# enhanced insulin receptor signalling capacity
in two different models of mouse obesity.
Thus,
JNK is a crucial mediator of
obesity and insulin resistance .
Inhibitory serine phosphorylation of
insulin receptor substrate (IRS)-1
was previously shown to be responsible for
both {TNF-alpha, FFA}-induced insulin resistance .]

fructose is ok with high fiber:
. an orange has 20 calories,
10 of which are fructose and has high fibre.
A glass of orange juice has
120 calories from 6 oranges
and there’s no fibre.
so by all means eat the fruit,
just don’t drink the juice.

Miles Faith had an article in
Pediatrics, December 2006
showing that in toddlers,
in inner city Harlem in New York,
in toddlers the number of juice servings
correlated with the degree of BMI increase.

. what about regulators for
The Corn Refiners Association
and the Juice Products Association?
. the International Obesity Task Force
has the Sydney principles,
for regulation of marketing to children .
In fact in Europe, 52 health ministers agreed
that marketing to children had to stop.
Well in fact
that is not happening in America.

Lustig (2008)`Limbic Triangle

Childhood Obesity: Adrift in the “Limbic Triangle”
Michelle L. Mietus-Snyder and Robert H. Lustig
Annual Review of Medicine 59:147-162 (February 2008)
. there's an increasing prevalence of obesity
worldwide (22).
. public health media campaigns
[can't trump cultural dietary norms .]
This review outlines the complex network of
genetic, behavioral, and environmental barriers
that thwart our attempts control obesity .

. the “limbic triangle” is the
Neuroendocrine mechanisms within the limbic brain that
# prevent starvation (ventromedial hypothalamus),
# heighten reward (ventral tegmental area and nucleus accumbens),
# attenuate stress (amygdala),
in order to promote food-seeking behavior
and to conserve energy output.

The “limbic triangle” is a set of 3 areas of the CNS
that conspire to drive food intake
and reduce physical activity,
resulting in persistent weight gain.
The ventromedial hypothalamus (VMH)
transduces the leptin signal from adipocytes
to reduce energy intake and increase energy expenditure;
however, hyperinsulinemia prevents leptin signaling,
promoting the “starvation response.”
The ventral tegmental area (VTA)
transduces the leptin signal
to reduce dopamine neurotransmission to the
nucleus accumbens (NA), reducing food intake;
however,
hyperinsulinemia prevents leptin signaling
here as well,
increasing dopamine
and promoting the “reward” of food.
The amygdala transduces fear and stress,
which results in increased cortisol release
from the adrenal cortex.
The elevated cortisol also drives
energy-rich food intake
and promotes insulin resistance,
further interfering with leptin signaling
at the other two CNS sites.
Thus, activation of any aspect of the limbic triangle
turns on a positive feedback loop,
promoting continued weight gain and obesity.

CHO, carbohydrate;
REE, resting energy expenditure;
SNS, sympathetic nervous system.

. the Healthy People 2010 goal is to
reduce the prevalence of obese children to 5%.
. sources in the current rise of childhood obesity
include
decreased physical activity,
increased television time,
and increased consumption of
sugar-sweetened beverages .

A recent review found some new sources of
across usa people of all ages:
sleep debt;
endocrine disruptors in the food chain;
decreased variability in ambient temperature
due to heating and air conditioning;
decreased smoking;
increased use of pharmacotherapies
(notably steroids and antipsychotics
that alter energy balance);
demographic changes toward ethnicities with
higher prevalences of obesity
and toward older age brackets
in which individuals are more likely to
accumulate extra adiposity;
increase in gravida age;
greater reproductive fitness at
moderate degrees of overweight
(although severe overweight promotes infertility)
and assortative mate selection
for obesogenic genes .

Others posit that obesity is the result of
chronic stress in modern life,
coupled with frequent dieting
or self-imposed food restriction,
with synergistic effects that increase the
reward value of palatable foods .
The increasing prevalence of
micronutrient deficiencies
in highly processed, energy-dense diets
can be linked to numerous chronic conditions
including obesity .
A link between changes in our gut microbial flora
and the increasing prevalence of obesity,
metabolic syndrome, and type 2 diabetes
has also been postulated .

Although the contribution of
any one of these risk factors may be small,
their combined impact is probably considerable
and possibly synergistic .

March 2008: How Bad Is Fructose: Pure White and Deadly

Fructose: Is It Bad For Our Health?
A commentary prepared for a joint
ILSI North America/USDA Workshop:
State-of-the-Science on Dietary Sweeteners Containing Fructose,
Author: George A. Bray, MD
Boyd Professor LSU System
Pennington Biomedical Research Center

The current epidemic of obesity could be explained by
the consumption of an extra 20-ounce soft drink each day.
. an extra 50 kcal per day
could account for a weight gain of 1 kg in 1 year.
In addition to the calories and fructose they provide,
soft drinks have little else to contribute to our diet.
High-fructose corn syrup (HFCS) is clearly
a marker for highly refined foods
-- the kind of food we want to avoid in our diet.

“If then there is reason to be concerned about
a dietary cause of a widespread disease,
one should look for some constituent of man's diet
that has been introduced recently
or has increased considerably, recently (1).”

“Some factor of diet and/or lifestyle
must be driving weight upward,
because human biology and our underlying genetic code
cannot change in such a short time (2).”

Just as HFCS was appearing in the US food supply,
Professor Yudkin (1) wrote a book titled
Pure, White and Deadly,
in which he attributed the rising risks of
obesity and heart disease to sugar.
Professor Yudkin’s ideas were not
taken very seriously ...

The law of energy balance does not explain the
biological control of food intake
nor how fat is distributed over the body.
The hedonic effects of food
are not factored into the equation
nor does energy balance help us to understand
genetic influences,
which we know account for a significant amount of
the susceptibility to obesity .

. fructose is more chemically reactive than glucose,
and it circulates in blood at a much lower
concentration than glucose.
Fructose is an intermediate in the
formation of trioses from glucose.
The fructose 1-phosphate formed when
fructose is absorbed into the liver
can be readily converted to glycerol 3-phosphate,
the precursor of triglyceride synthesis.

Glucose directly stimulates insulin release
from the pancreatic beta-cell,
but fructose does not.
Fructose also enters muscle and other cells
without depending on insulin,
whereas most glucose enters cells
in an insulin-dependent manner.
Finally once inside the cell,
fructose can enter the pathways that provide
the triglyceride backbone (glycerol)
more efficiently than glucose.
Thus, high consumption of fructose,
may be a “fat equivalent” .

good science: bad sodas

In one of the few randomized,
 well controlled intervention studies,
 Danish investigators (27) showed that
10 weeks of drinking sugar(half fructose)
gained weight,
whereas subjects drinking the same amount of
artificially sweetened beverages
lost weight.
Equally important,
drinking sugar-sweetened beverages
was associated with a small but significant
increase in blood pressure.

In a study of Swiss children,
higher intake of fructose predicted
a smaller LDL particle size
--the higher risk for LDL-cholesterol .

Fructose, unlike other sugars,
increases serum uric acid levels.
. ATP is used by the enzyme phosphofructokinase
to phosphorylate fructose to fructose-1-phosphate.
The adenosine-5’- diphosphate can be further broken down
to adenosine-5’-monophosphate,
then to inosine 5'-phosphate and finally to uric acid.
. high levels of uric acid could set the stage for
advancing cardiovascular disease by
reducing the availability of nitric oxide (NO),
which is crucial for maintaining
normal function of the vessel walls
including blood pressure regulation .

Framingham Study,

Soft-drink consumption has been linked to the
development of cardio-metabolic risk factors
and the metabolic syndrome .
Individuals consuming one or more soft drinks per day
had a higher prevalence of the metabolic syndrome
(OR = 1.48; 95% CI = 1.30-1.69)
and an increased risk of developing
the metabolic syndrome over 4 years of follow-up.
Conclusion
The attribution "pure, white, and deadly"
to sugar by Professor Yudkin in 1972
may yet be partly right: about fructose .
As Yudkin said 25 years ago (1),
"(I suppose it is natural
for the vast and powerful sugar interests
to seek to protect themselves,
since in the wealthier countries
sugar makes a greater contribution to our diets,
measured in calories, than does meat or bread
or any other single commodity).
Literature Cited
1. Yudkin J. Pure, white and deadly:
the problem of sugar. London: Viking; 1986.
2. Taubes G. Good calories bad calories.
Challenging the conventional wisdom on diet,
  weight control and disease. New York: Knopf; 2007.
3. Cleave TL.
The saccharine disease. The master disease of our time.
New Canaan, CT:  Keats Pub; 1974.
4. Bray GA.
The metabolic syndrome and obesity.
Totawa, NJ: Humana Press; 2007.
[...] .
27. Raben A, Vasilaras TH, Møller AC, Astrup AA.
Sucrose compared with artificial sweeteners:
different effects on ad libitum food intake
and body weight after 10 wk of supplementation
in overweight subjects.
Am J Clin Nutr. 2002;76:721-9

7.28: fan's of Lustig's message:

180degreehealth:

7.13: news.health/fructose/180degreehealth:
. a comment on Dr.Mercola's site
introduced me to Lustig with this link:
holy-grail-of-fructose-information .
. it introduced Lustig's video
"(Sugar: The Bitter Truth)
180degreehealth's page at mercola:
. Author and independent health researcher.
. Creator of www.180degreehealth.com
and associated blogs:
www.180degreehealth.blogspot.com
www.180kitchen.wordpress.com
- confronting mainstream dogma:
nutrition, health, lifestyle, and medical .
Publishes quarterly eBooks, monthly eZine,
and weekly audio podcasts to free membership base.

7.15: thatpaleoguy.blogspot.com:

about Jamie Scott:

"( I believe the ultimate control
one can have in their life
is control over their own health.
That requires knowledge
- knowledge of yourself,
the environment you operate in,
and the interaction between the two.
I hold post-graduate diplomas in
sport & exercise medicine
and in nutritional medicine.)

Scott quoted these Lustig papers:
Fructose: metabolic, hedonic, and societal parallels with ethanol.
 Lustig RH.
The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome.
Lim JS, Mietus-Snyder M, Valente A, Schwarz JM, Lustig RH.
and commented:
"( People need to get off the track of
worrying about fructose in their fruit
when there are other elephants in the room.
I think everyone agrees
that the problem with fructose
sits largely with that found in added sugars.)
7.28: more from Scott:

June 2010: Fructose: Making Your Kids Fatter

Endocrine Society's 92nd Annual Meeting
. high levels of fructose throughout childhood
may lead to an increase in visceral [abdominal] obesity,
which is associated with increased cardio-metabolic risk .

Scott July 2010: David Gillespie vs sugar

>  Have you seen the following wonderful
> 90 minute lecture (circa 2009) on Fructose ?
> Sugar - The Bitter Truth, by Robert Lustig
    Yes,
have watched that a couple of times now.
Great lecture.
Although not great enough to sway
some dietitians & nutritionists I know...
they still don't see a problem with it:
[eg,] an Australian Nutrition Scientist
(he's rebutting David Gillespie [@ abc.net.au]
- author of 'Sweet Poison')

David Gillespie said...

. here's my rebuttal of his 'rebuttal'
"(Sweet Poison is stuffed to the brim
with examples from the (over 3,000) studies
that show the damage being done by fructose, ...)

Scott October 2010 Fructose Intolerance:

"(I would disagree that a low fructose diet
is hard to follow.  Paleo/Primal nutrition.)
. see his FODMAP's page
-- Fermentable Oligo- Di- Mono-saccharides And Polyols .
. why we should all be more fructose intolerant ...
High Fructose in children promotes abdominal obesity
High Fructose Impairs Memory In Rats
High Fructose May Contribute to High Blood Pressure
Fructose Metabolism More Complicated Than Was Thought

Eating too much fructose can induce leptin resistance:

"( They found that the animals exposed to
the high-fructose diet,
the leptin resistant rats, ate more and
gained much more weight and fat
than the leptin responsive animals
on the fructose-free diet.
All told, this study showed that leptin resistance can:
# develop by eating a lot of fructose
# develop silently, that is,
with very little indication it is happening
# result in weight gain when paired with
a high fat, calorie dense diet .
"(This study may explain how
the global increase in fructose consumption
is related to the current obesity epidemic),
Shapiro said.
    How it happens:
. elevation in triglycerides produced by fructose
prevented leptin from reaching the brain.
If leptin does not reach the brain,
the brain will not send out
the signal to stop eating.
)
Scot's comment:
This is an important insight
as for decades
we have blamed the rise in obesity
on the consumption of a high-fat, calorie-dense diet.
It would seem however
(and has been pointed out in recent commentaries),
it is not the high fat foods per se,
rather, it is when these are paired with
high intakes of fructose
-- and, I would bet the farm, --
on high intakes of omega-6 fats also.
Think about it from an evolutionary point of view...
late summer/early autumn,
we would have had a relative abundance of
fruit (fructose) and nuts (omega-6),
probably alongside some of our other regular foods
such as sources of animal fat, starchy tubers, etc.
The perfect recipe for storing A LITTLE BIT
of extra fat for the winter months ahead.
But with our modern diet of
high fructose and omega-6 all year round,
every day is autumn to our metabolism.

7.15: other fans of low-fructose for childhood obesity:

Dr. Redmond, Metametrix Clinical Laboratories:

Aim for a diet with a low glycemic load.
Avoid high fructose corn sugar (HFCS).
Fructose increases lipogenesis which can lead to
fat accumulation in the liver .
--  co-author in the Laboratory Evaluations for
Integrative and Functional Medicine(2008) textbook.

Melania Manco, MD Ph.D:

Nonalcoholic Fatty Liver Disease in Children:
Non Alcoholic Fatty Liver Disease (NAFLD)
may be deemed as a worldwide problem in childhood .
The increase in its prevalence
parallels the epidemic obesity.
In genetically prone individuals,
excessive consumption of
saturated fats and refined sugars
leads to the derangement of the
adipose tissue architecture and homeostasis,
the peripheral and hepatic resistance to
insulin-stimulated glucose uptake,
thus favoring a condition of
chronic low-grade inflammation.
The present review focuses on pediatric
Non Alcoholic Fatty Liver Disease (NAFLD)
among co-morbidities, being the disease
yet under diagnosed and under treated
despite a prevalence growing exponentially.
Evidences suggest that the duration of the disease
affects probably the likelihood of
progression to more severe disease
(necro-inflammation or NASH
 (Non Alcoholic SteatoHepatitis),
fibrosis and cirrhosis).
NAFLD associates with abdominal obesity,
insulin resistance
and features of metabolic syndrome.
In view of the epidemic obesity in childhood,
facing the disease early becomes crucial .
 Observations in children as well as in adults
suggest that normal weight subjects
also may be insulin resistant
presenting an unhealthy phenotype characterised by
increased abdominal distribution of fat.
These individuals are prone to develop
all the features of the Metabolic Syndrome,
including NAFLD/NASH.
A recent review [Am J Clin Nutr86 :285– 300,2007(pdf)]
discusses systematically the effect of
carbohydrate, fat, and protein ratios
and specific food components,
such as soluble fiber, n-3 fatty acids,
and fructose,
on fatty liver disease in adults
with the intent to enable clinicians to
evaluate the most appropriate diet for NAFLD/NASH patients
and make rational decisions based on this perspective
—in the absence of controlled trials—
to help their patients .

Zivkovic AM, German JB, Sanyal AJ:

Comparative review of diets for the metabolic syndrome:
implications for nonalcoholic fatty liver disease.
Am J Clin Nutr86 :285– 300,2007
Sucrose and fructose:
Several studies have shown that high intakes of fructose
increase  de novo lipogenesis (DNL) in both
animal models and humans (106-108).
One study of lean and obese women found
a trend toward a higher increase with sucrose
[half fructose, half glucose]
than with glucose [without fructose].
These data suggest that some individuals may be
more sensitive to fructose-induced stimulation of DNL.

Studies of the effects of fructose consumption
on whole-body energy metabolism
suggest that a high consumption of
fructose and glucose in the form of
sweetened beverages
may lead to changes in long-term
energy balance regulation
which favors increased calorie consumption
and weight gain.
Sweetened drinks, such as sodas,
are typically consumed as additional calories
and lead to excess intake of as much as 150–300 kcal/d (112).
It is recommended that intakes of refined sugars
and high-fructose or high-glucose foods
should be reduced in the NAFLD population.
High intakes of fructose and glucose
as simple [defibered] sugars
stimulate the de novo synthesis of fatty acids,
especially in individuals with insulin resistance
and in those who are overweight .
refs:
Dietary Fructose and Glucose Differentially Affect
Lipid and Glucose Homeostasis
J. Nutr. 2009 139: 1257S-1262S
Fructose Ingestion:
Dose-Dependent Responses in Health Research
J. Nutr. 2009 139: 1246S-1252S
Fructose consumption and consequences for
glycation, plasma triacylglycerol, and body weight:
meta-analyses and meta-regression models
of intervention studies
Am J Clin Nutr 2008 88: 1419-1437

ucsf.edu`Jeffrey Norris on June 25, 2009:

. here are links related to the Lustig video
"(Sugar: The Bitter Truth):
Fructose consumption as a risk factor
for non-alcoholic fatty
J Hepatol. 2008 June; 48(6): 993–999.
Adolescent Overweight and
Future Adult Coronary Heart Disease
Kirsten Bibbins-Domingo, Pamela Coxson, Mark T. Pletcher,
James Lightwood and Lee Goldman
New England Journal of Medicine, 357(23):2371-2379 (Dec. 6, 2007)

Overweight Adolescents Projected to Have
More Heart Disease in Young Adulthood
UCSF News Release, Dec. 5, 2007

Kirsten Bibbins-Domingo, PhD, MD:

. lead author on the study reported in
New England Journal of Medicine. Dec. 6, 2007:
. UCSF assistant professor in
medicine, epidemiology and biostatistics;
and, co-director of the UCSF Center for
Vulnerable Populations
at San Francisco General Hospital .

A new study investigating the health effects of
being overweight during adolescence
projects alarming increases in the rates of
heart disease and premature death
by the time today’s teenagers reach young adulthood.
A team of researchers used a computer-based
statistical modeling system known as
the Coronary Heart Disease (CHD) Policy Model
to estimate the potential impact
of an increasingly overweight U.S. adolescent population
on future adult health nationwide.
Based on the numbers of overweight adolescents in 2000,
the study found that up to
37 % of males and 44 % of females will be obese
when these teenagers turn 35 years old in 2020.
The model estimated more than 100,000
extra cases of heart disease by 2035,
which is a 16 % increase over today’s figures,
and a rise by as much as 19 %
in obesity-related CHD[coronary heart disease] deaths .
“This study highlights the importance of
preventing obesity before it starts in children.
The current high rate of overweight
is not just a problem for adolescents and their parents,
it’s something that will affect all of us
well into the future” .