Low carb diets

"Lyle McDonald" wrote in message
...
Aaron wrote:

"Lyle McDonald" wrote in message
...
OmegaZero2003 wrote:

"Lyle McDonald" wrote in message
...
OmegaZero2003 wrote:
\
Low carb need not be a form of or mean calorie restriction. The
calories
decreased via the low-carb approach can be added back in by
taking
some
additional EFAs like fish/flax oils, to very good effect.

Think nutrient partitioning- taking advantage of what the body
does
with
certain types of nutrients (e.g., leptin- and insulin-modulated
partitioning) and, as an extension, timing the intake of those
different
nutrients to best work with the body's metabolistic parameters
governing
their - well - metabolism!

So are you suggesting that, via nutrient partitioning, a
maintenance
calories (i.e. not restricted in calories) low-carb diet will
somehow
cause something to occur wrt: body fat?

Well - I read your previous posts on the matter, along with about 30
studies
(some posted in another thread), that nutrient partitioning (via
differntial
response of metabolic parameters such as insulin and leptin etc.)
will
cause
loss of bf and maint of lean body mass.

Only when you are looking at increasing protein from subadequate to
adequate levels in fat people. Of course, since protein is less
energetically efficient (in terms of providing ATP to the body),
switching out carbs/fat to protein results in a technically lower
calorie diet.

A little over 50% of the aminos from dietary protein are available for
ATP production so for every 200 calories of carbs you replace with 200
calories of protein, you're getting ~100 calories less dietary energy.
So at 2000 ostensible calories, a higher protein diet is technically
NOT
providing 2000 calories of useable energy.

The weight-loss issue is not what I am aiming at here, but bf loss
vs
lean
muscle maint.

No ****.

Lyle

in terms of bunk studies, I have one GI study that showed the low GI
maintained RMR better than the high GI diet, and produced more weight
loss
(however not significantly more) but the fuktards made these relatively
obese (~100kg) people eat a 15% protein High GI to a 25% low GI, which
resulted in 0.4 vs 0.8g/kg protein intake!
****tards, you would 'hope' that somebody as big in the GI world like
Ludwig
would actually ****ing pick that to start with.

that was the first one Omega cited, that I mentioned had 4 independent
variables


you mean I was meant to read thru that pile of papers for a mention of it?

it had varying GI, varying amounts of protein (about double in the low
GI group), varying amounts of carbs and varying amounts of fats.

I have seen both Berardi and Kreider hang 'A calorie is not a calorie'
arguments on that study (arguing that low GI is protein sparing in
Krieder's case).

A ****ty study and ****tier conclusions drawn from it.

Lyle

about the only thing of worth that you get out of it, is the 2day ad lib
intake of high/low gi styff is that a high protein low GI diet will cuase a
spontaneous reduction in calories compared to a high GI low protien...

weeee

what fun

Whats the reference for the drink carbs all at once vs drip feeding it in,
cos I cant be bothered hunting on pubmed... its sorta similar to borries
(sp?) second protien speed study where they drip fed whey to 'simulate'
casein.

---
Aaron

Aaron wrote:

"Lyle McDonald" wrote in message

in terms of bunk studies, I have one GI study that showed the low GI
maintained RMR better than the high GI diet, and produced more weight
loss
(however not significantly more) but the fuktards made these relatively
obese (~100kg) people eat a 15% protein High GI to a 25% low GI, which
resulted in 0.4 vs 0.8g/kg protein intake!
****tards, you would 'hope' that somebody as big in the GI world like
Ludwig
would actually ****ing pick that to start with.

that was the first one Omega cited, that I mentioned had 4 independent
variables

you mean I was meant to read thru that pile of papers for a mention of it?

See, this is what happens when you found a country with nothign but
criminals and let them breed: you end up with a bunch of lazy ass ****s
like you.

about the only thing of worth that you get out of it, is the 2day ad lib
intake of high/low gi styff is that a high protein low GI diet will cuase a
spontaneous reduction in calories compared to a high GI low protien...

weeee

yeah and no **** on that.
Reminds me of this brilliant conclusion I read ina review a while back

"While the optimal diet for obesity is not know, a diet based around
sufficient amounts of protein, unrefined carbohydrates and healthy fats
would seem to be ideal."

Yeah, well no ****. Three decades and 30 billion dollars worth of
nutrition research and this is the best they can do?


what fun

Whats the reference for the drink carbs all at once vs drip feeding it in,
cos I cant be bothered hunting on pubmed... its sorta similar to borries
(sp?) second protien speed study where they drip fed whey to 'simulate'
casein.

still don't have it handy. It was one of those things that I saw
referenced in a review paper (probably on insulin sensitivity) and never
bothered to actually look up.

Lyle

Elzinator wrote:

"OmegaZero2003" wrote in message ws.com...
"Lyle McDonald" wrote in message
...
After all of these studies and 30+ years of research, the basic
conclusion is that all diets work, as long as people follow them. And
unless they are totally retarded, they all generate about teh same
weight/fat loss (and for the majority of dieters, small differences in
LBM retention are an irrelevancy; that only matters for athletes and
bodybuilders and tha'ts a tiny percentage of the dieting public).

Meaning this: pick the dietary approach (which is going to depend on
personal food preferences, activity, etc) that YOU CAN BEST STICK TO. I
have been saying this for years.

Oh I agree with this 100%.

But it is interesting to look at the mechanisms and theories.

Dude, mechanisms rool. (Lyle only likes endpoints

I am interested in mechanisms as long as they lead to applicable endpoints.
Most of the molecular/gene level stuff does not.

Lyle

On Thu, 18 Dec 2003 21:42:20 -0600, Lyle McDonald
wrote:

yeah and no **** on that.
Reminds me of this brilliant conclusion I read ina review a while back

"While the optimal diet for obesity is not know, a diet based around
sufficient amounts of protein, unrefined carbohydrates and healthy fats
would seem to be ideal."

Yeah, well no ****. Three decades and 30 billion dollars worth of
nutrition research and this is the best they can do?

Well what do you expect? That's a bare bones minimum of three
independent variables. How you gonna design a non-bogus experiment
when you've got that to contend with?

---
Proton Soup

"If I drink water I will have to go to the bathroom and
how can I use the bathroom when my people are in bondage?"
-Saddam Hussein

Lyle McDonald wrote:

still don't have it handy. It was one of those things that I saw
referenced in a review paper (probably on insulin sensitivity) and never
bothered to actually look up.

Amazingly, I managed to track it down on Pubmed.

Lyle

***
Diabetes. 1990 Jul;39(7):775-81.

Metabolic effects of reducing rate of glucose ingestion by single bolus versus
continuous sipping.

Jenkins DJ, Wolever TM, Ocana AM, Vuksan V, Cunnane SC, Jenkins M, Wong GS,
Singer W, Bloom SR, Blendis LM, et al.

Department of Nutritional Sciences, Faculty of Medicine, University of Toronto,
Ontario, Canada.

Modifying the rate of absorption has been proposed as a therapeutic
principle of
specific relevance to diabetes. To demonstrate clearly the metabolic benefits
that might result from reducing the rate of nutrient delivery, nine healthy
volunteers took 50 g glucose in 700 ml water on two occasions: over 5-10 min
(bolus) and at a constant rate over 3.5 h (sipping). Despite similar 4-h blood
glucose areas, large reductions were seen in serum insulin (54 +/- 10%,
P less
than 0.001) and C-peptide (47 +/- 12%, P less than 0.01) areas after sipping,
together with lower gastric inhibitory polypeptide and enteroglucagon
levels and
urinary catecholamine output. There was also prolonged suppression of plasma
glucagon, growth hormone, and free-fatty acid (FFA) levels after sipping,
whereas these levels rose 3-4 h after the glucose bolus. An intravenous glucose
tolerance test at 4 h demonstrated a 48 +/- 10% (P less than 0.01) more rapid
decline in blood glucose (Kg) after sipping than after the bolus. Furthermore,
FFA and total branched-chain amino acid levels as additional markers of insulin
action were lower over this period despite similar absolute levels of insulin
and C-peptide. These findings indicate that prolonging the rate of glucose
absorption enhances insulin economy and glucose disposal.

"Lyle McDonald" wrote in message
...
Aaron wrote:

"Lyle McDonald" wrote in message

in terms of bunk studies, I have one GI study that showed the low GI
maintained RMR better than the high GI diet, and produced more
weight
loss
(however not significantly more) but the fuktards made these
relatively
obese (~100kg) people eat a 15% protein High GI to a 25% low GI,
which
resulted in 0.4 vs 0.8g/kg protein intake!
****tards, you would 'hope' that somebody as big in the GI world
like
Ludwig
would actually ****ing pick that to start with.

that was the first one Omega cited, that I mentioned had 4 independent
variables

you mean I was meant to read thru that pile of papers for a mention of
it?

See, this is what happens when you found a country with nothign but
criminals and let them breed: you end up with a bunch of lazy ass ****s
like you.

no, NZ is based on immigrants, aussie is based upon criminals

texas is based upon cows innit?

about the only thing of worth that you get out of it, is the 2day ad lib
intake of high/low gi styff is that a high protein low GI diet will
cuase a
spontaneous reduction in calories compared to a high GI low protien...

weeee

yeah and no **** on that.
Reminds me of this brilliant conclusion I read ina review a while back

"While the optimal diet for obesity is not know, a diet based around
sufficient amounts of protein, unrefined carbohydrates and healthy fats
would seem to be ideal."

Yeah, well no ****. Three decades and 30 billion dollars worth of
nutrition research and this is the best they can do?

yip

by the time they have spent 25billion on buying some computerds, downloading
porn and the likes, there aint much left over for studies of any value (and
that research in the states costs 10x that it costs here...)


what fun

Whats the reference for the drink carbs all at once vs drip feeding it
in,
cos I cant be bothered hunting on pubmed... its sorta similar to
borries
(sp?) second protien speed study where they drip fed whey to 'simulate'
casein.

still don't have it handy. It was one of those things that I saw
referenced in a review paper (probably on insulin sensitivity) and never
bothered to actually look up.

*******. Oh well, it will be a late nite so I may as well surf pubmed

----
Aaron

"Lyle McDonald" wrote in message
...
Lyle McDonald wrote:

still don't have it handy. It was one of those things that I saw
referenced in a review paper (probably on insulin sensitivity) and never
bothered to actually look up.

Amazingly, I managed to track it down on Pubmed.

Lyle

***
Diabetes. 1990 Jul;39(7):775-81.

Metabolic effects of reducing rate of glucose ingestion by single bolus
versus
continuous sipping.

Jenkins DJ, Wolever TM, Ocana AM, Vuksan V, Cunnane SC, Jenkins M, Wong
GS,
Singer W, Bloom SR, Blendis LM, et al.

Department of Nutritional Sciences, Faculty of Medicine, University of
Toronto,
Ontario, Canada.

Modifying the rate of absorption has been proposed as a therapeutic
principle of
specific relevance to diabetes. To demonstrate clearly the metabolic
benefits
that might result from reducing the rate of nutrient delivery, nine
healthy
volunteers took 50 g glucose in 700 ml water on two occasions: over 5-10
min
(bolus) and at a constant rate over 3.5 h (sipping). Despite similar 4-h
blood
glucose areas, large reductions were seen in serum insulin (54 +/- 10%,
P less
than 0.001) and C-peptide (47 +/- 12%, P less than 0.01) areas after
sipping,
together with lower gastric inhibitory polypeptide and enteroglucagon
levels and
urinary catecholamine output. There was also prolonged suppression of
plasma
glucagon, growth hormone, and free-fatty acid (FFA) levels after sipping,
whereas these levels rose 3-4 h after the glucose bolus. An intravenous
glucose
tolerance test at 4 h demonstrated a 48 +/- 10% (P less than 0.01) more
rapid
decline in blood glucose (Kg) after sipping than after the bolus.
Furthermore,
FFA and total branched-chain amino acid levels as additional markers of
insulin
action were lower over this period despite similar absolute levels of
insulin
and C-peptide. These findings indicate that prolonging the rate of glucose
absorption enhances insulin economy and glucose disposal.


it was done in canada

that rules it out to start with...

"Elzinator" wrote in message
om...
Lyle McDonald wrote in message
.. .
OmegaZero2003 wrote:

Meaning this: pick the dietary approach (which is going to depend on
personal food preferences, activity, etc) that YOU CAN BEST STICK
TO. I
have been saying this for years.

Oh I agree with this 100%.

But it is interesting to look at the mechanisms and theories.

No doubt. But the more you look, the more you find it comes down, more
or less to the above.

I mean, fundamentally, weight loss is a function of

eat less (or eat differently so that you automatically eat less)
exercise (or not)
repeat
forever

most of the mechanistic stuff has to do with determining the details of
those 4 steps.

Which has more relavence for pathophysiologies and age-related issues
than the general populace. I agree that mechanistic knowledge is not
as important for the general populace, and, as you mention later in
your post, it is easy to attain weight loss (and maintain it) by
adjusting the two components: diet and exericse. However, age-related
changes in gene expression and metabolism alter the effects of both
diet and exericse. Pathophysiologies are often associated with genetic
mutations and resulting congenital or acquired phenotypes in which the
effects of diet and exercise may be dissimilar with normal
individuals.

After the symposium that I attended today on lipodystrophy, the
multifactorial nature of these pathophysiologies was very apparent;
not one treatment or therapy will result in equal response in all
individuals.

This is very similar to the issues facing cancer researchers.

Three very different mechanisms/theories using separate processes all
interacting to produce the endpoint.


This is why pursuing mechanistic studies in diet and exercise and
weight regulation is imperative. And why I find it so fascinating and
challenging.

What to eat and does it even matter what the composition of the diet is?
Given a few requirements (which I stated previously), the differences
are minor approaching 4/5th of **** all (they certainly aren't that
important for your average obese individual; a few pounds either way may
be huge for an athlete or bodybuilder). So all diets basically work as
long as you reduce calories. One issue is whether or not the diet is
going to be strictly controlled or you're allowing ad-lib intakes. If
the latter, you need to pick a diet that spontaneously makes folks
reduce food intake. Both low-fat and low-carb approaches have studies
to back them (reducing fat tends to reduce calories in the short-term
because of the high energy density, in that carbs typically make up 50%
or more of the daily diet, reducing/removing them tends to reduce
calories as well). High-fiber is key and protein is turning out to be
the big player as it decreases hunger/appetite the most. A high fiber,
high protein, low GI carb, and low to moderate fat diet would probably
lead to the greatest spontaneous reduction in caloric intake.

Exercise. What type, how much, how often? Studies are showing that
exercise has a bigger role in preventing weight regain (but it takes a
lot) than in causing weight or fat loss per se. Of course, most
exercise studies use pretty paltry intervenions. Of course, the average
person won't do/can't handle intense exercise, at least not at first.

Exercise also plays a large role in other traits, such as
cardioprotection and aiding the immune system. Reduction of diabetes
and CVD risk, ETC. What we don't know is what exercise prescription to
assign for each of these, or all for that matter. I suspect that it is
a combinatin of resistance and aerobic training. Each confers benefits
the other may not.


On and on it goes. One of these days I'll write a real diet book and
adress all of the above issues in the anal retentive detail I'm known
for.

Uh, yeah....

Allow me to paste in the introduction of a very recent review authored
by one of my favorite reserchers in molecular/cellular biology of
exericse, Dr. Frank Booth (who up until a few years ago, was in
Houston) and a co-author:

"On a superficial level, many would consider it intuitive to
make the statement that exercise in general is a good thing.
However, when the layers of the exercise onion are peeled, the
answer to the question of how exactly at the mechanistic level
is exercise beneficial for human health does not seem that
obvious to the general scientific community, although there is
extensive literature at a descriptive level documenting the
precise benefits of exercise for many aspects of human health.

If, peeling those layers even further, we then consider the
notion that gene selection during the eons of human evolution
was likely influenced by physical activity to support human
health, we would suspect the reaction would be one of great
skepticism.

Hmmm - the selection-for mechanisms have been theorized to include a way to
reward both curiosity and activity given the nature of the nature most of
homo sapiens' ancestors faced. Even the theory of neuronal group selection
is based on (appropriate) activation upon perturbation (sensory modalities,
motor skills etc.)


.. Therefore, the major objectives of this review are
1) to amalgamate the presently known information, parts of which have
been separately developed from previous investigators
(5, 12-16, 21, 39, 40), that support the above notion of
an evolutionarily derived need for undertaking regular physical
activity to maintain normality of specific metabolic functions,
and 2) to present a hypothesis that the combination of continuous
food abundance and a sedentary lifestyle results in metabolic
derangements because of the stalling of the evolutionarily

Deranged - now that's somethin I can identify with...

programmed metabolic cycles that were selected to support
cycles of feast and famine and of physical activity and
rest.

We contend that achieving such an understanding of
potential gene selection will provide further avenues for fruitful
research into dissecting the cellular and molecular mechanisms
of physical inactivity-mediated chronic diseases."

Very well put (and a very excellent review).

"Aaron" hunt354 at hotmail dot com wrote in message
...

"Lyle McDonald" wrote in message
...
Aaron wrote:

"Lyle McDonald" wrote in message
...
OmegaZero2003 wrote:

"Lyle McDonald" wrote in message
...
OmegaZero2003 wrote:
\
Low carb need not be a form of or mean calorie restriction.
The
calories
decreased via the low-carb approach can be added back in by
taking
some
additional EFAs like fish/flax oils, to very good effect.

Think nutrient partitioning- taking advantage of what the body
does
with
certain types of nutrients (e.g., leptin- and
insulin-modulated
partitioning) and, as an extension, timing the intake of those
different
nutrients to best work with the body's metabolistic parameters
governing
their - well - metabolism!

So are you suggesting that, via nutrient partitioning, a
maintenance
calories (i.e. not restricted in calories) low-carb diet will
somehow
cause something to occur wrt: body fat?

Well - I read your previous posts on the matter, along with about
30
studies
(some posted in another thread), that nutrient partitioning (via
differntial
response of metabolic parameters such as insulin and leptin etc.)
will
cause
loss of bf and maint of lean body mass.

Only when you are looking at increasing protein from subadequate to
adequate levels in fat people. Of course, since protein is less
energetically efficient (in terms of providing ATP to the body),
switching out carbs/fat to protein results in a technically lower
calorie diet.

A little over 50% of the aminos from dietary protein are available
for
ATP production so for every 200 calories of carbs you replace with
200
calories of protein, you're getting ~100 calories less dietary
energy.
So at 2000 ostensible calories, a higher protein diet is technically
NOT
providing 2000 calories of useable energy.

The weight-loss issue is not what I am aiming at here, but bf loss
vs
lean
muscle maint.

No ****.

Lyle

in terms of bunk studies, I have one GI study that showed the low GI
maintained RMR better than the high GI diet, and produced more weight
loss
(however not significantly more) but the fuktards made these
relatively
obese (~100kg) people eat a 15% protein High GI to a 25% low GI, which
resulted in 0.4 vs 0.8g/kg protein intake!
****tards, you would 'hope' that somebody as big in the GI world like
Ludwig
would actually ****ing pick that to start with.

that was the first one Omega cited, that I mentioned had 4 independent
variables


you mean I was meant to read thru that pile of papers for a mention of it?

it had varying GI, varying amounts of protein (about double in the low
GI group), varying amounts of carbs and varying amounts of fats.

I have seen both Berardi and Kreider hang 'A calorie is not a calorie'
arguments on that study (arguing that low GI is protein sparing in
Krieder's case).

A ****ty study and ****tier conclusions drawn from it.

Lyle

about the only thing of worth that you get out of it, is the 2day ad lib
intake of high/low gi styff is that a high protein low GI diet will cuase
a
spontaneous reduction in calories compared to a high GI low protien...

But not for those with adequate protein to start with! One does not need a
reduction in calories to change bodycomp.


weeee

what fun

Whats the reference for the drink carbs all at once vs drip feeding it in,
cos I cant be bothered hunting on pubmed... its sorta similar to borries
(sp?) second protien speed study where they drip fed whey to 'simulate'
casein.

---
Aaron

"OmegaZero2003" wrote in message
s.com...

"Aaron" hunt354 at hotmail dot com wrote in message
...

"Lyle McDonald" wrote in message
...
Aaron wrote:

"Lyle McDonald" wrote in message
...
OmegaZero2003 wrote:

"Lyle McDonald" wrote in
message
...
OmegaZero2003 wrote:
\
Low carb need not be a form of or mean calorie restriction.
The
calories
decreased via the low-carb approach can be added back in by
taking
some
additional EFAs like fish/flax oils, to very good effect.

Think nutrient partitioning- taking advantage of what the
body
does
with
certain types of nutrients (e.g., leptin- and
insulin-modulated
partitioning) and, as an extension, timing the intake of
those
different
nutrients to best work with the body's metabolistic
parameters
governing
their - well - metabolism!

So are you suggesting that, via nutrient partitioning, a
maintenance
calories (i.e. not restricted in calories) low-carb diet will
somehow
cause something to occur wrt: body fat?

Well - I read your previous posts on the matter, along with
about
30
studies
(some posted in another thread), that nutrient partitioning (via
differntial

response of metabolic parameters such as insulin and leptin
etc.)
will
cause
loss of bf and maint of lean body mass.

Only when you are looking at increasing protein from subadequate
to
adequate levels in fat people. Of course, since protein is less
energetically efficient (in terms of providing ATP to the body),
switching out carbs/fat to protein results in a technically lower
calorie diet.

A little over 50% of the aminos from dietary protein are available
for
ATP production so for every 200 calories of carbs you replace with
200
calories of protein, you're getting ~100 calories less dietary
energy.
So at 2000 ostensible calories, a higher protein diet is
technically
NOT
providing 2000 calories of useable energy.

The weight-loss issue is not what I am aiming at here, but bf
loss
vs
lean
muscle maint.

No ****.

Lyle

in terms of bunk studies, I have one GI study that showed the low GI
maintained RMR better than the high GI diet, and produced more
weight
loss
(however not significantly more) but the fuktards made these
relatively
obese (~100kg) people eat a 15% protein High GI to a 25% low GI,
which
resulted in 0.4 vs 0.8g/kg protein intake!
****tards, you would 'hope' that somebody as big in the GI world
like
Ludwig
would actually ****ing pick that to start with.

that was the first one Omega cited, that I mentioned had 4 independent
variables


you mean I was meant to read thru that pile of papers for a mention of
it?

it had varying GI, varying amounts of protein (about double in the low
GI group), varying amounts of carbs and varying amounts of fats.

I have seen both Berardi and Kreider hang 'A calorie is not a calorie'
arguments on that study (arguing that low GI is protein sparing in
Krieder's case).

A ****ty study and ****tier conclusions drawn from it.

Lyle

about the only thing of worth that you get out of it, is the 2day ad lib
intake of high/low gi styff is that a high protein low GI diet will
cuase
a
spontaneous reduction in calories compared to a high GI low protien...

But not for those with adequate protein to start with! One does not need a
reduction in calories to change bodycomp.

no, but it will happen slower, if not at all. And not in sedentary subjects
to any great extent.




weeee

what fun

Whats the reference for the drink carbs all at once vs drip feeding it
in,
cos I cant be bothered hunting on pubmed... its sorta similar to
borries
(sp?) second protien speed study where they drip fed whey to 'simulate'
casein.

---
Aaron