Dr. Atkins' Dietetic Revolution: Mu Critique?

1. Very fat people die earlier than people of normal weight because
hypertension, diabetes and coronary disease are more frequent among the
markedly obese. Most obese subjects, however, are only slightly overweight
and their mortality is not significantly elevated. Reasons for dieting are
more often psychological than somatic.

2. Reducing diets are ineffective because the obese rarely follow them.
Total fasting and intestinal bypass may provide better results, but are
more dangerous.

3. Atkins' diet eliminates carbohydrates from food without restricting
protein and fat intake. Deprived of carbohydrates, the body uses fat for
fuel. A small part of metabolized fat is eliminated in the urine as ketone
bodies, and this is why such diets are called "ketogenic". They have been
known at least since 1863.

4. Caloric loss due to ketonuria does not exceed 100 Cal/day in the
non-diabetic. It is maximal during total fasting and cannot be increased by
a ketogenic diet.

5. In the short run, such diets produce rapid weight loss due to polyuria.
On the other hand, refeeding carbohydrates causes water retention and
weight gain.

6. The diet decreases appetite: some patients eat less without feeling
severe hunger and without measuring their food intake.

7. Orthostatic hypotension, fatigue, and nausea are frequent, despite what
Dr. ATKINS claims.

8. The diet increases plasma cholesterol and uric acid. It may be dangerous
in diabetes (anorexia, acidosis) and in heart or kidney failure
(hypokalemia).

9. The diet, though far from good, is better than the book. ATKINS'
theories are at best half-truths, and the results he claims lack
credibility. The obese subject's disappointment with traditional reducing
diets and the book's hard-sell style account for ATKINS' success.

MU wrote:
|| 1. Very fat people die earlier than people of normal weight because
|| hypertension, diabetes and coronary disease are more frequent among
|| the markedly obese.

|| Most obese subjects, however, are only slightly
|| overweight and their mortality is not significantly elevated.
|| Reasons for dieting are more often psychological than somatic.
||

What?


|| 2. Reducing diets are ineffective because the obese rarely follow
|| them. Total fasting and intestinal bypass may provide better
|| results, but are more dangerous.

So the 2pd is not a reducing diet?

||
|| 3. Atkins' diet eliminates carbohydrates from food without
|| restricting protein and fat intake. Deprived of carbohydrates, the
|| body uses fat for fuel. A small part of metabolized fat is
|| eliminated in the urine as ketone bodies, and this is why such diets
|| are called "ketogenic". They have been known at least since 1863.

So?

||
|| 4. Caloric loss due to ketonuria does not exceed 100 Cal/day in the
|| non-diabetic. It is maximal during total fasting and cannot be
|| increased by a ketogenic diet.

So?

||
|| 5. In the short run, such diets produce rapid weight loss due to
|| polyuria. On the other hand, refeeding carbohydrates causes water
|| retention and weight gain.

So?

||
|| 6. The diet decreases appetite: some patients eat less without
|| feeling severe hunger and without measuring their food intake.
||
|| 7. Orthostatic hypotension, fatigue, and nausea are frequent,
|| despite what Dr. ATKINS claims.

That sounds just like propaganda.

||
|| 8. The diet increases plasma cholesterol and uric acid. It may be
|| dangerous in diabetes (anorexia, acidosis) and in heart or kidney
|| failure (hypokalemia).

Really? Not according to my diabetic body.

||
|| 9. The diet, though far from good, is better than the book. ATKINS'
|| theories are at best half-truths, and the results he claims lack
|| credibility. The obese subject's disappointment with traditional
|| reducing diets and the book's hard-sell style account for ATKINS'
|| success.

You're such a moron, Mu.

MU wrote:

1. Very fat people die earlier than people of normal weight because
hypertension, diabetes and coronary disease are more frequent among the
markedly obese. Most obese subjects, however, are only slightly overweight
and their mortality is not significantly elevated. Reasons for dieting are
more often psychological than somatic.

There are many who develop metabolic syndrome (MetS) with just being
mild to moderately overweight. This number is growing and is now
estimated to be 40-60 million Americans at higher risk for
cardiovascular events.

2. Reducing diets are ineffective because the obese rarely follow them.

Ime, they are ineffective because they miss the boat by failing to
educate people to "watch *how much* they are eating" and instead have
people "watch what they are eating."

The "see food diet" simply does not work.

Total fasting and intestinal bypass may provide better results, but are
more dangerous.

Fasting is not sustainable. Bariatic surgery still fails when folks do
not show they can watch how much they are eating.

3. Atkins' diet eliminates carbohydrates from food without restricting
protein and fat intake. Deprived of carbohydrates, the body uses fat for
fuel.

The initially burns fat very efficiently until it runs out of body carbs
(glycogen).

A small part of metabolized fat is eliminated in the urine as ketone
bodies, and this is why such diets are called "ketogenic". They have been
known at least since 1863.

This starts happening when glycogen stores are used up.


4. Caloric loss due to ketonuria does not exceed 100 Cal/day in the
non-diabetic. It is maximal during total fasting and cannot be increased by
a ketogenic diet.

The ketonuria is comparable to what occurs during fasting. For this
reason, many will say that Atkin's simulates the appetite suppression
that occurs with prolonged fasting.


5. In the short run, such diets produce rapid weight loss due to polyuria.

There is a diuresis. Also, the glycogen stored up in liver and muscle
can weigh up to 10-15 lbs. This glycogen has a high water content (like
play dough) and is used up within a few days resulting in a rapid 10-15
lb weight loss.

On the other hand, refeeding carbohydrates causes water retention and
weight gain.

10-15 lbs of glycogen coming back (imagine expanding overcooked pasta).

6. The diet decreases appetite: some patients eat less without feeling
severe hunger and without measuring their food intake.

Ironically, better health leads to healthier (ie bigger) appetites.


7. Orthostatic hypotension, fatigue, and nausea are frequent, despite what
Dr. ATKINS claims.

8. The diet increases plasma cholesterol and uric acid. It may be dangerous
in diabetes (anorexia, acidosis) and in heart or kidney failure
(hypokalemia).

Hyperketonemia leading to higher rates of lipid peroxidation would be
the most pressing cardiovascular concern. When there is weight loss
with the Atkin's diet, cholesterol should still decrease though there
may be a higher amount of oxidized LDL which may lead to more
atherogenic potential. Hyperuricemia is a problem primarily for those
predisposed to gout.


9. The diet, though far from good, is better than the book. ATKINS'
theories are at best half-truths, and the results he claims lack
credibility. The obese subject's disappointment with traditional reducing
diets and the book's hard-sell style account for ATKINS' success.

The rapid 10-15 lb glycogen weight loss hooks a lot of people during
induction.


Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
http://www.heartmdphd.com/

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Hyperketonemia leading to higher rates of lipid peroxidation would be
the most pressing cardiovascular concern.

Is this claim of yours still based on single croatian study?

Or you have something new in this area?

Mirek

"Mirek Fídler" wrote:

Hyperketonemia leading to higher rates of lipid peroxidation would be
the most pressing cardiovascular concern.

Is this claim of yours still based on single croatian study?

The biochemistry of hyperketonemia causing higher rates of lipid
peroxidation (via increased production of reactive oxygen species or
ROS) has been confirmed multiple times by more than one independent
group.

For example (from Lousiana State University):

http://makeashorterlink.com/?J3A222DF9

Another example (from the University of Oklahoma):

http://makeashorterlink.com/?O1F261DF9

Other examples:

http://makeashorterlink.com/?J21323DF9

http://makeashorterlink.com/?M23321DF9

http://makeashorterlink.com/?Z25362DF9

http://makeashorterlink.com/?F26312DF9

http://makeashorterlink.com/?J17322DF9

Or you have something new in this area?

President Clinton's recent experience with low-carbing would be a new
development.


Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
http://www.heartmdphd.com/

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http://makeashorterlink.com/?L26062048

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Is this claim of yours still based on single croatian study?

The biochemistry of hyperketonemia causing higher rates of lipid
peroxidation (via increased production of reactive oxygen species or
ROS) has been confirmed multiple times by more than one independent
group.

Actually, I tend to agree with you about this topic, I was just curious if
there is something else to read about it...

In the end, in a very simplified way, if ketones are there to substitute
glucose (not quite correct, but let us say so), and we all know that high
glucose levels are dangerous, it seems to be logical that high ketone levels
are dangerous too.

Anyway, now the question is what level of ketones is dangerous and how much
carbs you need to avoid it... I guess that with more than 70g/day you will
hardly exceed 1mmol/dl... From what I know, some people are unable to pass
this limit even at "atkins induction" levels, as there is quite effective
insulin feedback mechanism... (which, surprisingly, seems to work well even
for TypeII diabetics - perhaps much slower absorbtion of fat is the cause).

In any case it seems very stupid to me to overeat fat just to get better
ketostick results...

President Clinton's recent experience with low-carbing would be a new
development.

Actually, IF Clinton's recent experience was caused by dietary
hyperketonemia, THEN he was NOT following his choosen plan (SB diet is
non-ketogenic).

Mirek

On Fri, 10 Dec 2004 17:20:34 +0100, Mirek Fídler wrote:

Is this claim of yours still based on single croatian study?

The biochemistry of hyperketonemia causing higher rates of lipid
peroxidation (via increased production of reactive oxygen species or
ROS) has been confirmed multiple times by more than one independent
group.

Actually, I tend to agree with you about this topic, I was just curious
if
there is something else to read about it...

In the end, in a very simplified way, if ketones are there to substitute
glucose (not quite correct, but let us say so), and we all know that
high
glucose levels are dangerous, it seems to be logical that high ketone
levels
are dangerous too.

No, it doesn't at all. While it may be true, just because glucose is bad
does not infer that ketones are bad.

Anyway, now the question is what level of ketones is dangerous and how
much
carbs you need to avoid it... I guess that with more than 70g/day you
will
hardly exceed 1mmol/dl... From what I know, some people are unable to
pass
this limit even at "atkins induction" levels, as there is quite effective
insulin feedback mechanism... (which, surprisingly, seems to work well
even
for TypeII diabetics - perhaps much slower absorbtion of fat is the
cause).

In any case it seems very stupid to me to overeat fat just to get better
ketostick results...

President Clinton's recent experience with low-carbing would be a new
development.

So, clogged arteries occur after only a few months of a diet? And not
because he's relatively old? (If there's one truth about clogged
arteries, it's the older you get, the more likely you are to have them.)

Actually, IF Clinton's recent experience was caused by dietary
hyperketonemia, THEN he was NOT following his choosen plan (SB diet is
non-ketogenic).

Mirek





--
Bob in CT

"Mirek Fídler" wrote:

Is this claim of yours still based on single croatian study?

The biochemistry of hyperketonemia causing higher rates of lipid
peroxidation (via increased production of reactive oxygen species or
ROS) has been confirmed multiple times by more than one independent
group.

Actually, I tend to agree with you about this topic, I was just curious if
there is something else to read about it...

In the end, in a very simplified way, if ketones are there to substitute
glucose (not quite correct, but let us say so), and we all know that high
glucose levels are dangerous, it seems to be logical that high ketone levels
are dangerous too.

We know that one of the ketones (acetone) is outright lethal if ingested
from the fingernail polish remover bottle.

Anyway, now the question is what level of ketones is dangerous and how much
carbs you need to avoid it... I guess that with more than 70g/day you will
hardly exceed 1mmol/dl... From what I know, some people are unable to pass
this limit even at "atkins induction" levels, as there is quite effective
insulin feedback mechanism... (which, surprisingly, seems to work well even
for TypeII diabetics - perhaps much slower absorbtion of fat is the cause).

In any case it seems very stupid to me to overeat fat just to get better
ketostick results...

There are people doing just that to suppress their hunger.

President Clinton's recent experience with low-carbing would be a new
development.

Actually, IF Clinton's recent experience was caused by dietary
hyperketonemia, THEN he was NOT following his choosen plan (SB diet is
non-ketogenic).

It is not clear that Clinton was doing anything more specific than
"low-carbing," which in his case probably was hamburgers with the buns
removed. This more likely than not brought about hyperketonemia.


Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
http://www.heartmdphd.com/

**
Who is the humblest person in the universe?
http://makeashorterlink.com/?L26062048

What is all this about?
http://makeashorterlink.com/?R20632B48

Is this spam?
http://makeashorterlink.com/?N69721867

"Dr. Andrew B. Chung, MD/PhD" wrote

The biochemistry of hyperketonemia causing higher rates of lipid
peroxidation (via increased production of reactive oxygen species or
ROS) has been confirmed multiple times by more than one independent
group.

For example (from Lousiana State University):

http://makeashorterlink.com/?J3A222DF9

Another example (from the University of Oklahoma):

http://makeashorterlink.com/?O1F261DF9

Other examples:

http://makeashorterlink.com/?J21323DF9

http://makeashorterlink.com/?M23321DF9

http://makeashorterlink.com/?Z25362DF9

http://makeashorterlink.com/?F26312DF9

http://makeashorterlink.com/?J17322DF9


These are interesting studies, and I appreciate the effort you've gone to in
providing cites, but it should be noted that they are ALL specific to Type I
diabetics and in vitro studies, and demonstrate associative relationships
between specific ketone bodies, not causative. This leads me to a couple of
concerns.

First, what is going on biochemical in a Type I diabetic with significantly
elevated ketone levels is significantly different from a non-insulin
dependent diabetic, or especially a relatively healthy person who has
induced ketone production through dietary means. Blood glucose levels, blood
lipid levels, and doubtless many other factors will be quite different.
Until these studies are repeated on non-insulin dependent diabetics and
non-diabetics, conclusions drawn re effects of ketones on lipids should be
considered suspect at best.

Secondly, associations do not prove causation. In short, these studies,
while interesting and certainly pertinent for Type I diabetics, don't serve
for much more than an indication that similar studies need to be carried out
on non-diabetic subjects.

Being cautious, I'd say that it is probably a good idea to keep your carb
intake as high as is compatible with weight loss, but I already believe that
anyhow and it's part of the Atkins program to do that. Low-starch vegetables
and low-sugar fruits are full of antioxidants of various kinds, and the
Atkins program encourages us to load up on these, rather than grain
products, sugars, and other relatively "empty calorie" carb sources . Atkins
has always recommended taking supplemental antioxidant nutrients, too, which
would tend to mitigate effects of elevated ketone levels, if indeed there
are such effects in non-TI diabetics. (These studies do *not* demonstrate
such).

HG

Hannah Gruen wrote:

"Dr. Andrew B. Chung, MD/PhD" wrote

The biochemistry of hyperketonemia causing higher rates of lipid
peroxidation (via increased production of reactive oxygen species or
ROS) has been confirmed multiple times by more than one independent
group.

For example (from Lousiana State University):

http://makeashorterlink.com/?J3A222DF9

Another example (from the University of Oklahoma):

http://makeashorterlink.com/?O1F261DF9

Other examples:

http://makeashorterlink.com/?J21323DF9

http://makeashorterlink.com/?M23321DF9

http://makeashorterlink.com/?Z25362DF9

http://makeashorterlink.com/?F26312DF9

http://makeashorterlink.com/?J17322DF9


These are interesting studies, and I appreciate the effort you've gone to in
providing cites,

You are welcome.

but it should be noted that they are ALL specific to Type I
diabetics and in vitro studies,

Actually they are a mix of in vivo and in vitro studies.

and demonstrate associative relationships
between specific ketone bodies, not causative.

Actually, the in vitro parts of some of these studies provide data that
suggest causation.

This leads me to a couple of
concerns.

First, what is going on biochemical in a Type I diabetic with significantly
elevated ketone levels is significantly different from a non-insulin
dependent diabetic, or especially a relatively healthy person who has
induced ketone production through dietary means. Blood glucose levels, blood
lipid levels, and doubtless many other factors will be quite different.

Actually, for the in vitro studies, the main difference between Type I
and Type II is the insulin concentration. The Type I condition would be
low insulin. The Type II would be high. Because physiologically normal
insulin levels were used in the in vitro studies (necessary for cell
culture), the data is actually as applicable to Type IIs as to Type Is.
Indeed, there is much gathering evidence that insulin is pro-atherogenic
so that the Type II condition of *more* insulin may very well increase
lipid peroxidation.


Until these studies are repeated on non-insulin dependent diabetics and
non-diabetics, conclusions drawn re effects of ketones on lipids should be
considered suspect at best.

It remains a concern that hyperketonemia will cause vascular harm.


Secondly, associations do not prove causation.

However, in vitro studies do provide data that suggest causation.

In short, these studies,
while interesting and certainly pertinent for Type I diabetics, don't serve
for much more than an indication that similar studies need to be carried out
on non-diabetic subjects.

See above.

Being cautious, I'd say that it is probably a good idea to keep your carb
intake as high as is compatible with weight loss, but I already believe that
anyhow and it's part of the Atkins program to do that. Low-starch vegetables
and low-sugar fruits are full of antioxidants of various kinds, and the
Atkins program encourages us to load up on these, rather than grain
products, sugars, and other relatively "empty calorie" carb sources . Atkins
has always recommended taking supplemental antioxidant nutrients, too, which
would tend to mitigate effects of elevated ketone levels, if indeed there
are such effects in non-TI diabetics. (These studies do *not* demonstrate
such).

HG

The concern remains.



Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
http://www.heartmdphd.com/

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