Very low fat versus very low carb diets
runnswim@aol.com (Larry Weisenthal)
Care.
http://www.patientcareonline.com/patcare/article/articleDetail.jsp?id=197815#
- Larry W
jt
<runn...@aol.com> wrote:
I like how 30% calories from fat is considered low fat in these
studies? I Believe the USDA recommends no more than 30% calories come
from fat.
I agree with the articles findings as I do not consume more than 10%
of calories from fat and can I really don't have to watch calories at
all. I am 6' and have weighed around 150 pounds for the last 18
years. I am always interested in new ideas stupid or not so I tried a
variation of the coconut mans diet of lots of butter, coconut, full
fat dairy and very little protein or carbs. In about 10 days I had
gained 12 pounds.
Rob
Very interesting but what happens to hair and skin under such tight
fat restrictions? Can one get an adequate supply of EFAs on a diet
consisting of 10% total fat? Also, I have a hard time believing that
the key is dietary fat reduction rather than total calories that is
responsible for fat loss. Wasn't one of the problems we always heard
about low-fat diets was that people thought they could eat all the
low-fat food items they wanted. Sure, they cut out a lot of fat but
they overate on low-fat foods thereby causing weight gain.
Rob
runnswim@aol.com (Larry Weisenthal)
fat restrictions? Can one get an adequate supply of EFAs on a diet
consisting of 10% total fat? Also, I have a hard time believing that
the key is dietary fat reduction rather than total calories that is
responsible for fat loss. Wasn't one of the problems we always heard
about low-fat diets was that people thought they could eat all the
low-fat food items they wanted. Sure, they cut out a lot of fat but
they overate on low-fat foods thereby causing weight gain.<<
I think that the take home message of the last 20 years of diet wars
and nutrition research is that there is no one size fits all diet plan.
Like everything else in health and medicine, it (diet) should be
individualized.
I haven't eaten red meat or other than non-fat dairy since 1971 and
I've been following a (10% cals as fat) Pritikin Diet since the early
1980s. I'm 6', 165 #, which are exactly where I was when I graduated
from HS in 1965. I've got a full head of hair and nice finger nails
without the dreaded vertical ridges made famous by Gittelfinger. My
lipids and other health markers are also just fine. I don't restrict
calories at all. Just eat what I want, but read labels and hassle
waiters to make sure that gratuitous butter and/or cream and/or cheese
doesn't find its way into what I (carefully) order. So it works for
me.
On the other hand, I got into an argument with this guy who calls
himself "The Omnivore" and is a proponent of an Atkins-like approach.
He says that he tried Pritikin and it almost killed him. He says that
he does great on Atkins. I don't disbelieve him. He was conscientious
about trying things, and he found out what worked for him.
The nice thing is that we certainly have an abundance of choices.
There is literally a diet for everyone. I personally don't make the
claim that an ultra low fat diet is right for everyone, but neither do
I like it when people claim that carbohydrates are toxic, when I know
that to be nonsense, at least from the point of view of my own anatomy,
physiology, and biochemistry.
- larry w
Enrico C
<news:jqnso1570e6g5685f...@4ax.com> on sci.med.nutrition
:
Speaking of USDA recommendations, here's some.
In short, they say no more than 35 percent, no less than 20.
QUOTE "Dietary Guidelines for Americans 2005"
[...]
Fats
OVERVIEW
Fats and oils are part of a healthful diet,but the type of
fat makes a difference to heart health,and the total
amount of fat consumed is also important. High intake of
saturated fats,transfats,and cholesterol increases the risk
of unhealthy blood lipid levels,which,in turn,may increase
the risk of coronary heart disease. A high intake of fat
(greater than 35 percent of calories) generally increases
saturated fat intake and makes it more difficult to avoid
consuming excess calories. A low intake of fats and oils
(less than 20 percent of calories) increases the risk of inad-
equate intakes of vitamin E and of essential fatty acids and
may contribute to unfavorable changes in high-density
lipoprotein (HDL) blood cholesterol and triglycerides.
[...]
KEY RECOMMENDATIONS
* Consume less than 10 percent of calories from
saturated fatty acids and less than 300 mg/day
of cholesterol, and keep trans fatty acid consumption
as low as possible.
* Keep total fat intake between 20 to 35 percent of calo-
ries, with most fats coming from sources of
polyunsaturated and monounsaturated fatty acids,
such as fish, nuts, and vegetable oils.
* When selecting and preparing meat, poultry, dry beans,
and milk or milk products, make choices that are lean,
low-fat, or fat-free.
* Limit intake of fats and oils high in saturated and/or
trans fatty acids, and choose products low in such
fats and oils.
Key Recommendations for Specific Population Groups
* Children and adolescents. Keep total fat intake
between 30 to 35 percent of calories for children 2 to
3 years of age and between 25 to 35 percent of calo-
ries for children and adolescents 4 to 18 years of age,
with most fats coming from sources of polyunsatu-
rated and monounsaturated fatty acids, such as fish,
nuts, and vegetable oils.
[...]
UNQUOTE
TC
Carbs toxic? I've never heard anyone make that statement. Especially
among low carbers.
Fresh whole food carbs are the absolute bedrock fundamental basis of
good health. As well as good healthy animal fats and proteins from good
healthy well-raised animals.
On the other hand let's look at High Fructose Corn Syrup, refined wheat
flour and sugar.
Can you equivocally say that these three highly processed un-natural
carbs are not toxic, even to some minor degree?
TC
Pizzza Girl
"jt" <nob...@anywhere.com> wrote in message
news:jqnso1570e6g5685f...@4ax.com...
> gained 12 pounds. .
runnswim@aol.com (Larry Weisenthal)
flour and sugar.
Can you equivocally say that these three highly processed un-natural
carbs are not toxic, even to some minor degree? <<
Good grief. This is precisely the sort of talk that sets me off.
At the time Pritikin wrote his books in the late 70s/early 80s, no one
but no one was talking about glycemic index and stuff like that. The
thing people focus on is the 10% calories as fat. Even Ornish did it.
Ornish basically ripped off Pritikin and never gave Pritikin any
credit. But Ornish didn't distinguish between what we'd now call
"good" carbs and "bad" carbs, the way that Pritikin did from the start.
Pritikin (working, as he did, in the pre-glycemic index era) didn't
know about glycemic index, but his diet consisted of veggies, fruits,
and unrefined cereal grains. The one thing hyper-anti-carb purists
would cluck cluck about was the fact that Pritikin said that things
like potatoes and carrots and what all (ostensibly high glycemic foods)
were just fine. But he mostly got it right.
Now, having said that, let's agree that sugar and high fructose corn
syrup are to be avoided. That's what Pritikin said. He suggested the
use of frozen concentrated natural apple juice, in small quantities, as
a sweetener, if something like that was required. I don't put
sweeteners in anything.
But I have no problem eating baked or mashed potatoes, or popcorn, or
chewy white flour bagels, or al dente pasta, or chewy Italian bread.
I'll even have make a supper out of a mixed salad, couple of baked
potatoes, and some broccoli or spinach, along with a big glass of
non-fat milk. Then a nightly late night snack of unsweetened mixed
berries, mainly because I like them and only secondarily for the remote
chance that the anti-oxidants might be of tangible benefit.
No, I don't think that any of the above are "toxic," even to a minor
degree....for me. I presume that I'm descended from people who ate a
lot of grains and potatoes and didn't have a problem with it. I'm half
Finnish and I don't have a hint of lactose intolerance, so I can drink
a quart of non fat milk per day, if I like. And I have the genetics to
thrive on it.
Other people probably would have problems with my diet. So I am not
out to get everyone to eat the way I do.
What people should do is to monitor their weight, and lipids, and blood
pressure, and bowel movements, and whatever else concerns them and find
some sort of diet that consists of foods they like to eat and which
keeps their various health related parameters where they want them to
be.
- Larry W
TC
runnswim@aol.com (Larry Weisenthal)
with the theoretical arguments. However, there is a great saying in my
profession (cancer medicine): "Many a beautiful theory has been ruined
by an ugly fact."
Let me preface the following by again saying that I have no interest in
fighting "Diet Wars" or in maintaining that any one form of diet is
better than any other form of diet for everyone. There is no such
thing as one size fits all medicine, and that goes for diet as well as
for anything else.
The "fact" that I'd like to refer to is this: When you take people
with Type II diabetes (those seeming most at risk for the deleterious
effects of carbohydrates) and put them on a Pritikin-type diet plus
sensible moderate exercise, they do very well: lipids fall, serum
glucose and serum insulin fall, Blood pressure falls, etc. Now, people
may argue that this sort of diet would not work in a type II diabetic
who wasn't willing to continue with the exercise plan. Perhaps so.
Maybe the reason that my diet has worked so well for me for such a long
time (less strict Pritikin since 1971, fairly strict Pritikin, but
"cheating" by eating white flour bagels - plain or with non-fat cream
cheese," chewy Italian bread (mostly dry), and regular al dente pasta -
since 1981) is that I've always gotten regular exercise (hence my long
standing AOL "handle"). So a high carbohydrate, ultra low fat diet
works in people who are willing to put in the effort to do the sort of
exercise that absolutely every health authority recommends. Maybe it
doesn't work for couch potatoes. I wouldn't know. But that's my
point. Diets, as in everything else in life, should be individualized.
If it works, keep doing it. If it does't work, try something else
until you find something which does work.
Common sense.
- Larry W
runnswim@aol.com (Larry Weisenthal)
absolutely not true. <<
Good grief. You are arguing against a whole lot of published, peer
reviewed research.
I really didn't want to end up fighting diet wars, but, if you insist,
I'll do it. No time now (at work) but I'll get back to this.
What I really, really, really hate is when someone says look, I tried
this and it didn't work, so that means that this is the way that it is.
The clinical trial with an "N" of 1 !
But let's look at the literature, shall we?
More later.
- Larry W
runnswim@aol.com (Larry Weisenthal)
your biases.<<
Susan,
Why don't you give me the chance to present my side of the debate
first, as I said that I'd do after work tonight or perhaps tomorrow?
After I have done so, then you can provide counter-arguments and/or
present your own data/published studies/whatever. And then I can
comment on those, if I wish; or perhaps I'll agree with you. Who can
say? After we are finished, then you can conclude if I am biased or
objective, OK?
- Larry W
TC
runn...@aol.com (Larry Weisenthal) wrote:
> >>As a type 2 diabetic, and former Ornish dieter, I can say that's
> absolutely not true. <<
>
> Good grief. You are arguing against a whole lot of published, peer
> reviewed research.
Nope. That is your failing.
>
> I really didn't want to end up fighting diet wars, but, if you insist,
> I'll do it. No time now (at work) but I'll get back to this.
>
> What I really, really, really hate is when someone says look, I tried
> this and it didn't work, so that means that this is the way that it is.
If you really hate it why do you insist that your experience is the end
all and be all on diet? That is so oxymoronish, with the emphasis on
moron.
>
> The clinical trial with an "N" of 1 !
>
> But let's look at the literature, shall we?
>
> More later.
>
> - Larry W
I suggest that you take some time to review ALL the literature and not
just what matches your opinion.
Pritikin and Ornish are guilty of doing their own research to further
their own diets. I suggest you read anything that is not done by these
two biased profiteering greedy bastards.
TC
runnswim@aol.com (Larry Weisenthal)
all and be all on diet? That is so oxymoronish, with the emphasis on
moron. <<
Will you please go back and read what I wrote and not what you claim I
wrote. I was very careful to state that what works for me works for me
and what works for someone else may be different from what works for
me.
And I ask you for the same courtesy currently being extended to me by
Susan. That you give me the chance to state my case, and then you'll
have the chance to rebut this case, and then we can either go back and
forth or reach some common understanding or whatever. After we are
finished, you are then free to pronounce me biased (Susan's word) or a
moron (your word). But at least give me a chance, OK?
- Larry W
TC
You said that you hate it when people use their own personal diet
anecdotes to declare that it is the way things are, and you also went
on at length about your personal experience with the Pritikin diet.
Which is it? Are anecdotes worthy of your hatred or is your anecdote
valid proof?
TC
jt
>I suggest that you take some time to review ALL the literature and not
>just what matches your opinion.
>
Of course anything not matching your opinion is biased or paid for by
big corporations.
runnswim@aol.com (Larry Weisenthal)
The anecdotes were being used for two different things. I used an
anecdote to buttress my claim that, despite currently conventional
wisdom, high carbohydrate diets are not toxic for everyone and may even
be helpful for certain people (in this case me). I was very careful to
emphasize that my own, personal experience may not be broadly
generalizable, and I offered my opinion that my own unique genetics may
make such a diet work for me. Even Barry Sears, in his original Zone
Diet book (trashing the ultra low fat approach) said that (based on
what, he didn't say) about 25% of people seem to do OK on such diets.
I'm not even arguing for a percentage (what is the "lowest common
denominator" diet which works of the most people). I was just arguing
that the number was certainly above ZERO, based on my own described
anecdotal experience.
In the other situation, the discusser made the blanket statement that
high carb diets were unsuitable for Type II diabetics, based on her own
anecdotal experience. I opined that I hated when people did this (used
their own personal experience to generalize to the whole world).
More later...
Doug Freese
"TC" <tund...@hotmail.com> wrote in message
news:1134673844.4...@g14g2000cwa.googlegroups.com...
> I suggest that you take some time to review ALL the literature and not
> just what matches your opinion.
TC, why don't you tie you fingers in knot for a few and give Larry a
chance. Why don't you google Larry and SMN and you will find him
extremely balanced, rational and very informed about nutrition. To make
a statement such as above is your usual close minded approach to all
that disagree.
> Pritikin and Ornish are guilty of doing their own research to further
> their own diets. I suggest you read anything that is not done by these
> two biased profiteering greedy bastards.
And Atkins wasn't. Pot, kettle, black.
Larry, thanks for stopping in. Damn we need some rational nutrition
thought. You will find that no matter what study you show TC he will
claim they are on the take and thus you can't have a rational discussion
but please continue to post.
-DF
Doug Freese
"Susan" <neve...@nomail.com> wrote in message
news:40ego4F...@individual.net...
> I'm not holding out much hope, at this point, that you're capable of
> conducting a discussion with integrity.
And you claim TC has a short fuse? In don't see a difference between
the two of you other than gender.
-DF
TC
Doug Freese wrote:
> "TC" <tund...@hotmail.com> wrote in message
> news:1134673844.4...@g14g2000cwa.googlegroups.com...
> > I suggest that you take some time to review ALL the literature and not
> > just what matches your opinion.
>
> TC, why don't you tie you fingers in knot for a few and give Larry a
> chance. Why don't you google Larry and SMN and you will find him
> extremely balanced, rational and very informed about nutrition. To make
> a statement such as above is your usual close minded approach to all
> that disagree.
>
> > Pritikin and Ornish are guilty of doing their own research to further
> > their own diets. I suggest you read anything that is not done by these
> > two biased profiteering greedy bastards.
>
> And Atkins wasn't. Pot, kettle, black.
Actually no. Atkins financed independent researchers and let the chips
fall where they may. You can do that when you know that your idea is
based in science and the researchers are interested in science.
>
> Larry, thanks for stopping in. Damn we need some rational nutrition
> thought. You will find that no matter what study you show TC he will
> claim they are on the take and thus you can't have a rational discussion
> but please continue to post.
>
> -DF
I don't see how he can be too too rational when he rants against people
using anecdotes from their experiences to justify an alternative view
and he goes ahead and does exactly the same to support his views on
Pritikin.
But, hey, if he wants to throw in his two cents worth, nothing is
stopping him.
And anyone who sees pritikin as any kind of reasonable alternative
can't be too reliable, either.
TC
runnswim@aol.com (Larry Weisenthal)
biomedical literature. I agreed to hear you out, but if you continue
making untrue statements and assumptions, I'll just assume everything
you say is a pile of crap. <<
Look Susan, Read what I wrote and then read what you wrote. You made
the blanket statement that the Pritikin Diet was harmful to Type II
diabetics and you did not cite
"extensive review of the biomedical literature;" rather you cited your
own experience.
I made not one single untrue statement. I'm sorry it has taken me so
long to get back to this thread; I pulled an all-nighter at work
getting together a patent application which had to be express mailed
today. Finally put that one to bed, and you are now job number one.
Hope to get this back to you this evening (I'm on the west coast).
And can we PLEASE keep the personal attacks to a minimum. At worst,
we'll end up having an honest difference of opinion. You certainly
have no basis to go attacking my "integrity" for gosh sakes.
Back later.
Hell hath no fury like someone who's dietary views have been
challenged. It's worse than politics and religion.
- Larry W
runnswim@aol.com (Larry Weisenthal)
only in jest, but I understand why you were offended. I've had less
than 3 hours sleep in the past 38, and I'm getting a little punchy.
I'll try to stay more on task from here on in.
O.k.
First, a few general remarks.
As illustrated on this thread, few things provoke as much passion as
diet. Put Osama bin Laden and George Bush next to each other at a
lunch counter, and have both of them spontaneously order lamb and
baklava, and you'll have instant bonding, which transcends much of what
divides them. But put a low carb guy next to a low fat guy at the same
lunch counter, and they'll be mentally gagging over the sight of each
other's food. So we need to recognize this from the start. Virtually
nothing is a personally sacred to us as our food. Attack my food;
attack me. It's just what it is.
Second, nearly everyone (and this includes nutrition researchers) is
strongly biased by their affection for their own food.
Thirdly (and this was told to me by a prominent, well-published
nutrition Ph.D.), the world of nutrition research is populated by
people who generally couldn't make it in more competitive and rigorous
scientific disciplines. The people who tend to do nutrition studies
are, therefore, (1) strongly biased on a personal level to begin with
in ways that just don't apply to most scientific disciplines (who has a
lot of personal emotion wrapped up in p53 gene expression?) and are (2)
at the bottom of the biomedical research food chain.
Fourthly, there are few types of clinical trials harder to complete
than definitive diet and lifestyle interventional studies. For a whole
lot of obvious reasons, beginning with the fact that you are (1) trying
to change something as personal as someone's diet and (2) you are
trying to get inherently lazy 21st century people to commit to a
lifelong program of regular exercise. Also, it takes decades to
determine effects on longevity, which is the main gold standard which
really matters.
I'm not a believer in the lowest common denominator approach to
anything -- in this case, the effort to define the sort of diet which
works best for the average person, in a world where few people are
truly average. Susan has provided her experience; I've provided mine.
Both of us are telling the truth. I believe Susan when she says that
she suffered ill effects from the Ornish diet. The experience may well
have motivated her to show the passion expressed in her various
messages on this thread. Hopefully, Susan believes what I said about
my own experience with my own diet of more than 3 decades. Susan isn't
"average," and neither am I! Who would even want to be "average?"
Now, let's narrow things down a bit.
Here's what Susan and I have been arguing about. It all started when I
was glowing about my fondness for bagels, Italian bread, al dente white
flour pasta, and baked potatoes (all consumed in a background of a
10-15% calories as fat diet and regular, vigorous exercise). Susan
said that high carbohydrate diets were unhealthful for Type II
diabetics. I said that the Pritikin experience proved that a high
carbohydrate diet (of the type defined by Pritikin in the setting of a
regular exercise program) was beneficial for type II diabetics (I did
not qualify this by saying "most diabetics," but it was just a brief
exchange). At this point Susan developed a case of unwarranted
certitude, and her anger was compounded by a spat over who was more
eqregiously generalizing a personal anecdote. And then I tossed out my
gratuitous "Hell hath no fury" line, and we really are not getting
along.
Here's the point of contention: I assert that a Pritikin-type diet and
exercise program improves the health of many (but obviously not all)
Type II diabetics. Susan asserts that the medical and scientific
literature (of which she has an impressive command) proves otherwise.
Susan is giving me a chance to state my case. Then she'll offer
counter arguments.
My case will be stated in 3 parts:
1. Data supporting my assertions of the beneficial effect of the
Pritikin diet/exercise program for Type II diabetics.
2. General critique of studies purporting to show deleterious effects
of high carbohydrate diets.
3. A simple explanation of why it's not at all remarkable that a high
carbohydrate diet and exercise program could be helpful to (many) type
II diabetics (and even more helpful to - many, but not all - non-type
II diabetics).
Alas, however, I've been up for 35 of the last 38 hours and I need to
take a nap before driving up to LAX to pick up my younger daughter
(returning from college for Christmas break).
I'll dive into (1), (2), and (3) either later tonight or tomorrow (I
suspect the latter).
- Larry W
runnswim@aol.com (Larry Weisenthal)
fall where they may. You can do that when you know that your idea is
based in science and the researchers are interested in science. <<
Let's hold that thought....
- Larry
Doug Freese
> Longevity isn't in play here. Health and quality of life is.
>
> You seem to be unaware of the larger body of biomedical science that
> doesn't rely on diet studies.
So regardless of what data he shows you, you are stating before hand,
that is is bogus. Gotta love a closed mind.
> This better be brief; I'm bored to tears already.
Why, can't read more than a page per day?
> You apparently flatter yourself that the rest of the international
> internet community gives a shit about you and I and this discussion.
> Get over yourself.
You and TC are perfect reasons cloning should never be allowed.
> This should be fun, if I don't fall asleep.
There is some help for narcolepsy.
> You can't imagine how unlikely I am to read a single additional post
> by you. You've now posted about 5 times, now at GREAT LENGTH to
> explain why you are too busy and have no time to substantiate your
> remarks.
Fortunately there are others that do care.
-DF
Pizzza Girl
example of yourhypocrasy inside the same
paragraph...LOL
So typical of you, George
"I just gag at folks who make unfounded,
unsubstantiated claims without scientific merit based
upon their own biases and little else. I don't give a
rat's ass what you eat or what you think of my diet.
I care a lot about accuracy."
"Susan" <neve...@nomail.com> wrote in message
news:40hq76F...@individual.net...
> x-no-archive: yes
>
> runn...@aol.com (Larry Weisenthal) wrote:
> > Susan, I do apologize for the "Hell hath no fury"
remark. I meant it
> > only in jest, but I understand why you were
offended. I've had less
> > than 3 hours sleep in the past 38, and I'm getting
a little punchy.
> > I'll try to stay more on task from here on in.
>
> You'll have to.
>
> >
> > O.k.
> >
> > First, a few general remarks.
> >
> > As illustrated on this thread, few things provoke
as much passion as
> > diet. Put Osama bin Laden and George Bush next to
each other at a
> > lunch counter, and have both of them spontaneously
order lamb and
> > baklava, and you'll have instant bonding, which
transcends much of what
> > divides them. But put a low carb guy next to a low
fat guy at the same
> > lunch counter, and they'll be mentally gagging over
the sight of each
> > other's food. So we need to recognize this from
the start. Virtually
> > nothing is a personally sacred to us as our food.
Attack my food;
> > attack me. It's just what it is.
>
> Maybe that's true of you, but not true of me. I just
gag at folks who
> make unfounded, unsubstantiated claims without
scientific merit based
> upon their own biases and little else. I don't give
a rat's ass what
> you eat or what you think of my diet.
>
> I care a lot about accuracy.
>
> >
> > Second, nearly everyone (and this includes
nutrition researchers) is
> > strongly biased by their affection for their own
food.
>
> Affection is a very odd word to use when discussing
the most healthful
> way for a diabetic to eat.
>
> >
> > Thirdly (and this was told to me by a prominent,
well-published
> > nutrition Ph.D.), the world of nutrition research
is populated by
> > people who generally couldn't make it in more
competitive and rigorous
> > scientific disciplines. The people who tend to do
nutrition studies
> > are, therefore, (1) strongly biased on a personal
level to begin with
> > in ways that just don't apply to most scientific
disciplines (who has a
> > lot of personal emotion wrapped up in p53 gene
expression?) and are (2)
> > at the bottom of the biomedical research food
chain.
>
> Oh, who cares what some supercilious special friend
of yours thinks of
> others he likes to look down on?
>
> >
> > Fourthly, there are few types of clinical trials
harder to complete
> > than definitive diet and lifestyle interventional
studies. For a whole
> > lot of obvious reasons, beginning with the fact
that you are (1) trying
> > to change something as personal as someone's diet
and (2) you are
> > trying to get inherently lazy 21st century people
to commit to a
> > lifelong program of regular exercise. Also, it
takes decades to
> > determine effects on longevity, which is the main
gold standard which
> > really matters.
>
> Longevity isn't in play here. Health and quality of
life is.
>
> You seem to be unaware of the larger body of
biomedical science that
> doesn't rely on diet studies.
>
> >
> > I'm not a believer in the lowest common denominator
approach to
> > anything -- in this case, the effort to define the
sort of diet which
> > works best for the average person, in a world where
few people are
> > truly average. Susan has provided her experience;
I've provided mine.
> > Both of us are telling the truth. I believe Susan
when she says that
> > she suffered ill effects from the Ornish diet. The
experience may well
> > have motivated her to show the passion expressed in
her various
> > messages on this thread. Hopefully, Susan believes
what I said about
> > my own experience with my own diet of more than 3
decades. Susan isn't
> > "average," and neither am I! Who would even want
to be "average?"
>
> I'm not convinced that "average" wouldn't be
flattering you. I'm not
> yet impressed that you're anything but someone in
love with the sound
> and sight of his own words.
> This better be brief; I'm bored to tears already.
You apparently
> flatter yourself that the rest of the international
internet community
> gives a shit about you and I and this discussion.
Get over yourself.
>
> >
> > 1. Data supporting my assertions of the beneficial
effect of the
> > Pritikin diet/exercise program for Type II
diabetics.
>
> Compared to Burger King, maybe.
>
> >
> > 2. General critique of studies purporting to show
deleterious effects
> > of high carbohydrate diets.
>
> This should be fun, if I don't fall asleep.
>
> >
> > 3. A simple explanation of why it's not at all
remarkable that a high
> > carbohydrate diet and exercise program could be
helpful to (many) type
> > II diabetics (and even more helpful to - many, but
not all - non-type
> > II diabetics).
>
> It's like selling gluten to celiacs.
>
> >
> > Alas, however, I've been up for 35 of the last 38
hours and I need to
> > take a nap before driving up to LAX to pick up my
younger daughter
> > (returning from college for Christmas break).
> >
> > I'll dive into (1), (2), and (3) either later
tonight or tomorrow (I
> > suspect the latter).
>
> You can't imagine how unlikely I am to read a single
additional post by
> you. You've now posted about 5 times, now at GREAT
LENGTH to explain
> why you are too busy and have no time to substantiate
your remarks.
>
> Susan
RBR
wrote:
>
>This better be brief; I'm bored to tears already. You apparently
>flatter yourself that the rest of the international internet community
>gives a shit about you and I and this discussion. Get over yourself.
>
A tad hostile, don't you think?
>>
>> 1. Data supporting my assertions of the beneficial effect of the
>> Pritikin diet/exercise program for Type II diabetics.
>
>Compared to Burger King, maybe.
>
Sarcasm? This really helps your case.
>>
>> 2. General critique of studies purporting to show deleterious effects
>> of high carbohydrate diets.
>
>This should be fun, if I don't fall asleep.
>
>>
<sigh>
>> 3. A simple explanation of why it's not at all remarkable that a high
>> carbohydrate diet and exercise program could be helpful to (many) type
>> II diabetics (and even more helpful to - many, but not all - non-type
>> II diabetics).
>
>It's like selling gluten to celiacs.
>
>>
>> Alas, however, I've been up for 35 of the last 38 hours and I need to
>> take a nap before driving up to LAX to pick up my younger daughter
>> (returning from college for Christmas break).
>>
>> I'll dive into (1), (2), and (3) either later tonight or tomorrow (I
>> suspect the latter).
>
>You can't imagine how unlikely I am to read a single additional post by
>you. You've now posted about 5 times, now at GREAT LENGTH to explain
>why you are too busy and have no time to substantiate your remarks.
>
>Susan
One certainly gets the impression that you have no intention
whatsoever to debate runnswim and are doing whatever you can to
sabotage the debate before it even begins.
RBR
Matti Narkia
<1133393845.3...@o13g2000cwo.googlegroups.com> "runn...@aol.com
(Larry Weisenthal)" <runn...@aol.com> wrote:
>High quality editorial review in the November 2005 issue of Patient
>Care.
>
>http://www.patientcareonline.com/patcare/article/articleDetail.jsp?id=197815#
>
Here a few more interesting articles:
Effects of Protein, Monounsaturated Fat, and Carbohydrate Intake on Blood
Pressure and Serum Lipids: Results of the OmniHeart Randomized Trial
Lawrence J. Appel; Frank M. Sacks; Vincent J. Carey; Eva Obarzanek; Janis F.
Swain; Edgar R. Miller III; Paul R. Conlin; Thomas P. Erlinger; Bernard A.
Rosner; Nancy M. Laranjo; Jeanne Charleston; Phyllis McCarron; Louise M.
Bishop; for the OmniHeart Collaborative Research Group
JAMA. 2005;294:2455-2464.
<http://jama.ama-assn.org/cgi/content/abstract/294/19/2455>
"Conclusion In the setting of a healthful diet, partial substitution of
carbohydrate with either protein or monounsaturated fat can further
lower blood pressure, improve lipid levels, and reduce estimated
cardiovascular risk."
Comments in
Replacing Some Carbohydrates With Protein And Unsaturated Fat May Enhance
Heart Health Benefits
<http://www.sciencedaily.com/releases/2005/11/051117114505.htm>:
"Compared with the study diet containing more carbohydrates, the diet
with greater protein:
* lowered blood pressure, LDL “bad” cholesterol, and triglycerides, and
* lowered HDL “good” cholesterol.
The diet with more unsaturated fat, primarily monounsaturated fat:
* lowered blood pressure and triglycerides,
* raised HDL, and
* did not lower LDL."
Carbohydrate restriction improves the features of Metabolic Syndrome.
Metabolic Syndrome may be defined by the response to carbohydrate
restriction
Jeff S Volek, Richard D Feinman
Nutrition & Metabolism 2005, 2:31 (16 November 2005)
<http://www.nutritionandmetabolism.com/content/2/1/31/abstract>
<http://www.nutritionandmetabolism.com/content/pdf/1743-7075-2-31.pdf>
Comments in
Low-carb Diet Better Than Low-fat Diet At Improving Metabolic Syndrome
<http://www.sciencedaily.com/releases/2005/11/051116090318.htm>
Merchant AT, Anand SS, Vuksan V, Jacobs R, Davis B, Teo K, Yusuf S; SHARE
and SHARE-AP Investigators.
Protein intake is inversely associated with abdominal obesity in a
multi-ethnic population.
J Nutr. 2005 May;135(5):1196-201.
PMID: 15867303 [PubMed - indexed for MEDLINE]
<http://www.nutrition.org/cgi/content/abstract/135/5/1196>
"Substituting a modest amount of protein for carbohydrate may reduce
abdominal obesity in a diverse multi-ethnic population."
Lofgren IE, Herron KL, West KL, Zern TL, Patalay M, Koo SI, Fernandez ML.
Carbohydrate intake is correlated with biomarkers for coronary heart disease
in a population of overweight premenopausal women.
J Nutr Biochem. 2005 Apr;16(4):245-50.
PMID: 15808329 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15808329>
"... Participants were divided into low (<53% of energy)
or high (> or = 53% energy) carbohydrate intake groups.
Individuals in the <53% carbohydrate group consumed more
cholesterol and total fat, but also had higher intake of
polyunsaturated and monounsaturated fatty acids (SFAs). In
contrast, subjects in the > or =53% group consumed higher
concentrations of glucose and fructose than those in the
low-carbohydrate (LC) group. In addition, subjects
consuming <53% carbohydrate had lower concentrations of
LDL-C and apo B (P < .01) and a larger LDL diameter (P <
.05) than the > or =53% group. These results suggest that
the lower LDL-C in the LC group may be related to both the
amount of carbohydrate and the type of fatty acids
consumed by these subjects."
Mozaffarian D, Rimm EB, Herrington DM.
Dietary fats, carbohydrate, and progression of coronary atherosclerosis in
postmenopausal women.
Am J Clin Nutr. 2004 Nov;80(5):1175-84. Erratum in: Am J Clin Nutr. 2005
Jan;81(1):199.
PMID: 15531663 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/80/5/1175>
"Conclusions: In postmenopausal women with relatively low total fat
intake, a greater saturated fat intake is associated with less
progression of coronary atherosclerosis, whereas carbohydrate intake is
associated with a greater progression."
Aude YW, Agatston AS, Lopez-Jimenez F, Lieberman EH, Marie Almon, Hansen M,
Rojas G, Lamas GA, Hennekens CH.
The national cholesterol education program diet vs a diet lower in
carbohydrates and higher in protein and monounsaturated fat: a randomized
trial.
Arch Intern Med. 2004 Oct 25;164(19):2141-6.
PMID: 15505128 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15505128>
"CONCLUSIONS: Compared with the NCEP diet, the MLC diet, which is lower
in total carbohydrates but higher in complex carbohydrates, protein, and
monounsaturated fat, caused significantly greater weight loss over 12
weeks. There were no significant differences between the groups in blood
lipid levels, but favorable changes were observed within the MLC diet
group."
Rodriguez-Villar C, Perez-Heras A, Mercade I, Casals E, Ros E
Comparison of a high-carbohydrate and a high-monounsaturated fat, olive
oil-rich diet on the susceptibility of LDL to oxidative modification in
subjects with Type 2 diabetes mellitus.
Diabet Med. 2004 Feb;21(2):142-9.
PMID: 14984449 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14984449>
Archer WR, Lamarche B, St-Pierre AC, Mauger JF, Deriaz O, Landry N, Corneau
L, Despres JP, Bergeron J, Couture P, Bergeron N.
High carbohydrate and high monounsaturated fatty acid diets similarly affect
LDL electrophoretic characteristics in men who are losing weight.
J Nutr. 2003 Oct;133(10):3124-9.
PMID: 14519795 [PubMed - indexed for MEDLINE]
<http://www.nutrition.org/cgi/content/full/133/10/3124>
"... These results suggest that, when associated with
weight loss, ad libitum consumption of high CHO and high
MUFA diets may be considered to be equally beneficial for
the management of LDL-related atherogenic dyslipidemia.
However, the high MUFA diet more favorably affected
triglyceride levels, suggesting that it may be preferable
to a high CHO diet in cardiovascular disease prevention."
Colette C, Percheron C, Pares-Herbute N, Michel F, Pham TC, Brillant L,
Descomps B, Monnier L.
Exchanging carbohydrates for monounsaturated fats in energy-restricted
diets: effects on metabolic profile and other cardiovascular risk factors.
Int J Obes Relat Metab Disord. 2003 Jun;27(6):648-56.
PMID: 12833107 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12833107>
"CONCLUSIONS: The MUFA-rich diet showed better effects on serum TG than
the CHO-rich diet, even with energy restriction and weight loss. The
results suggest also a protective effect of oleic acid on oxidative
stress and SMC proliferation, two other important cardiovascular risk
factors."
Strychar I, Ishac A, Rivard M, Lussier-Cacan S, Beauregard H, Aris-Jilwan N,
Radwan F, Yale JF.
Impact of a high-monounsaturated-fat diet on lipid profile in subjects with
type 1 diabetes.
J Am Diet Assoc. 2003 Apr;103(4):467-74.
PMID: 12669010 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12669010>
"... A high-monounsaturated-fat diet seemed to have a favorable effect
on fasting lipoprotein profile in people with type 1 diabetes. ..."
Hung T, Sievenpiper JL, Marchie A, Kendall CW, Jenkins DJ.
Fat versus carbohydrate in insulin resistance, obesity, diabetes and
cardiovascular disease.
Curr Opin Clin Nutr Metab Care. 2003 Mar;6(2):165-76. Review.
PMID: 12589186 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12589186>
Brynes AE, Mark Edwards C, Ghatei MA, Dornhorst A, Morgan LM, Bloom SR,
Frost GS.
A randomised four-intervention crossover study investigating the effect of
carbohydrates on daytime profiles of insulin, glucose, non-esterified fatty
acids and triacylglycerols in middle-aged men.
Br J Nutr. 2003 Feb;89(2):207-18.
PMID: 12575905 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12575905>
"In conclusion the HIGH-FAT diet had a beneficial effect on postprandial
glucose and insulin over time but it was associated with higher
postprandial concentrations of TG and NEFA. Conversely the HIGH-GI diet
appeared to increase postprandial insulin resistance over the study
period."
Sacks FM, Katan M.
Randomized clinical trials on the effects of dietary fat and carbohydrate on
plasma lipoproteins and cardiovascular disease.
Am J Med. 2002 Dec 30;113 Suppl 9B:13S-24S. Review.
PMID: 12566134 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12566134>
Perez-Jimenez F, Lopez-Miranda J, Mata P.
Protective effect of dietary monounsaturated fat on arteriosclerosis: beyond
cholesterol.
Atherosclerosis. 2002 Aug;163(2):385-98. Review.
PMID: 12052487 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12052487>
Kris-Etherton PM.
AHA Science Advisory. Monounsaturated fatty acids and risk of cardiovascular
disease. American Heart Association. Nutrition Committee.
Circulation. 1999 Sep 14;100(11):1253-8.
PMID: 10484550 [PubMed - indexed for MEDLINE]
<http://circ.ahajournals.org/cgi/content/full/100/11/1253>
"MUFA Versus Carbohydrate as a Replacement for SFA
[...]
... Although HDL cholesterol decreased on both blood
cholesterol–lowering diets compared with the AAD, the
decrease in HDL cholesterol was less on the high-MUFA
diet (4.3%) than on the Step 1 diet (7.2%). Thus, HDL
cholesterol levels are higher and triglycerides are lower
on a high-MUFA than a low-fat/carbohydrate-rich, blood
cholesterol–lowering diet. ..."
--
Matti Narkia
Matti Narkia
<7hd9q1ho045vkm8ml...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>30 Nov 2005 15:37:25 -0800 in article
><1133393845.3...@o13g2000cwo.googlegroups.com> "runn...@aol.com
>(Larry Weisenthal)" <runn...@aol.com> wrote:
>
>>High quality editorial review in the November 2005 issue of Patient
>>Care.
>>
>>http://www.patientcareonline.com/patcare/article/articleDetail.jsp?id=197815#
>>
>Here a few more interesting articles:
>
>Effects of Protein, Monounsaturated Fat, and Carbohydrate Intake on Blood
>Pressure and Serum Lipids: Results of the OmniHeart Randomized Trial
>Lawrence J. Appel; Frank M. Sacks; Vincent J. Carey; Eva Obarzanek; Janis F.
>Swain; Edgar R. Miller III; Paul R. Conlin; Thomas P. Erlinger; Bernard A.
>Rosner; Nancy M. Laranjo; Jeanne Charleston; Phyllis McCarron; Louise M.
>Bishop; for the OmniHeart Collaborative Research Group
>JAMA. 2005;294:2455-2464.
><http://jama.ama-assn.org/cgi/content/abstract/294/19/2455>
>
Here's another useful article:
Walter C Willett, MD, DrPH
Concepts and Controversies on Diet: Stop Recommending Low-Fat Diets!
<http://xnet.kp.org/permanentejournal/sum03/concepts.html>
--
Matti Narkia
Matti Narkia
<h2e9q1dg8qeuk7lgf...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
This article gives something to think about:
Dreon DM, Fernstrom HA, Williams PT, Krauss RM.
Reduced LDL particle size in children consuming a very-low-fat diet
is related to parental LDL-subclass patterns.
Am J Clin Nutr. 2000 Jun;71(6):1611-6.
PMID: 10837306 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/71/6/1611>
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=10837306&dopt=Abstract>
Comments in
Extreme low-fat diets can increase heart disease risk for some
<http://www.lbl.gov/Science-Articles/Archive/extremediet-patternb.html>
--
Matti Narkia
Matti Narkia
<gce9q15q02dvee7fs...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
A related article:
Dreon DM, Fernstrom HA, Williams PT, Krauss RM.
A very low-fat diet is not associated with improved lipoprotein profiles in
men with a predominance of large, low-density lipoproteins.
Am J Clin Nutr. 1999 Mar;69(3):411-8.
PMID: 10075324 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/69/3/411>
"Conclusions: There is no apparent lipoprotein benefit of reduction in
dietary fat from 20–24% to 10% in men with large LDL particles:
LDL-cholesterol concentration was not reduced, and in a subset of
subjects there was a shift to small LDL along with increased
triacylglycerol and reduced HDL-cholesterol concentrations."
--
Matti Narkia
runnswim@aol.com (Larry Weisenthal)
I've read the abstracts (previously) of all those papers and I have the
full texts of most of them.
I stand 100% behind my previous statements, and I'll back them up, as I
said I would.
Sorry it's taking me longer than I'd planned.
To those folks who are still around, thanks for giving me the benefit
of the doubt until I've been able to make my case. For those who have
run out of patience, if you later on have an interest in this, you'll
be able to see how it turned out by Googling "runnswim" on the
sci.med.nutrition newsgroup and sorting by date.
- Larry Weisenthal
Matti Narkia
<1134989324.3...@g43g2000cwa.googlegroups.com> "runn...@aol.com
(Larry Weisenthal)" <runn...@aol.com> wrote:
>Hey Matti,
>
>I've read the abstracts (previously) of all those papers and I have the
>full texts of most of them.
>
Great, here a couple of new ones:
Yancy WS Jr, Foy M, Chalecki AM, Vernon MC, Westman EC.
A low-carbohydrate, ketogenic diet to treat type 2 diabetes.
Nutr Metab (Lond). 2005 Dec 1;2(1):34 [Epub ahead of print]
PMID: 16318637 [PubMed - as supplied by publisher]
<http://www.nutritionandmetabolism.com/content/2/1/34>
<http://www.nutritionandmetabolism.com/content/pdf/1743-7075-2-34.pdf>
Westman EC, Yancy WS Jr, Olsen MK, Dudley T, Guyton JR.
Effect of a low-carbohydrate, ketogenic diet program compared to a low-fat
diet on fasting lipoprotein subclasses.
Int J Cardiol. 2005 Nov 15; [Epub ahead of print]
PMID: 16297472 [PubMed - as supplied by publisher]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16297472>
>I stand 100% behind my previous statements, and I'll back them up, as I
>said I would.
>
What can I say, it seems that you are a true _believer_ ;-).
--
Matti Narkia
runnswim@aol.com (Larry Weisenthal)
>>Matti Narkia
Thanks for the smiley, and for keeping our exchange dispassionate .
...just curious, are you Finnish/writing from Finland?
- Larry W
Matti Narkia
<1134992842.9...@g47g2000cwa.googlegroups.com> "runn...@aol.com
(Larry Weisenthal)" <runn...@aol.com> wrote:
Yep. What gave me up? My use of english language, my name, my ISP, or
googling usenet groups for my posting history? :-)
--
Matti Narkia
Matti Narkia
<1134608289.14aa409ba0...@roc.usenetexchange.com> "Pizzza
Girl" <P...@yahoo.com> wrote:
>Dairy is bad for you.
>
Milk and butter perhaps, but not _moderate_ consumption of fermented milk
products yogurt and cheese, IMHO, especially if they are made of milk from
grass-fed cows, goats or sheep. They contain much less lactose than milk
(cheese has hardly any at all) and may have some useful probiotics. See
Gill HS, Guarner F.
Probiotics and human health: a clinical perspective.
Postgrad Med J. 2004 Sep;80(947):516-26. Review.
PMID: 15356352 [PubMed - indexed for MEDLINE]
<http://pmj.bmjjournals.com/cgi/content/full/80/947/516>
Anderson JW, Gilliland SE.
Effect of fermented milk (yogurt) containing Lactobacillus acidophilus L1 on
serum cholesterol in hypercholesterolemic humans.
J Am Coll Nutr. 1999 Feb;18(1):43-50.
PMID: 10067658 [PubMed - indexed for MEDLINE]
<http://www.jacn.org/cgi/content/full/18/1/43>
Xiao JZ, Kondo S, Takahashi N, Miyaji K, Oshida K, Hiramatsu A, Iwatsuki K,
Kokubo S, Hosono A
Effects of milk products fermented by Bifidobacterium longum on blood lipids
in rats and healthy adult male volunteers.
J Dairy Sci. 2003 Jul;86(7):2452-61.
PMID: 12906063 [PubMed - indexed for MEDLINE]
<http://jds.fass.org/cgi/content/full/86/7/2452>
Kiessling G, Schneider J, Jahreis G.
Long-term consumption of fermented dairy products over 6 months increases
HDL cholesterol.
Eur J Clin Nutr. 2002 Sep;56(9):843-9.
PMID: 12209372 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12209372>
Kullisaar T, Songisepp E, Mikelsaar M, Zilmer K, Vihalemm T, Zilmer M.
Antioxidative probiotic fermented goats' milk decreases oxidative
stress-mediated atherogenicity in human subjects.
Br J Nutr. 2003 Aug;90(2):449-56.
PMID: 12908907 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12908907>
Terahara M, Kurama S, Takemoto N.
Prevention by lactic acid bacteria of the oxidation of human LDL.
Biosci Biotechnol Biochem. 2001 Aug;65(8):1864-8.
PMID: 11577730 [PubMed - indexed for MEDLINE]
<http://www.jstage.jst.go.jp/article/bbb/65/8/65_1864/_article/-char/en>
<http://www.jstage.jst.go.jp/article/bbb/65/8/1864/_pdf>
<http://www.jstage.jst.go.jp/article/bbb/65/8/65_1864/_cit>
Aihara K, Kajimoto O, Hirata H, Takahashi R, Nakamura Y.
Effect of powdered fermented milk with Lactobacillus helveticus on subjects
with high-normal blood pressure or mild hypertension.
J Am Coll Nutr. 2005 Aug;24(4):257-65.
PMID: 16093403 [PubMed - indexed for MEDLINE]
<http://www.jacn.org/cgi/content/abstract/24/4/257>
Tuomilehto J, Lindstrom J, Hyyrynen J, Korpela R, Karhunen ML, Mikkola L,
Jauhiainen T, Seppo L, Nissinen A.
Effect of ingesting sour milk fermented using Lactobacillus helveticus
bacteria producing tripeptides on blood pressure in subjects with mild
hypertension.
J Hum Hypertens. 2004 Nov;18(11):795-802.
PMID: 15175633 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15175633>
FitzGerald RJ, Murray BA, Walsh DJ.
Hypotensive peptides from milk proteins.
J Nutr. 2004 Apr;134(4):980S-8S. Review.
PMID: 15051858 [PubMed - indexed for MEDLINE]
<http://www.nutrition.org/cgi/content/full/134/4/980S>
Seppo L, Jauhiainen T, Poussa T, Korpela R.
A fermented milk high in bioactive peptides has a blood pressure-lowering
effect in hypertensive subjects.
Am J Clin Nutr. 2003 Feb;77(2):326-30.
PMID: 12540390 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/77/2/326>
Fuglsang A, Rattray FP, Nilsson D, Nyborg NC.
Lactic acid bacteria: inhibition of angiotensin converting enzyme in vitro
and in vivo.
Antonie Van Leeuwenhoek. 2003;83(1):27-34.
PMID: 12755477 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12755477>
Saito T, Nakamura T, Kitazawa H, Kawai Y, Itoh T.
Isolation and structural analysis of antihypertensive peptides that exist
naturally in Gouda cheese.
J Dairy Sci. 2000 Jul;83(7):1434-40.
PMID: 10908049 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=10908049&dopt=Abstract>
<http://jds.fass.org/cgi/reprint/83/7/1434>
Yamamoto N, Maeno M, Takano T.
Purification and characterization of an antihypertensive peptide from a
yogurt-like product fermented by Lactobacillus helveticus CPN4.
J Dairy Sci. 1999 Jul;82(7):1388-93.
PMID: 10416158 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10416158>
<http://jds.fass.org/cgi/reprint/82/7/1388>
Nakamura Y, Yamamoto N, Sakai K, Takano T.
Antihypertensive effect of sour milk and peptides isolated from it that are
inhibitors to angiotensin I-converting enzyme.
J Dairy Sci. 1995 Jun;78(6):1253-7.
PMID: 7673515 [PubMed - indexed for MEDLINE]
<http://jds.fass.org/cgi/reprint/78/6/1253>
Nakamura Y, Yamamoto N, Sakai K, Okubo A, Yamazaki S, Takano T.
Purification and characterization of angiotensin I-converting enzyme
inhibitors from sour milk.
J Dairy Sci. 1995 Apr;78(4):777-83.
PMID: 7790570 [PubMed - indexed for MEDLINE]
<http://jds.fass.org/cgi/reprint/78/4/777>
Yamamoto N, Akino A, Takano T.
Antihypertensive effect of the peptides derived from casein by an
extracellular proteinase from Lactobacillus helveticus CP790.
J Dairy Sci. 1994 Apr;77(4):917-22.
PMID: 8201050 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8201050>
<http://jds.fass.org/cgi/reprint/77/4/917>
--
Matti Narkia
Matti Narkia
<49ddq1tskcbv5g36j...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>Thu, 15 Dec 2005 00:58:09 +0000 in article
><1134608289.14aa409ba0...@roc.usenetexchange.com> "Pizzza
>Girl" <P...@yahoo.com> wrote:
>
>>Dairy is bad for you.
>>
>Milk and butter perhaps, but not _moderate_ consumption of fermented milk
>products yogurt and cheese, IMHO, especially if they are made of milk from
>grass-fed cows, goats or sheep. They contain much less lactose than milk
>(cheese has hardly any at all) and may have some useful probiotics. See
>
Here some interesting cheese references:
Hauswirth CB, Scheeder MR, Beer JH.
High {omega}-3 Fatty Acid Content in Alpine Cheese. The Basis for an
Alpine Paradox.
Circulation. 2003 Dec 15 [Epub ahead of print]
PMID: 14676141 [PubMed - as supplied by publisher]
<http://circ.ahajournals.org/cgi/content/full/109/1/103>
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14676141&dopt=Abstract>
Abstract:
"BACKGROUND: alpha-Linolenic acid (ALA) may protect from
cardiovascular disease. Because fresh alpine grass contains
high amounts of ALA, we hypothesized that the levels of
omega-3 fatty acids would concentrate to nutritional
relevance in the cheese of milk from cows with alpine grass
feeding compared with cheese from silage and concentrate
feeding; the newly available cheese produced from cows fed
with linseed supplementation should contain even higher ALA
concentrations. METHODS AND RESULTS: Forty different
cheeses were analyzed by gas chromatography for their fatty
acid profile: (1) 12 from well-defined alpine regions
around Gstaad, Switzerland; (2) 7 commercially available
English cheddar cheeses; (3) 6 cheeses from cows fed with
linseed supplementation; (4) 7 industrial-type Emmentals;
and (5) 8 alpine cheeses with partial silage feeding. The
alpine cheese contained 4 times more linolenic acid
(C18:3omega-3) compared with cheddar, more total omega-3
fatty acids, and showed a significantly lower n-6:omega-3
ratio. Conjugated linoleic acid (C18:2 c9/t11) was 3-fold
higher, whereas the amount of palmitic acid was 20% lower.
The Emmental reached 40% of the ALA content compared with
alpine cheese, and surprisingly, cheese from linseed-
supplemented cows contained only 49% of that of the alpine
cheese (P<0.001 for each trait in the 5 cheese groups).
CONCLUSIONS: Cheese made of milk from cows grazed on alpine
pastures had a more favorable fatty acid profile than all
other cheese types. Alpine cheese may be a relevant source
of ALA and other cardioprotective fatty acids."
Nestel PJ, Chronopulos A, Cehun M.
Dairy fat in cheese raises LDL cholesterol less than that in butter in
mildly hypercholesterolaemic subjects.
Eur J Clin Nutr. 2005 Sep;59(9):1059-63.
PMID: 16015270 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16015270>
"... CONCLUSION: A total of 40 g dairy fat eaten daily for 4 weeks as
butter, but not as cheese, raised total and LDL cholesterol
significantly compared with a diet containing significantly less
saturated fat. Dietary advice regarding cheese consumption may require
modification."
Biong AS, Muller H, Seljeflot I, Veierod MB, Pedersen JI.
A comparison of the effects of cheese and butter on serum lipids,
haemostatic variables and homocysteine.
Br J Nutr. 2004 Nov;92(5):791-7.
PMID: 15533268 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15533268>
"... Total cholesterol was significantly lower after the CH diet
than after the BC diet (-0.27 mmol/l; P=0.03), while the
difference in LDL-cholesterol was found to be below
significance level (-0.22 mmol/l; P=0.06). There were no
significant differences in HDL-cholesterol, triacylglycerols,
apo A-I, apo B or lipoprotein (a), haemostatic variables and
homocysteine between the diets. The results indicate that, at
equal fat content, cheese may be less cholesterol increasing
than butter. ..."
Tholstrup T, Hoy CE, Andersen LN, Christensen RD, Sandstrom B.
Does fat in milk, butter and cheese affect blood lipids and
cholesterol differently?
J Am Coll Nutr. 2004 Apr;23(2):169-76.
PMID: 15047684 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15047684>
"... RESULTS: Fasting LDL cholesterol concentration was
significantly higher after butter than cheese diet (p = 0.037),
with a borderline significant difference in total cholesterol
(p = 0.054) after the experimental periods of three weeks.
Postprandial glucose showed a higher response after cheese diet
than after milk diet (p = 0.010, diet x time interaction).
CONCLUSIONS: A different effect of fat in milk and butter could
not be confirmed in this study. The moderately lower LDL
cholesterol after cheese diet compared to butter diet should be
investigated further..."
Colquhoun DM, Somerset S, Irish K, Leontjew LM.
Cheese added to a low fat diet does not affect serum lipids.
Asia Pac J Clin Nutr. 2003;12 Suppl:S65.
PMID: 15023695 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15023695>
" .. Conclusions - On the background of a LF diet, including cheese is
not associated with adverse effects on serum lipids. Fermentation
presumably is responsible for these favorable effects."
Segall JJ.
Why is cheese safe for the coronary arteries?
Int J Cardiol. 1992 May;35(2):281-3. No abstract available.
PMID: 1572753 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1572753>
--
Matti Narkia
Matti Narkia
<hf5dq1hne87jqmtqk...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>19 Dec 2005 02:48:44 -0800 in article
><1134989324.3...@g43g2000cwa.googlegroups.com> "runn...@aol.com
>(Larry Weisenthal)" <runn...@aol.com> wrote:
>
>>Hey Matti,
>>
>>I've read the abstracts (previously) of all those papers and I have the
>>full texts of most of them.
>>
>Great, here a couple of new ones:
>
>Yancy WS Jr, Foy M, Chalecki AM, Vernon MC, Westman EC.
>A low-carbohydrate, ketogenic diet to treat type 2 diabetes.
>Nutr Metab (Lond). 2005 Dec 1;2(1):34 [Epub ahead of print]
>PMID: 16318637 [PubMed - as supplied by publisher]
><http://www.nutritionandmetabolism.com/content/2/1/34>
><http://www.nutritionandmetabolism.com/content/pdf/1743-7075-2-34.pdf>
>
Additional references about low-carbohydrate diet in type 2 diabetes;
Nielsen JV, Jonsson E, Nilsson AK.
Lasting improvement of hyperglycaemia and bodyweight: low-carbohydrate diet
in type 2 diabetes. A brief report.
Ups J Med Sci. 2005;110(2):179-83.
PMID: 16075898 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16075898>
"... A low-carbohydrate diet is an effective tool in the treatment of
obese patients with type 2 diabetes."
Arora SK, McFarlane SI
The case for low carbohydrate diets in diabetes management.
Nutr Metab (Lond). 2005 Jul 14;2:16.
PMID: 16018812 [PubMed]
<http://www.nutritionandmetabolism.com/content/2/1/16>
"A low fat, high carbohydrate diet in combination with
regular exercise is the traditional recommendation for
treating diabetes. Compliance with these lifestyle
modifications is less than satisfactory, however, and a
high carbohydrate diet raises postprandial plasma glucose
and insulin secretion, thereby increasing risk of CVD,
hypertension, dyslipidemia, obesity and diabetes.
Moreover, the current epidemic of diabetes and obesity
has been, over the past three decades, accompanied by a
significant decrease in fat consumption and an increase
in carbohydrate consumption. This apparent failure of the
traditional diet, from a public health point of view,
indicates that alternative dietary approaches are needed.
Because carbohydrate is the major secretagogue of
insulin, some form of carbohydrate restriction is a prima
facie candidate for dietary control of diabetes. Evidence
from various randomized controlled trials in recent years
has convinced us that such diets are safe and effective,
at least in short-term. These data show low carbohydrate
diets to be comparable or better than traditional low fat
high carbohydrate diets for weight reduction, improvement
in the dyslipidemia of diabetes and metabolic syndrome as
well as control of blood pressure, postprandial glycemia
and insulin secretion. Furthermore, the ability of low
carbohydrate diets to reduce triglycerides and to
increase HDL is of particular importance. Resistance to
such strategies has been due, in part, to equating it
with the popular Atkins diet. However, there are many
variations and room for individual physician planning.
Some form of low carbohydrate diet, in combination with
exercise, is a viable option for patients with diabetes.
However, the extreme reduction of carbohydrate of popular
diets (<30 g/day) cannot be recommended for a diabetic
population at this time without further study. On the
other hand, the dire objections continually raised in the
literature appear to have very little scientific basis.
Whereas it is traditional to say that more work needs to
be done, the same is true of the assumed standard low fat
diets which have an ambiguous record at best. We see
current trends in the national dietary recommendations as
a positive sign and an appropriate move in the right
direction."
Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP.
Effect of a low-carbohydrate diet on appetite, blood glucose levels, and
insulin resistance in obese patients with type 2 diabetes.
Ann Intern Med. 2005 Mar 15;142(6):403-11. Summary for patients in: Ann
Intern Med. 2005 Mar 15;142(6):I44.
PMID: 15767618 [PubMed - indexed for MEDLINE]
<http://www.annals.org/cgi/content/abstract/142/6/403>
<http://www.annals.org/cgi/reprint/142/6/403.pdf>
Leon-Sanz M, Garcia-Luna PP, Sanz-Paris A, Gomez-Candela C, Casimiro C,
Chamorro J, Pereira-Cunill JL, Martin-Palmero A, Trallero R, Martinez J,
Ordonez FJ, Garcia-Peris P, Camarero E, Gomez-Enterria P, Cabrerizo L,
Perez-de-la-Cruz A, Sanchez C, Garcia-de-Lorenzo A, Rodriguez N, Usan L;
Abbott SPAI-97-004 Study Cooperative Group.
Glycemic and lipid control in hospitalized type 2 diabetic patients:
evaluation of 2 enteral nutrition formulas (low carbohydrate-high
monounsaturated fat vs high carbohydrate).
JPEN J Parenter Enteral Nutr. 2005 Jan-Feb;29(1):21-9.
PMID: 15715270 [PubMed - indexed for MEDLINE]
<http://jpen.aspenjournals.org/cgi/content/abstract/29/1/21>
Garg A, Bantle JP, Henry RR, Coulston AM, Griver KA, Raatz SK, Brinkley L,
Chen YD, Grundy SM, Huet BA, et al.
Effects of varying carbohydrate content of diet in patients with
non-insulin-dependent diabetes mellitus.
JAMA. 1994 May 11;271(18):1421-8.
PMID: 7848401 [PubMed - indexed for MEDLINE]
<http://jama.ama-assn.org/cgi/content/abstract/271/18/1421>
"... INTERVENTIONS--A high-carbohydrate diet containing
55% of the total energy as carbohydrates and 30% as fats
was compared with a high-monounsaturated-fat diet
containing 40% carbohydrates and 45% fats. The amounts of
saturated fats, polyunsaturated fats, cholesterol,
sucrose, and protein were similar.
[...]
CONCLUSIONS--In NIDDM patients, high-carbohydrate diets
compared with high-monounsaturated-fat diets caused
persistent deterioration of glycemic control and
accentuation of hyperinsulinemia, as well as increased
plasma triglyceride and very-low-density lipoprotein
cholesterol levels, which may not be desirable."
--
Matti Narkia
Matti Narkia
<7hd9q1ho045vkm8ml...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>30 Nov 2005 15:37:25 -0800 in article
><1133393845.3...@o13g2000cwo.googlegroups.com> "runn...@aol.com
>(Larry Weisenthal)" <runn...@aol.com> wrote:
>
>>High quality editorial review in the November 2005 issue of Patient
>>Care.
>>
>>http://www.patientcareonline.com/patcare/article/articleDetail.jsp?id=197815#
>>
>Here a few more interesting articles:
>
[snip]
>
>Carbohydrate restriction improves the features of Metabolic Syndrome.
>Metabolic Syndrome may be defined by the response to carbohydrate
>restriction
>Jeff S Volek, Richard D Feinman
>Nutrition & Metabolism 2005, 2:31 (16 November 2005)
><http://www.nutritionandmetabolism.com/content/2/1/31/abstract>
><http://www.nutritionandmetabolism.com/content/pdf/1743-7075-2-31.pdf>
>
>Comments in
>
>Low-carb Diet Better Than Low-fat Diet At Improving Metabolic Syndrome
><http://www.sciencedaily.com/releases/2005/11/051116090318.htm>
>
A related study:
Hickey JT, Hickey L, Yancy WS, Juanita H, C.Westman E.
Clinical use of a carbohydrate-restricted diet to treat the dyslipidemia of
the metabolic syndrome.
Metabolic syndrome and related disorders, Sep 2003, Vol. 1, No. 3: 227-232
<http://www.liebertonline.com/doi/abs/10.1089%2F154041903322716705>
"Conclusions: A carbohydrate-restricted diet
recommendation led to improvements in lipid profiles and
lipoprotein subclass traits of the metabolic syndrome in
a clinical outpatient setting, and should be considered
as a treatment for the metabolic syndrome."
--
Matti Narkia
Matti Narkia
<hf5dq1hne87jqmtqk...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>19 Dec 2005 02:48:44 -0800 in article
><1134989324.3...@g43g2000cwa.googlegroups.com> "runn...@aol.com
>(Larry Weisenthal)" <runn...@aol.com> wrote:
>
>>Hey Matti,
>>
>>I've read the abstracts (previously) of all those papers and I have the
>>full texts of most of them.
>>
>Great, here a couple of new ones:
>
>Yancy WS Jr, Foy M, Chalecki AM, Vernon MC, Westman EC.
>A low-carbohydrate, ketogenic diet to treat type 2 diabetes.
>Nutr Metab (Lond). 2005 Dec 1;2(1):34 [Epub ahead of print]
>PMID: 16318637 [PubMed - as supplied by publisher]
><http://www.nutritionandmetabolism.com/content/2/1/34>
><http://www.nutritionandmetabolism.com/content/pdf/1743-7075-2-34.pdf>
>
>Westman EC, Yancy WS Jr, Olsen MK, Dudley T, Guyton JR.
>Effect of a low-carbohydrate, ketogenic diet program compared to a low-fat
>diet on fasting lipoprotein subclasses.
>Int J Cardiol. 2005 Nov 15; [Epub ahead of print]
>PMID: 16297472 [PubMed - as supplied by publisher]
><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16297472>
>
Here's a recent animal study, which should raise some interest:
A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of
Alzheimer's disease
Ingrid Van der Auwera, Stefaan Wera, Fred Van Leuven, Samuel T Henderson
Nutrition & Metabolism 2005, 2:28 (17 October 2005)
<http://www.nutritionandmetabolism.com/content/2/1/28/abstract>
<http://www.nutritionandmetabolism.com/content/pdf/1743-7075-2-28.pdf>
"Background
Alzheimer's disease (AD) is a progressive
neurodegenerative disorder that primarily strikes the
elderly. Studies in both humans and animal models have
linked the consumption of cholesterol and saturated fats
with amyloid-beta (Abeta) deposition and development of
AD. Yet, these studies did not examine high fat diets in
combination with reduced carbohydrate intake. Here we
tested the effect of a high saturated fat / low
carbohydrate diet on a transgenic mouse model of AD.
Results
Starting at three months of age, two groups of female
transgenic mice carrying the "London" APP mutation
(APP/V717I) were fed either, a standard diet (SD) composed
of high carbohydrate / low fat chow, or a ketogenic diet
(KD) composed of very low carbohydrate / high saturated
fat chow for 43 days. Animals fed the KD exhibited greatly
elevated serum ketone body levels, as measured by beta-
hydroxybutyrate (3.85 + 2.6 mM), compared to SD fed
animals (0.29 + 0.06 mM). In addition, animals fed the KD
lost body weight (SD 22.2 + 0.6 g vs. KD 17.5 + 1.4 g, p=
0.0067). In contrast to earlier studies, the brief KD
feeding regime significantly reduced total brain Abeta
levels by approximately 25%. Despite changes in ketone
levels, body weight, and Abeta levels, the KD diet did not
alter behavioral measures.
Conclusions
Previous studies have suggested that diets rich in
cholesterol and saturated fats increased the deposition of
Abeta and the risk of developing AD. Here we demonstrate
that a diet rich in saturated fats and low in
carbohydrates can actually reduce levels of Abeta.
Therefore, dietary strategies aimed at reducing Abeta
levels should take into account interactions of dietary
components and the metabolic outcomes, in particular,
levels of carbohydrates, total calories, and presence of
ketone bodies should be considered."
Comments in
Editorial
When is a high fat diet not a high fat diet?
Richard D Feinman
Nutrition & Metabolism 2005, 2:27 (17 October 2005)
<http://www.nutritionandmetabolism.com/content/pdf/1743-7075-2-27.pdf>
and in
A High Fat, Low Carbohydrate Diet Improves Alzheimer's Disease In Mice
<http://www.sciencedaily.com/releases/2005/10/051017072307.htm>
"Mice with the mouse model of Alzheimer's disease show
improvements in their condition when treated with a high-
fat, low-carbohydrate diet. A report published today in
the peer-reviewed, open access journal Nutrition and
Metabolism, showed that a brain protein, amyloid-beta,
which is an indicator of Alzheimer's disease, is reduced
in mice on the so-called ketogenic diet.
[...]
The authors believe that Insulin and the related hormone,
insulin-related growth factor-1 (IGF-1), are the key
players. "Insulin is often considered a storage hormone,
since it promotes deposition of fat but insulin may also
work to encourage amyloid-beta production."
Richard Feinman, editor of the journal, explains the
relation between nutrients: "You might say that fat is the
bomb, and insulin (from carbohydrate) is the fuse. Most
studies of the deleterious effects of fat have been done
in the presence of high carbohydrate. If carbs are high,
dietary fat is not oxidized and is instead stored as body
fat." When carbohydrates are very low and fat is high,
compounds called ketone bodies are generated (ketosis) and
these compounds may play a role in the observed reduction
in amyloid-beta. In association with a group from
University of Washington led by Dr. Suzanne Craft,
Henderson has previously shown cognitive improvement in
patients with mild AD who were given a diet that raises
ketone bodies."
--
Matti Narkia
Matti Narkia
(Larry Weisenthal)" <runn...@aol.com> wrote:
>High quality editorial review in the November 2005 issue of Patient
>Care.
>
>http://www.patientcareonline.com/patcare/article/articleDetail.jsp?id=197815#
>
The title of the article is "VIEWPOINT: Very-low-fat diets are superior to
low-carbohydrate diets". The article just does not deliver what the title
promises. Reasons:
1) The scope of the article is very limited: it only discusses weight loss
diets. Other health aspects don't get much attention. I did not for example
find anything about the effects on type 2 diabetes, which was Susan's
concern, but perhaps I just browsed through the article too quickly.
2) Most of the article concentrated in critisizing successful low
carbyhodrate weight loss trials with.
3) No _evidence_ for the claimed superiority of the very-low-fat diet was
given.
4) No long term health effects were discussed.
5) The article's bias shows in that it does not mention any of the articles
which find no association between dietary fat and body fat. Below some
examples of these:
Willett WC, Leibel RL.
Dietary fat is not a major determinant of body fat.
Am J Med. 2002 Dec 30;113 Suppl 9B:47S-59S. Review.
PMID: 12566139 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12566139>
Willett WC.
Dietary fat plays a major role in obesity: no.
Obes Rev. 2002 May;3(2):59-68. Review.
PMID: 12120421 [PubMed - indexed for MEDLINE]
<http://www.blackwell-synergy.com/links/doi/10.1046/j.1467-789X.2002.00060.x/abs/>
Willett WC.
Is dietary fat a major determinant of body fat?
Am J Clin Nutr. 1998 Mar;67(3 Suppl):556S-562S. Review. Erratum in: Am J
Clin Nutr 1999 Aug;70(2):304.
PMID: 9497170 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/reprint/67/3/556S>
<http://www.ajcn.org/cgi/content/full/70/2/304> (Erratum)
An opposing view to the previous article:
Bray GA, Popkin BM.
Dietary fat intake does affect obesity!
Am J Clin Nutr. 1998 Dec;68(6):1157-73. Review.
PMID: 9846842 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/reprint/68/6/1157>
Willett's reply to Bray and Popkin:
Willett WC.
Dietary fat and obesity: an unconvincing relation.
Am J Clin Nutr. 1998 Dec;68(6):1149-50.
<http://www.ajcn.org/cgi/reprint/68/6/1149>
--
Matti Narkia
Matti Narkia
Susan <neve...@nomail.com> wrote:
>
>Matti, you've kind of gone off point, here, though you've furnished a
>lot of good information.
>
The title of the article which started this thread is "VIEWPOINT:
Very-low-fat diets are superior to low-carbohydrate diets". That gives quite
a lot of scope, although it turned out that the article only dealt with
weight loss diets. See also the title of this thread. Diversion to type 2
diabetes came later.
>Larry's contention is that studies show that Pritikin is a suitable
>intervention, with exercise, for type 2 diabetes. Why not take a look
>at those studies as I have? I think you'll find that not only did the
>diabetics remain in the range that cellular damage is occurring
>(diabetes not well controlled) but that the effect demonstrated is
>likely from the exercise alone.
>
I might have look at those as well, but why don't you post a few, because
you are already familiar with them.
--
Matti Narkia
Matti Narkia
Susan <neve...@nomail.com> wrote:
I took the liberty to find complete references and links to full text for
your citations, hope that's ok :-).
>
>HbA1c and triglycerides are both elevated by high carb diets, even more
>so if they're low fat:
>
>
>
>**************************************
>A low fat - high carbohydrate diet often raises triglycerides. For
>example the very lean Dean Ornish program raises triglycerides 60% or
>more. My triglycerides are 63. On a low fat diet they were 239.
>Anything over 150 is considered a risk factor for heart disease and
>stroke. Some studies (at Harvard Medical School) have suggested that
>the ratio of triglycerides to HDL cholesterol is a much more accurate
>predictor of risk factor than total cholesterol. Your ratio
>Triglycerides / HDL =
>2.0 or less.
>
>"A new study suggests that level of triglyceride in the blood may help
>predict heart attack risk as well as other more well-known blood fats
>such as LDL and HDL cholesterol. High triglycerides alone increased
>the risk of heart attack nearly three-fold, according to a report in
>the current issue of Circulation. And people with the highest ratio of
>triglycerides to HDL -- the "good" cholesterol -- had 16 times the
>risk of heart attack as those with the lowest ratio of triglycerides
>to HDL in the study of 340 heart attack patients and 340 of their
>healthy, same age counterparts. The ratio of triglycerides to HDL was
>the strongest predictor of a heart attack, even more accurate than the
>LDL/HDL ratio," reported Harvard lead study author.
>Triglycerides, a mixture of fatty acids and glycerol that make up the
>principle fats in the blood, bind to carrier proteins, forming
>compounds known as lipoproteins. Other types of lipoproteins that
>carry cholesterol, such as LDL and HDL, are known to be related to the
>risk of heart disease because of their propensity to deposit -- or not
>deposit -- fat in coronary arteries. However, it has not been clear if
>triglyceride level could predict heart attack risk, despite years of
>research." Circulation (1997;96:2520-2525)
>
Gaziano JM, Hennekens CH, O'Donnell CJ, Breslow JL, Buring JE.
Fasting triglycerides, high-density lipoprotein, and risk of myocardial
infarction.
Circulation. 1997 Oct 21;96(8):2520-5.
PMID: 9355888 [PubMed - indexed for MEDLINE]
<http://circ.ahajournals.org/cgi/content/full/96/8/2520>
>
>"When the researchers accounted for other risk factors for stroke,
>people with more than 200 mg of triglycerides per dl of blood were
>nearly 30% more likely to have an ischemic stroke or TIA than people
>with lower levels of the blood fats.
>Ischemic strokes, which occur when a clot or narrowed artery cuts off
>the brain's blood supply, account for about 80% of all strokes. The
>other 20% are due to broken blood vessels in the brain
>High triglycerides and the low levels of HDL, or "good," cholesterol
>that usually coexist are important risk factors for the main type of
>stroke, called ischemic stroke, among patients with heart disease."
>Circulation December 11, 2001;104:2892-2897
>
Tanne D, Koren-Morag N, Graff E, Goldbourt U.
Blood lipids and first-ever ischemic stroke/transient ischemic attack in the
Bezafibrate Infarction Prevention (BIP) Registry: high triglycerides
constitute an independent risk factor.
Circulation. 2001 Dec 11;104(24):2892-7.
PMID: 11739302 [PubMed - indexed for MEDLINE]
<http://circ.ahajournals.org/cgi/content/full/104/24/2892>
>
>************************************************
>
>
>
>
>High-Grain Diet May Increase Risk of Cardiovascular Disease
>
>American Journal Clinical Nutrition January 2003 77: 43-50
>
>When humans consume more carbohydrates than can be stored, the excess
>carbohydrate energy is converted to fat by the liver. This process may
>maintain blood sugar control and prevent diabetes in the short-term,
>however it may also increase triglyceride concentrations, which may
>increase the risk of cardiovascular disease.
>
>In the last decade, researchers established that fat production by the
>liver varies depending on dietary habits and health status.
>
>The typical Western diet has a high fat content, which means that only
>a limited amount of carbohydrates are available for liver fat
>production, and liver fat production tends to be very low among
>individuals who eat this type of diet. However, when too many
>carbohydrates were consumed, both liver fat and sugar production were
>increased.
>
>A very low-fat (10 percent of energy) and very high-carbohydrate (75
>percent of energy) diet also leads to increased liver fat production,
>with the increase being even more pronounced when more than half of
>the carbohydrate was consumed as simple sugars. This points to the
>importance of carbohydrate quality, as another study using 68 percent
>of energy from complex carbohydrate resulted in minimal liver fat
>production.
>
>However, it was found that obese individuals with high insulin levels
>who consume a high-fat (40 percent of energy) diet had a liver fat
>production rate three to four times higher than that of lean
>individuals with normal insulin levels. But, both normal and high
>insulin groups had lower liver fat production on the high-fat diet
>than on a low-fat, high-carbohydrate diet.
>
>Moreover, the low-fat, high-carbohydrate diet caused an increase in
>triglyceride concentrations, a risk factor for coronary heart disease,
>which was associated with the liver fat production in both normal and
>high-insulin individuals.
>
>Researchers concluded that the low-fat, high-carbohydrate diet might
>not be ideal, as it can induce liver fat production and insulin
>resistance. This is especially true when most of the carbohydrate is
>in the form of simple sugars.
Schwarz JM, Linfoot P, Dare D, Aghajanian K.
Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic
subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate
isoenergetic diets.
Am J Clin Nutr. 2003 Jan;77(1):43-50.
PMID: 12499321 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/77/1/43>
--
Matti Narkia
Matti Narkia
Susan <neve...@nomail.com> wrote:
>x-no-archive: yes
>
>Matti Narkia wrote:
>> Mon, 19 Dec 2005 11:03:51 -0500 in article <40o3v6F...@individual.net>
>> Susan <neve...@nomail.com> wrote:
>>
>>>Matti, you've kind of gone off point, here, though you've furnished a
>>>lot of good information.
>>>
>>
>> The title of the article which started this thread is "VIEWPOINT:
>> Very-low-fat diets are superior to low-carbohydrate diets". That gives quite
>> a lot of scope, although it turned out that the article only dealt with
>> weight loss diets. See also the title of this thread. Diversion to type 2
>> diabetes came later.
>
>This discussion began with Larry agreeing to furnish good evidence to me
>of the benefits of very high carb/very low fat for diabetics. Unless I'm
>misremembering?
>
That was fairly late in the thread, IMHO. My first post was a reply to
Larry's first post, which dealt with the above article. I gather that my
scope is perhaps a bit wider than yours as apparently was Larry's original
scope. Let's continue according our respective scopes and interests :-).
>
>> I might have look at those as well, but why don't you post a few, because
>> you are already familiar with them.
>>
>
>I haven't furnished them because he said *he* would, over and over and
>over and over... I said I'd wait for his good evidence of the salutary
>effect of very high carb low fat for type 2 diabetes before critiquing.
>His unwillingness to post the Pritikin studies may mean he's looked at
>them, too, and found a minor effect, all of which can be attributed to
>exercise overcoming some of the damage done to diabetics by the diet.
>
>In fact, the studies show that bg remains in the danger zone, that diet
>has to be overcome to the degree possible by exercise, and that TGLs and
>HDL go in the wrong directions on such diets; these are markers for
>worsening insulin resistance, as you know.
>
Yep.
--
Matti Narkia
Matti Narkia
<87pdq1pkj32vnaena...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>Mon, 19 Dec 2005 11:25:01 -0500 in article <40o56tF...@individual.net>
>Susan <neve...@nomail.com> wrote:
>
>I took the liberty to find complete references and links to full text for
>your citations, hope that's ok :-).
>
It seems that I missed reference and link to full text for Susan's last
citation. Here they are:
McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven G.
Use of metabolic markers to identify overweight individuals who are insulin
resistant.
Ann Intern Med. 2003 Nov 18;139(10):802-9. Summary for patients in: Ann
Intern Med. 2003 Nov 18;139(10):I16.
PMID: 14623617 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=14623617>
<http://www.annals.org/cgi/content/abstract/139/10/802>
<http://www.annals.org/cgi/reprint/139/10/802.pdf> (free full text)
--
Matti Narkia
Matti Narkia
Susan <neve...@nomail.com> wrote:
>
>Matti Narkia wrote:
>> Mon, 19 Dec 2005 11:45:01 -0500 in article <40o6cdF...@individual.net>
>
>> Larry's first post, which dealt with the above article. I gather that my
>> scope is perhaps a bit wider than yours as apparently was Larry's original
>> scope. Let's continue according our respective scopes and interests :-).
>
Chronologically, yes, but at an earlier location in the thread.
--
Matti Narkia
runnswim@aol.com (Larry Weisenthal)
>>Yep. What gave me up? My use of english language, my name, my ISP, or
googling usenet groups for my posting history? :-) <<
None of the above. I recognized the ethnicity of your name and saw
that you were writing to me at 3 AM Pacific Standard Time (when I was
writing to you; I often wake up in the middle of the night, and that's
when I have the most time to do my Usenetting). So I thought there was
a good chance you were writing from Europe.
I'm half-Finnish. Both sets of maternal great-parents (named
Hendrickson and Rautio, respectively were born in Finland). They came
to the US to take advantage of the homestead act, which gave immigrants
160 acres of free land if they built a house and farmed the land.
Interesting story with my maternal great-grandfather. He came to the
US in 1874. Built a house. Farmed land for nearly two years, then
"sent" for his wife and daughter. Tragically, their ship sunk in the
North Atlantic and they perished. Heartbroken, my great-grandfather
returned to Finland, eventually met and married another woman (my
great-grandmother) and returned with her to Wisconsin. Were it not for
that North Atlantic tragedy 130 years ago, I'd never have been born.
My grandmother and mother were born on the homesteaded land, which my
family finally sold in the early 1950s. My best friend (who does all
of the computer/software stuff for my business) is a "full-blooded"
Finn who still lives on HIS family's homestead, dating to the 1880s.
My grandmother and grandfather were the last generation to be fluent in
Finnish, which was still widely spoken in northern Wisconsin and
northern Michigan when I was growing up in the 1950s (we used to spend
summers there). I've read that modern day Finnish linguists have
studied the speech of the Finns of the Northern midwest, because it is
supposed to be closer to the Finnish language of the 19th century than
is the language in Finland today.
But don't let any of that above lead you to believe that I'm going to
go easy on you in our little diet debate!
- Larry W
Matti Narkia
<1135014968.3...@g47g2000cwa.googlegroups.com> "runn...@aol.com
(Larry Weisenthal)" <runn...@aol.com> wrote:
>>From Matti ->
>
>>>Yep. What gave me up? My use of english language, my name, my ISP, or
>googling usenet groups for my posting history? :-) <<
>
>None of the above. I recognized the ethnicity of your name and saw
>that you were writing to me at 3 AM Pacific Standard Time (when I was
>writing to you; I often wake up in the middle of the night, and that's
>when I have the most time to do my Usenetting). So I thought there was
>a good chance you were writing from Europe.
>
> I'm half-Finnish. Both sets of maternal great-parents (named
>Hendrickson and Rautio, respectively were born in Finland). They came
>to the US to take advantage of the homestead act, which gave immigrants
>160 acres of free land if they built a house and farmed the land.
>
So having partly Finnish roots perhaps helped you to recognize that my name
is Finnish? If you know Finnish names at all, my first name will reveal my
origin. I haven't seen exactly the same spelling of that name been used in
other cultures, although some are very close, Matt in English for example.
One problem with my first name is that many English female names end with a
vowel and perhaps for that reason some English speakers mistakenly think I'm
a woman :-)-
Rautio is a typical Finnish name, but Hendrickson is a Swedish name. We have
a Swedish speaking minority in Finland, and even some only Finnish speaking
people may have Swedish name. Although my father was not Swedish speaking,
he had a Swedish last name, Nylund, but he changed to a Finnish name long
before I was born.
>Interesting story with my maternal great-grandfather. He came to the
>US in 1874. Built a house. Farmed land for nearly two years, then
>"sent" for his wife and daughter. Tragically, their ship sunk in the
>North Atlantic and they perished. Heartbroken, my great-grandfather
>returned to Finland, eventually met and married another woman (my
>great-grandmother) and returned with her to Wisconsin. Were it not for
>that North Atlantic tragedy 130 years ago, I'd never have been born.
>My grandmother and mother were born on the homesteaded land, which my
>family finally sold in the early 1950s. My best friend (who does all
>of the computer/software stuff for my business) is a "full-blooded"
>Finn who still lives on HIS family's homestead, dating to the 1880s.
>
Quite a story!
>My grandmother and grandfather were the last generation to be fluent in
>Finnish, which was still widely spoken in northern Wisconsin and
>northern Michigan when I was growing up in the 1950s (we used to spend
>summers there). I've read that modern day Finnish linguists have
>studied the speech of the Finns of the Northern midwest, because it is
>supposed to be closer to the Finnish language of the 19th century than
>is the language in Finland today.
>
I think that most Finns, who moved to USA in 1800s and early 1900s settled
in northern states: Minnesota, Michigan and Wisconsin. Perhaps they were
looking for similar climate than in Finland, although I can't understand why
:-).
>But don't let any of that above lead you to believe that I'm going to
>go easy on you in our little diet debate!
>
Ok, fair enough :-). I'll try to do the same ;-).
--
Matti Narkia
Matti Narkia
<h2e9q1dg8qeuk7lgf...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>Sun, 18 Dec 2005 03:11:22 +0200 in article
><7hd9q1ho045vkm8ml...@4ax.com> Matti Narkia <nar...@yahoo.com>
>wrote:
>
>>30 Nov 2005 15:37:25 -0800 in article
>><1133393845.3...@o13g2000cwo.googlegroups.com> "runn...@aol.com
>>(Larry Weisenthal)" <runn...@aol.com> wrote:
>>
>>>High quality editorial review in the November 2005 issue of Patient
>>>Care.
>>>
>>>http://www.patientcareonline.com/patcare/article/articleDetail.jsp?id=197815#
>>>
>>Here a few more interesting articles:
>>
>>Effects of Protein, Monounsaturated Fat, and Carbohydrate Intake on Blood
>>Pressure and Serum Lipids: Results of the OmniHeart Randomized Trial
>>Lawrence J. Appel; Frank M. Sacks; Vincent J. Carey; Eva Obarzanek; Janis F.
>>Swain; Edgar R. Miller III; Paul R. Conlin; Thomas P. Erlinger; Bernard A.
>>Rosner; Nancy M. Laranjo; Jeanne Charleston; Phyllis McCarron; Louise M.
>>Bishop; for the OmniHeart Collaborative Research Group
>>JAMA. 2005;294:2455-2464.
>><http://jama.ama-assn.org/cgi/content/abstract/294/19/2455>
>>
>Here's another useful article:
>
>Walter C Willett, MD, DrPH
>Concepts and Controversies on Diet: Stop Recommending Low-Fat Diets!
><http://xnet.kp.org/permanentejournal/sum03/concepts.html>
Related articles:
Jeppesen J, Schaaf P, Jones C, Zhou MY, Chen YD, Reaven GM.
Effects of low-fat, high-carbohydrate diets on risk factors for ischemic
heart disease in postmenopausal women.
Am J Clin Nutr. 1997 Apr;65(4):1027-33. Erratum in: Am J Clin Nutr 1997
Aug;66(2):437.
PMID: 9094889 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9094889>
<http://www.ajcn.org/cgi/reprint/65/4/1027> (free full text)
Katan MB, Grundy SM, Willett WC.
Should a low-fat, high-carbohydrate diet be recommended for everyone? Beyond
low-fat diets.
N Engl J Med. 1997 Aug 21;337(8):563-6; discussion 566-7. No abstract
available.
PMID: 9262504 [PubMed - indexed for MEDLINE]
<http://content.nejm.org/cgi/content/extract/337/8/562>
<http://content.nejm.org/cgi/content/full/337/8/562> (not free)
Katan MB.
Effect of low-fat diets on plasma high-density lipoprotein concentrations.
Am J Clin Nutr. 1998 Mar;67(3 Suppl):573S-576S. Review.
PMID: 9497172 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9497172>
<http://www.ajcn.org/cgi/reprint/67/3/573S> (free)
--
Matti Narkia
Matti Narkia
(Larry Weisenthal)" <runn...@aol.com> wrote:
>>From Matti ->
>
>>>Yep. What gave me up? My use of english language, my name, my ISP, or
>googling usenet groups for my posting history? :-) <<
>
>None of the above.
The reason I asked about googling usenet groups is that by doing that
appropriately you can within seconds find messages in Finnish language by
me:
--
Matti Narkia
Matti Narkia
<nmldq1ds9abogcva0...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>30 Nov 2005 15:37:25 -0800 in article
><1133393845.3...@o13g2000cwo.googlegroups.com> "runn...@aol.com
>(Larry Weisenthal)" <runn...@aol.com> wrote:
>
>>High quality editorial review in the November 2005 issue of Patient
>>Care.
>>
>>http://www.patientcareonline.com/patcare/article/articleDetail.jsp?id=197815#
>>
>The title of the article is "VIEWPOINT: Very-low-fat diets are superior to
>low-carbohydrate diets". The article just does not deliver what the title
>promises. Reasons:
>
>1) The scope of the article is very limited: it only discusses weight loss
>diets. Other health aspects don't get much attention. I did not for example
>find anything about the effects on type 2 diabetes, which was Susan's
>concern, but perhaps I just browsed through the article too quickly.
>
>2) Most of the article concentrated in critisizing successful low
>carbyhodrate weight loss trials with.
>
>3) No _evidence_ for the claimed superiority of the very-low-fat diet was
>given.
>
>4) No long term health effects were discussed.
>
>5) The article's bias shows in that it does not mention any of the articles
>which find no association between dietary fat and body fat. Below some
>examples of these:
>
AHA does not like very-low-fat diets either:
Krauss RM, Eckel RH, Howard B, Appel LJ, Daniels SR, Deckelbaum RJ, Erdman
JW Jr, Kris-Etherton P, Goldberg IJ, Kotchen TA, Lichtenstein AH, Mitch WE,
Mullis R, Robinson K, Wylie-Rosett J, St Jeor S, Suttie J, Tribble DL,
Bazzarre TL.
AHA Dietary Guidelines: revision 2000: A statement for healthcare
professionals from the Nutrition Committee of the American Heart
Association.
Circulation. 2000 Oct 31;102(18):2284-99.
PMID: 11056107 [PubMed - indexed for MEDLINE]
<http://circ.ahajournals.org/cgi/content/full/102/18/2284>
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11056107>
"Very-Low-Fat Diets
Although in certain individuals under physician supervision,
very-low-fat diets may lead to weight loss and improved lipid
profiles,143 144 145 they are not recommended for the general
population for several reasons. First, results of randomized
trials show that weight loss is not sustained.143 146 Second,
in extreme cases, very-low-fat diets may lead to nutritional
inadequacies for essential fatty acids. Third, very-low-fat
diets are often associated with the use of processed low-fat
foods that are calorie dense.147 Finally, in individuals with
certain metabolic disorders associated with increased coronary
disease risk, namely low HDL cholesterol, high triglyceride,
and high insulin levels, a very-low-fat diet can amplify these
abnormalities,148 149 150 and other more appropriate dietary
approaches are indicated, as described above."
References cited in the above excerpt:
Lichtenstein AH, Van Horn L.
Very low fat diets.
Circulation. 1998;98:935–939.
<http://circ.ahajournals.org/cgi/content/full/98/9/935>
144. Kasim-Karakas SE, Almario RU, Mueller WM, et al.
Changes in plasma lipoproteins during low-fat, high-carbohydrate diets:
effects of energy intake. Am J Clin Nutr.. 2000;71:1439–1447.
<http://www.ajcn.org/cgi/content/abstract/71/6/1439>
<http://www.ajcn.org/cgi/content/full/71/6/1439>
145. Lichtenstein AH, Ausman LM, Carrasco W, et al.
Short-term consumption of a low-fat diet beneficially affects plasma lipid
concentrations only when accompanied by weight loss: hypercholesterolemia,
low-fat diet, and plasma lipids. Arterioscler Thromb. 1994;14:1751–1760.
<http://atvb.ahajournals.org/cgi/content/abstract/14/11/1751>
146. Sheppard L, Kristal AR, Kushi LH.
Weight loss in women participating in a randomized trial of low-fat diets.
Am J Clin Nutr. 1991;54:821–828.
<http://www.ajcn.org/cgi/content/abstract/54/5/821>
147. Rolls BJ, Shide DJ. The influence of dietary fat on food intake and
body weight.
Nutr Rev. 1992;50:283–290.
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=1436763&dopt=Abstract>
148. Kris-Etherton PM, Pearson TA, Wan Y, et al.
High-monounsaturated fatty acid diets lower both plasma cholesterol and
triacylglycerol concentrations.
Am J Clin Nutr. 1999;70:1009–1015.
<http://www.ajcn.org/cgi/content/abstract/70/6/1009>
<http://www.ajcn.org/cgi/content/full/70/6/1009>
149. Kasim-Karakas SE, Almario RU, Mueller WM, et al.
Changes in plasma lipoproteins during low-fat, high-carbohydrate diets:
effects of energy intake.
Am J Clin Nutr. 2000;71:1439–1447.
<http://www.ajcn.org/cgi/content/abstract/71/6/1439>
<http://www.ajcn.org/cgi/content/full/71/6/1439>
150. Chen YD, Coulston AM, Zhou MY, et al.
Why do low-fat high-carbohydrate diets accentuate postprandial lipemia in
patients with NIDDM?
Diabetes Care. 1995;18:10–16.
<http://care.diabetesjournals.org/cgi/content/abstract/18/1/10>
--
Matti Narkia
Matti Narkia
<ls3eq1tga274dah47...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
A case report:
Piper CM, Carroll PB, Dunn FL.
Diet-induced essential fatty acid deficiency in ambulatory patient with type
I diabetes mellitus.
Diabetes Care. 1986 May-Jun;9(3):291-3.
PMID: 3731994 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3731994>
"We report a case of symptomatic essential fatty acid
deficiency (EFAD) occurring in a free-living individual with
type I diabetes mellitus who was voluntarily following a high-
carbohydrate, fat-restricted diet. The patient was 43 yr old
with type I diabetes for 18 yr and no chronic complications.
His self-imposed diet excluded all red meats, fats, and oils.
After several months of this diet, the patient developed
lethargy and a pruritic, diffuse, scaly, and erythematous rash.
Biochemical studies revealed a mildly elevated SGOT and
abnormally low levels of linoleic, linolenic, and arachidonic
fatty acids. Treatment with linoleic acid supplementation in
his diet improved the rash, normalized SGOT, and corrected the
fatty acid profile. We conclude that EFAD may occur in a free-
living individual after consuming a very-low-fat diet."
--
Matti Narkia
Matti Narkia
<1134617364....@g44g2000cwa.googlegroups.com> "runn...@aol.com
(Larry Weisenthal)" <runn...@aol.com> wrote:
>
>But I have no problem eating baked or mashed potatoes, or popcorn, or
>chewy white flour bagels, or al dente pasta, or chewy Italian bread.
>I'll even have make a supper out of a mixed salad, couple of baked
>potatoes, and some broccoli or spinach, along with a big glass of
>non-fat milk. Then a nightly late night snack of unsweetened mixed
>berries, mainly because I like them and only secondarily for the remote
>chance that the anti-oxidants might be of tangible benefit.
>
Broccoli and spinach are low carb, so are many berries. Restricting
carbohydrates does not mean giving up plant food. Mainly you have to watch
starches such as potatoes, rice and grain products.
Available carbohydrate in some food items:
50 vegetables in the order of their available carbohydrate content from
lowest to highest
<http://www.fineli.fi/topfoods.php?compid=2034&fuclass=vegfresh&specdiet=none&items=50&from=bottom&portion=100g&lang=en>
40 fruit in the order of their available carbohydrate content from lowest to
highest
<http://www.fineli.fi/topfoods.php?compid=2034&fuclass=frufresh&specdiet=none&items=40&from=bottom&portion=100g&lang=en>
Berries in the order of their available carbohydrate content from lowest to
highest
<http://www.fineli.fi/topfoods.php?compid=2034&fuclass=berfresh&specdiet=none&items=40&from=bottom&portion=100g&lang=en>
Mushrooms in the order of their carbohydrate content from lowest to highest
<http://www.fineli.fi/topfoods.php?compid=2034&fuclass=mushrdi&specdiet=none&items=40&from=bottom&portion=100g&lang=en>
Legumes in the order of their carbohydrate content from lowest to highest
<http://www.nutritiondata.com/foods-016000000000005000000-w.html>
Nuts and seeds in the order of their carbohydrate content from lowest to
highest
<http://www.nutritiondata.com/foods-012000000000005000000-w.html>
Fish in the order of their available carbohydrate content from lowest to
highest
<http://www.fineli.fi/topfoods.php?compid=2034&fuclass=fish&specdiet=none&items=100&from=bottom&portion=100g&lang=en>
>No, I don't think that any of the above are "toxic," even to a minor
>degree....for me. I presume that I'm descended from people who ate a
>lot of grains and potatoes and didn't have a problem with it. I'm half
>Finnish and I don't have a hint of lactose intolerance, so I can drink
>a quart of non fat milk per day, if I like. And I have the genetics to
>thrive on it.
>
I'm full Finnish and I can drink milk too, but I don't, I prefer yogurt and
cheese, which seem to be healthier choices that milk and butter ;-). My wife
is not of Finnish origin and she is lactose intolerant, but she can eat
cheese. Finns can tolerate milk, and most of them drink it, or at least used
to, but I'm not sure, if it is good for them, because Finland's coronary
mortality used to be among highest in the world, perhaps the highest (at
least in the Seven Countries Study it was the highest of the countries
included). It has come down quite a bit during last 40 years or so, but
think it is still relatively high.
As for cheese, it is low carbo, and to my knowledge perhaps the only milk
product which has never been associated with coronary heart disease (at
least not when used in moderation; a dose makes a poison).
>Other people probably would have problems with my diet. So I am not
>out to get everyone to eat the way I do.
>
>What people should do is to monitor their weight, and lipids, and blood
>pressure, and bowel movements, and whatever else concerns them and find
>some sort of diet that consists of foods they like to eat and which
>keeps their various health related parameters where they want them to
>be.
>
But these measurements don't tell everything. For example, In the Seven
Countries Study started in 60s, Cretans had by far the lowest coronary
mortality of all the countries included, although their cholesterol was
higher than in the countries with higher coronary mortality. See
Bruno Simini.
Serge Renaud: from French paradox to Cretan miracle
Lancet, Volume 355, Number 9197, 01 January 2000
<http://www.thelancet.com/journals/lancet/article/PIIS0140673605719905/fulltext>
"Then, “when I saw the results of the Seven Countries
Study in 1980”, he recalls, “I thought, Cretans must be
doing—or eating—something right”. Crete had by far the
lowest coronary mortality of the countries studied. Yet,
serum cholesterol concentrations were higher in Crete
than in other countries with higher coronary mortalities.
“Something protects Cretans which does not reduce their
cholesterol”, proposed Renaud.
Renaud guessed that the difference was a-linolenic acid
and set up the Lyon Diet Heart Study in 1985, a secondary
prevention trial. Overall, deaths and cardiovascular
events were reduced by at least 70%, with the protective
effect occurring within 2 months. This study, which was
published in The Lancet in 1994, was initially rejected
by the New England Journal of Medicine because the
“intervention induced no changes in serum lipids”, a fact
that left the referees “wondering how such a large
mortality reduction could have possibly been achieved”.
Renaud's answer is simple. The participants in the Lyon
study ate like Cretans: no butter, cream, or milk; lots
of vegetables, fruit, bread, and cereals; and little
meat. For the study, Renaud designed a margarine similar
in composition to olive oil, but enriched in a-linolenic
acid. Patients ate cheese (“a 9000 year old invention not
linked to coronary disease”) and, of course, drank wine.
Other linolenic acid-rich ingredients of the Cretan
diet—walnuts, snails, and purslane—were replaced by his
margarine. Although linolenic acid's protective effects
have been corroborated in other studies, Ducimetière
warns that “the extraordinary [Lyon] results await
confirmation”."
References related to Lyon Diet Heart Study:
de Lorgeril M, Renaud S, Mamelle N, Salen P, Martin JL, Monjaud I, Guidollet
J, Touboul P, Delaye J.
Mediterranean alpha-linolenic acid-rich diet in secondary
prevention of coronary heart disease.
Lancet. 1994 Jun 11;343(8911):1454-9. Erratum in: Lancet 1995 Mar
18;345(8951):738.
PMID: 7911176 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=7911176&dopt=Abstract>
Renaud S, de Lorgeril M, Delaye J, Guidollet J, Jacquard F, Mamelle N,
Martin JL, Monjaud I, Salen P, Toubol P.
Cretan Mediterranean diet for prevention of coronary heart disease.
Am J Clin Nutr. 1995 Jun;61(6 Suppl):1360S-1367S.
PMID: 7754988 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7754988&dopt=Abstract>
"As a result of the Seven Countries Study, the
Mediterranean diet has been popularized as a healthy
diet. Nevertheless, it has not replaced the prudent diet
commonly prescribed to coronary patients. Recently, we
completed a secondary, randomized, prospective prevention
trial in 605 patients recovering from myocardial
infarction in which we compared an adaptation of the
Cretan Mediterranean diet with the usual prescribed diet.
After a mean follow-up period of 27 mo, recurrent
myocardial infarction, all cardiovascular events, and
cardiac and total death were significantly decreased by >
70% in the group consuming the Mediterranean diet. These
protective effects were not related to serum
concentrations of total, low-density-lipoprotein (LDL),
or high-density-lipoprotein (HDL) cholesterol. In
contrast, protective effects were related to changes
observed in plasma fatty acids: an increase in n-3 fatty
acids and oleic acid and a decrease in linoleic acid that
resulted from higher intakes of linolenic and oleic
acids, but lower intakes of saturated fatty acids and
linoleic acid. In addition, higher plasma concentrations
of antioxidant vitamins C and E were observed. We
conclude that a Cretan Mediterranean diet adapted to a
Western population protected against coronary heart
disease much more efficiently than did the prudent diet.
Thus, it appears that the favorable life expectancy of
the Cretans could be largely due to their diet."
Michel de Lorgeril, MD; Patricia Salen, BSc; Jean-Louis Martin, PhD;
Isabelle Monjaud, BSc; Jacques Delaye, MD; Nicole Mamelle, PhD
Mediterranean Diet, Traditional Risk Factors, and the Rate of
Cardiovascular Complications After Myocardial Infarction
Final Report of the Lyon Diet Heart Study
Circulation. 1999;99:779-785
<http://circ.ahajournals.org/cgi/content/full/99/6/779>
Leaf, A.
Dietary Prevention of Coronary Heart Disease.
The Lyon Diet Heart Study.
Circulation 99: 733-735
<http://circ.ahajournals.org/cgi/content/full/99/6/733>
--
Matti Narkia
Matti Narkia
<o27eq19df003164ij...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>
>As for cheese, it is low carb, and to my knowledge perhaps the only milk
>product which has never been associated with coronary heart disease (at
>least not when used in moderation; a dose makes a poison).
>
unsweetened and low-fat. And lactid acid bacteria in it may do some good.
Still, Greek eat high fat yogurt (up to 10% of fat) and it doesn't seem to
harm them, when looking at their coronary mortality rates. But perhaps they
would be even better, if they switched to low or no fat. :-)
--
Matti Narkia
Matti Narkia
<1134693365.3...@g47g2000cwa.googlegroups.com> "runn...@aol.com
(Larry Weisenthal)" <runn...@aol.com> wrote:
>>>You said that you hate it when people use their own personal diet anecdotes to declare that it is the way things are, and you also went on at length about your personal experience with the Pritikin diet.<<
>
>The anecdotes were being used for two different things. I used an
>anecdote to buttress my claim that, despite currently conventional
>wisdom, high carbohydrate diets are not toxic for everyone and may even
>be helpful for certain people (in this case me). I was very careful to
>emphasize that my own, personal experience may not be broadly
>generalizable, and I offered my opinion that my own unique genetics may
>make such a diet work for me. Even Barry Sears, in his original Zone
>Diet book (trashing the ultra low fat approach) said that (based on
>what, he didn't say) about 25% of people seem to do OK on such diets.
>I'm not even arguing for a percentage (what is the "lowest common
>denominator" diet which works of the most people). I was just arguing
>that the number was certainly above ZERO, based on my own described
>anecdotal experience.
>
I can agree with that. But, if the number is above zero, but still would
represent only a small minority of the whole population, is there a valid
reason to recommend such a diet, and even claim its superiority?
--
Matti Narkia
Matti Narkia
>> unsweetened and low-fat.
>
>
For low carbers, probably, I'm not sure if the same is valid for moderate or
high carbers.
>
> And lactid acid bacteria in it may do some good.
>> Still, Greek eat high fat yogurt (up to 10% of fat) and it doesn't seem to
>> harm them, when looking at their coronary mortality rates. But perhaps they
>> would be even better, if they switched to low or no fat. :-)
>>
>
>HMG-CoA, the target of statin drugs.
>
I tried not to overstate my point ;-). Seems that I managed to understate it
:-). Actually, I posted today some references showing that some selected
probiotic cultures may lower LDL, inhibit oxidation of LDL, raise HDL and
lower blood pressure. But all this may not be achieved with one culture or
type of yogurt. In fact, the most common yogurt cultures didn't seem to be
the most promising ones in the studies I browsed.
--
Matti Narkia
Matti Narkia
>
>I haven't furnished them because he said *he* would, over and over and
>over and over... I said I'd wait for his good evidence of the salutary
>effect of very high carb low fat for type 2 diabetes before critiquing.
>His unwillingness to post the Pritikin studies may mean he's looked at
>them, too, and found a minor effect, all of which can be attributed to
>exercise overcoming some of the damage done to diabetics by the diet.
>
diabetes, references are below. As expected they suggest positive effect. It
may indeed be impossible to differentiate between the effects of exercise
and diet in a combined regimen.
Henriksen EJ.
Exercise training and the antioxidant alpha-lipoic acid in the treatment of
insulin resistance and type 2 diabetes.
Free Radic Biol Med. 2006 Jan 1;40(1):3-12.
PMID: 16337874 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16337874>
Cauza E, Hanusch-Enserer U, Strasser B, Kostner K, Dunky A, Haber P.
Strength and endurance training lead to different post exercise glucose
profiles in diabetic participants using a continuous subcutaneous glucose
monitoring system.
Eur J Clin Invest. 2005 Dec;35(12):745-51.
PMID: 16313250 [PubMed - in process]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16313250>
Sigal RJ, Kenny GP, Wasserman DH, Castaneda-Sceppa C.
Physical activity/exercise and type 2 diabetes.
Diabetes Care. 2004 Oct;27(10):2518-39. Review.
PMID: 15451933 [PubMed - indexed for MEDLINE]
<http://care.diabetesjournals.org/cgi/content/full/27/10/2518>
Boule NG, Haddad E, Kenny GP, Wells GA, Sigal RJ.
Effects of exercise on glycemic control and body mass in type 2 diabetes
mellitus: a meta-analysis of controlled clinical trials.
JAMA. 2001 Sep 12;286(10):1218-27. Review.
PMID: 11559268 [PubMed - indexed for MEDLINE]
<http://jama.ama-assn.org/cgi/content/full/286/10/1218>
--
Matti Narkia
Matti Narkia
>> diabetes, references are below. As expected they suggest positive effect. It
>> may indeed be impossible to differentiate between the effects of exercise
>> and diet in a combined regimen.
>
>helped. The bg numbers were very bad, and they chose to withdraw meds
>anyhoo, too, just so they could say they did.
>
I found these two very old studies co-authored by Pritikin about the
combined regimen:
Barnard RJ, Massey MR, Cherny S, O'Brien LT, Pritikin N.
Long-term use of a high-complex-carbohydrate, high-fiber, low-fat diet and
exercise in the treatment of NIDDM patients.
Diabetes Care. 1983 May-Jun;6(3):268-73.
PMID: 6307614 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6307614>
Barnard RJ, Lattimore L, Holly RG, Cherny S, Pritikin N.
Response of non-insulin-dependent diabetic patients to an intensive program
of diet and exercise.
Diabetes Care. 1982 Jul-Aug;5(4):370-4.
PMID: 7151652 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7151652>
I wonder if the full texts are available somewhere to check about
methodology? Any other related studies?
Here's a diet only low fat study
Nicholson AS, Sklar M, Barnard ND, Gore S, Sullivan R, Browning S.
Toward improved management of NIDDM: A randomized, controlled, pilot
intervention using a lowfat, vegetarian diet.
Prev Med. 1999 Aug;29(2):87-91.
PMID: 10446033 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10446033>
Strangely enough, they had decided to compare two low fat diets: a vegan on
and conventional one. Conclusion:
"CONCLUSION: The use of a low-fat, vegetarian diet in patients with
NIDDM was associated with significant reductions in fasting serum
glucose concentration and body weight in the absence of recommendations
for exercise. A larger study is needed for confirmation."
Very funny ;-). Why on earth they didn't have control group with higher fat
content?
--
Matti Narkia
Enrico C
<news:40on9cF...@individual.net> on sci.med.nutrition :
> x-no-archive: yes
>
> Matti Narkia wrote:
>
>> Well, I think that yogurt is pretty safe as well as long as it is
>> unsweetened and low-fat.
>
> Full fat is better, and just as healthy.
I like both kinds, low and full fat (unsweetened) yogurts, and have
one or the other according to appetite, but I find the full fat more
satiating, so I end up eating less when I have the full fat.
Speaking of fat, these days I feel like eating more fat than usual
(and fewer carbs and protein): I mean foods such as olive oil, fat
fish, nuts, dark chocolate, even fresh whipped cream... I guess it
must be the cold wheather! :)
--
Enrico C
* cut the ending "cut-togli.invalid" string when replying by email *
Matti Narkia
<gtaeq1l6m7glsbpou...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
Here's one that I didn't post today:
Naruszewicz M, Johansson ML, Zapolska-Downar D, Bukowska H.
Effect of Lactobacillus plantarum 299v on cardiovascular disease risk
factors in smokers.
Am J Clin Nutr. 2002 Dec;76(6):1249-55.
PMID: 12450890 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/76/6/1249>
There are some functional food products based on this bacterium. There's
some info about them on the page
<http://www.probi.com/standard.asp?id=1&lang=1>
--
Matti Narkia
Matti Narkia
<u3jeq11qptkb0b4sg...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>>>
>>I tried not to overstate my point ;-). Seems that I managed to understate it
>>:-). Actually, I posted today some references showing that some selected
>>probiotic cultures may lower LDL, inhibit oxidation of LDL, raise HDL and
>>lower blood pressure. But all this may not be achieved with one culture or
>>type of yogurt. In fact, the most common yogurt cultures didn't seem to be
>>the most promising ones in the studies I browsed.
>
>Here's one that I didn't post today:
>
>Naruszewicz M, Johansson ML, Zapolska-Downar D, Bukowska H.
>Effect of Lactobacillus plantarum 299v on cardiovascular disease risk
>factors in smokers.
>Am J Clin Nutr. 2002 Dec;76(6):1249-55.
>PMID: 12450890 [PubMed - indexed for MEDLINE]
><http://www.ajcn.org/cgi/content/full/76/6/1249>
>
is that Lactobacillus plantarum 299v is not to my knowledege used to make
yogurt. Lactobacillus plantarum is found in fermented foods of plant origin.
Here's a review about it:
Molin G.
Probiotics in foods not containing milk or milk constituents, with special
reference to Lactobacillus plantarum 299v.
Am J Clin Nutr. 2001 Feb;73(2 Suppl):380S-385S. Review.
PMID: 11157345 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/2/380S>
--
Matti Narkia
runnswim@aol.com (Larry Weisenthal)
Larry maintains that a Pritikin-type diet is healthful for many people
with Type II diabetes. Susan (and others) argue that it is unhealthful
(I presume Susan would maintain for virtually all) people with Type II
diabetes.
I will present my side of the argument in three parts, over the next
three days.
1. Direct evidence supporting my claim.
2. Explanation of why alleged evidence contradicting my claim is bogus.
3. Consideration of physiologic principles which indicate that my claim
is not only plausible, but also likely to be true.
I began by going through my files, but I was pleasantly surprised to
find a very comprehensive (409 peer-reviewed references, including 253
links to free, full text peer reviewed publications) and recent
(updated December 15, 2005) invited review published in the Journal of
Applied Physiology, by two well-published UCLA researchers.
Roberts, CK and Barnard (no, not the notorious PETA Barnard), R.J.
Effects of exercise and diet on chronic disease. J. Appl. Physiol.
98:3-30, 2005.
http://jap.physiology.org/cgi/content/full/98/1/3
The article costs $8.00 (which is a relative bargain in an era where
most journals charge $30 per article, and considering also that it does
contain 253 links to - free - recent, pertinent references).
This article is focused on the combined role of diet and exercise in
the genesis and treatment of coronary artery disease, hypertension,
diabetes, the metabolic syndrome, and cancer. It is particularly
pertinent to this debate, because it includes a detailed review of
studies of the Pritikin diet and exercise program in the setting of
Type II diabetes (as well as in heart disease and hyertension).
The Pritikin studies consisted largely of 26 day residential diet and
exercise intervention. Food consumption is ad libitum, and contains
10-15% calories as fat, 15-20% calories as protein, and 65-75% calories
as carbohydrate. The latter is in the form of high-fiber, whole grains
(5 or more servings per day), vegetables (4 or more servings), and
fruits (3 or more servings). Protein derives from plants, non-fat
dairy, and fish or chicken. It contains < 100 mg of dietary
cholesterol, and prohibits alcohol, tobacco, and caffeinated beverages.
The program also consists of 45 minutes to one hour per day of exercise
(treadmill) at which the heart rate is maintained at 70-85% of the
maximal heart rate obtained during a formal pre-enrollment treadmill
examination. Subjects also perform some resistance training.
All of the important publications were researched and written not by
Pritikin employees, but by independent UCLA researchers who had no
conflicts of interest. The Pritikin center was located in Santa Monica
(it has since moved to South Florida), in close proximity to the UCLA
medical school, facilitating the research.
Dealing ONLY with the diabetes data, 864 subjects were studied. There
were, overall, marked improvements in serum glucose, serum insulin,
blood pressure, triglycerides, and requirements for oral hypoglycemics
and insulin injections.
In a follow-up study (2 - 3 years post discharge), serum glucose remain
unchanged (markedly improved) in subjects continuing to adhere to the
program. However, in subjects who abandoned the program, medications
had been re-started.
These data (published in first rate journals) have never been
challenged or refuted.
I've got to go home and make dinner (two daughters home from college).
I'm making Italian style fish in red sauce, al dente pasta, salad,
vegetable, hearty Italian bread, and non-fat milk for the girls; a
glass of wine plus the milk for me.
Tomorrow I'll tell you the fatal flaws behind the studies that have
been cited to challenge the notion that high carbohydrate diets can,
indeed, be healthy for people with Type II diabetes.
- Larry W
runnswim@aol.com (Larry Weisenthal)
>>The reason I asked about googling usenet groups is that by doing that
appropriately you can within seconds find messages in Finnish language
by
me: <<
I'll do that.
I probably ought to e-mail you privately. My grandfather (Jacob Rautio)
was a (large animal/farm) veterinarian. He invented some bovine (cow)
obstetrical devices which were used for some time by him and his
colleagues and perhaps others (I don't know). His wife (my
grandmother) transcribed for him a beautifully illustrated, hand
written handbook on the topic of bovine veterinary science, which
included pictures of his inventions and how to use them. I'd like to
get in contact with someone in Finland about it (since it's all written
in Finnish, which I can't read). I'd scan it into a PDF file. It
might be of interest to someone in a Finnish university - perhaps for
several purposes.
- Larry W
Matti Narkia
<gtaeq1l6m7glsbpou...@4ax.com> Matti Narkia <nar...@yahoo.com>
wrote:
>Mon, 19 Dec 2005 16:33:34 -0500 in article <40on9cF...@individual.net>
I happen to have a collection of review articles about probiotics and
prebiotics. Here is the list of them with links;
Snelling AM.
Effects of probiotics on the gastrointestinal tract.
Curr Opin Infect Dis. 2005 Oct;18(5):420-6. Review.
PMID: 16148529 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16148529>
Meurman JH.
Probiotics: do they have a role in oral medicine and dentistry?
Eur J Oral Sci. 2005 Jun;113(3):188-96. Review.
PMID: 15953242 [PubMed - indexed for MEDLINE]
<http://www.blackwell-synergy.com/doi/abs/10.1111/j.1600-0722.2005.00191.x>
Salminen SJ, Gueimonde M, Isolauri E.
Probiotics that modify disease risk.
J Nutr. 2005 May;135(5):1294-8. Review.
PMID: 15867327 [PubMed - indexed for MEDLINE]
<http://www.nutrition.org/cgi/content/abstract/135/5/1294>
Jenkins B, Holsten S, Bengmark S, Martindale R.
Probiotics: a practical review of their role in specific clinical scenarios.
Nutr Clin Pract. 2005 Apr;20(2):262-70. Review.
PMID: 16207661 [PubMed - indexed for MEDLINE]
<http://ncp.aspenjournals.org/cgi/content/abstract/20/2/262>
Bengmark S, Martindale R.
Prebiotics and synbiotics in clinical medicine.
Nutr Clin Pract. 2005 Apr;20(2):244-61. Review.
PMID: 16207660 [PubMed - indexed for MEDLINE]
<http://ncp.aspenjournals.org/cgi/content/abstract/20/2/244>
Gill HS, Guarner F.
Probiotics and human health: a clinical perspective.
Postgrad Med J. 2004 Sep;80(947):516-26. Review.
PMID: 15356352 [PubMed - indexed for MEDLINE]
<http://pmj.bmjjournals.com/cgi/content/full/80/947/516>
Hamilton-Miller JM.
Probiotics and prebiotics in the elderly.
Postgrad Med J. 2004 Aug;80(946):447-51. Review.
PMID: 15299153 [PubMed - indexed for MEDLINE]
<http://pmj.bmjjournals.com/cgi/content/full/80/946/447>
Isolauri E.
Dietary modification of atopic disease: Use of probiotics in the prevention
of atopic dermatitis.
Curr Allergy Asthma Rep. 2004 Jul;4(4):270-5. Review.
PMID: 15175140 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15175140>
Marelli G, Papaleo E, Ferrari A.
Lactobacilli for prevention of urogenital infections: a review.
Eur Rev Med Pharmacol Sci. 2004 Mar-Apr;8(2):87-95. Review.
PMID: 15267122 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15267122>
Reid G, Bruce AW.
Urogenital infections in women: can probiotics help?
Postgrad Med J. 2003 Aug;79(934):428-32. Review.
PMID: 12954951 [PubMed - indexed for MEDLINE]
<http://pmj.bmjjournals.com/cgi/content/full/79/934/428>
Takano T.
Anti-hypertensive activity of fermented dairy products containing biogenic
peptides.
Antonie Van Leeuwenhoek. 2002 Aug;82(1-4):333-40. Review.
PMID: 12369200 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12369200>
Lactobacillus sporogenes.
Altern Med Rev. 2002 Aug;7(4):340-2. Review.
PMID: 12197786 [PubMed - indexed for MEDLINE]
<http://www.thorne.com/altmedrev/.fulltext/7/4/340.pdf>
D'Souza AL, Rajkumar C, Cooke J, Bulpitt CJ.
Probiotics in prevention of antibiotic associated diarrhoea: meta-analysis.
BMJ. 2002 Jun 8;324(7350):1361. Review.
PMID: 12052801 [PubMed - indexed for MEDLINE]
<http://bmj.bmjjournals.com/cgi/content/full/324/7350/1361>
<http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=12052801>
Marteau PR.
Probiotics in clinical conditions.
Clin Rev Allergy Immunol. 2002 Jun;22(3):255-73. Review.
PMID: 12043384 [PubMed - indexed for MEDLINE]
<http://www.humanapress.com/ArticleDetail.pasp?issn=1080-0549&acode=CRIAI:22:3:255>
Delzenne NM, Williams CM.
Prebiotics and lipid metabolism.
Curr Opin Lipidol. 2002 Feb;13(1):61-7. Review.
PMID: 11790964 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11790964>
Kaur IP, Chopra K, Saini A.
Probiotics: potential pharmaceutical applications.
Eur J Pharm Sci. 2002 Feb;15(1):1-9. Review.
PMID: 11803126 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11803126>
Pereira DI, Gibson GR.
Effects of consumption of probiotics and prebiotics on serum lipid levels in
humans.
Crit Rev Biochem Mol Biol. 2002;37(4):259-81. Review.
PMID: 12236466 [PubMed - indexed for MEDLINE]
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12236466>
Walker WA.
Introduction
Supplements:Probiotics in Health and Disease
Am J Clin Nutr. 2001 Jun;73(6):1121S-1123S. Review.
<http://www.ajcn.org/cgi/content/full/73/6/1121S>
Isolauri E.
Probiotics in human disease.
Am J Clin Nutr. 2001 Jun;73(6):1142S-1146S. Review.
PMID: 11393192 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/6/1142S>
Saavedra JM.
Clinical applications of probiotic agents.
Am J Clin Nutr. 2001 Jun;73(6):1147S-1151S. Review.
PMID: 11393193 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/6/1147S>
Vanderhoof JA.
Probiotics: future directions.
Am J Clin Nutr. 2001 Jun;73(6):1152S-1155S. Review.
PMID: 11393194 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/6/1152S>
Lu L, Walker WA.
Pathologic and physiologic interactions of bacteria with the
gastrointestinal epithelium.
Am J Clin Nutr. 2001 Jun;73(6):1124S-1130S. Review.
PMID: 11393190 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/6/1124S>
Drouault S, Corthier G.
[Health effects of lactic acid bacteria ingested in fermented milk.]
Vet Res. 2001 Mar-Apr;32(2):101-17. Review. French.
PMID: 11368077 [PubMed - indexed for MEDLINE]
<http://www.edpsciences.org/10.1051/vetres:2001115>
<http://www.edpsciences.org/articles/vetres/pdf/2001/02/v1201.pdf?access=ok>
Supplements:Probiotics and Prebiotics
Am J Clin Nutr. 2001 Feb;73(2 Suppl)
<http://www.ajcn.org/content/vol73/issue2/#SUPPLEMENTS>
Schrezenmeir J, de Vrese M.
Probiotics, prebiotics, and synbiotics--approaching a definition.
Am J Clin Nutr. 2001 Feb;73(2 Suppl):361S-364S. Review.
PMID: 11157342 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/2/361S>
Heller KJ.
Probiotic bacteria in fermented foods: product characteristics and starter
organisms.
Am J Clin Nutr. 2001 Feb;73(2 Suppl):374S-379S. Review.
PMID: 11157344 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/2/374S>
Molin G.
Probiotics in foods not containing milk or milk constituents, with special
reference to Lactobacillus plantarum 299v.
Am J Clin Nutr. 2001 Feb;73(2 Suppl):380S-385S. Review.
PMID: 11157345 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/2/380S>
Dunne C, O'Mahony L, Murphy L, Thornton G, Morrissey D, O'Halloran S, Feeney
M, Flynn S, Fitzgerald G, Daly C, Kiely B, O'Sullivan GC, Shanahan F,
Collins JK.
In vitro selection criteria for probiotic bacteria of human origin:
correlation with in vivo findings.
Am J Clin Nutr. 2001 Feb;73(2 Suppl):386S-392S. Review.
PMID: 11157346 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/2/386S>
Bezkorovainy A.
Probiotics: determinants of survival and growth in the gut.
Am J Clin Nutr. 2001 Feb;73(2 Suppl):399S-405S. Review.
PMID: 11157348 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/2/399S>
Roberfroid MB.
Prebiotics: preferential substrates for specific germs?
Am J Clin Nutr. 2001 Feb;73(2 Suppl):406S-409S. Review.
PMID: 11157349 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/2/406S>
Cummings JH, Macfarlane GT, Englyst HN.
Prebiotic digestion and fermentation.
Am J Clin Nutr. 2001 Feb;73(2 Suppl):415S-420S. Review.
PMID: 11157351 [PubMed - indexed for MEDLINE]
<http://www.ajcn.org/cgi/content/full/73/2/415S>
de Vrese M, Stegelmann A, Richter B, Fenselau S, Laue C, Schrezenmeir J.
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--
Matti Narkia
runnswim@aol.com (Larry Weisenthal)
(from the Journal of Applied Physiology):
Across two studies, Barnard et al. (29, 31) noted that diabetes may be
controlled by lifestyle modification. In 129 patients with diabetes
mellitus, 45 of 54 patients who were on oral hypoglycemic agents
discontinued medication, 26 of 35 patients who were taking insulin were
off medication at discharge, and most of the others had their dosage
reduced. In the first of these studies (29), data were obtained from 60
patients; fasting blood glucose was reduced from 194.9 ± 10.1 to 144.6
± 7.1 mg/dl and maximum work capacity increased from 5.6 ± 0.3 to 7.9
± 0.4 METs. In the second (31), glucose decreased from 180 ± 11 to
134 ± 4, and after a 2- to 3-yr follow-up blood glucose concentration
was unchanged; however, in those who did not adhere to the program,
oral agents were started. In 1992, Barnard et al. (33) documented that,
in individuals with diabetes or insulin resistance, lifestyle
modification significantly reduced hyperinsulinemia, blood pressure,
and hypertriglyceridemia. In the diabetic patients, decreases were
noted in glucose (200 ± 17 to 144 ± 14 mg/dl), insulin (40 ± 15 to
27 ± 11 µU/ml), blood pressure (142 ± 9 to 132 ± 6 mmHg systolic,
83 ± 3 to 71 ± 3 mmHg diastolic), and TG (353 ± 76 to 196 ± 31
mg/dl), and significant reductions were also noted in insulin-resistant
and normal groups (33). In a separate study (30), 70 hypertensive,
diabetic patients had reductions in blood pressure of 141 ± 2/81 ± 2
to 127 ± 2/75 ± 1 mmHg, with 37 of the 61 patients taking
antihypertensive medications having discounted their medications.
Glucose decreased from 198 ± 9 to 152 ± 5 with 20 of 28 discontinuing
oral hypoglycemics and 12 of 27 discontinuing insulin therapy after the
intervention. VO2max increased, and blood pressure at the same relative
work rate decreased from 183 ± 3/84 ± 2 to 161 ± 3/76 ± 1 mmHg. Of
the 4,587 individuals previously discussed (21), 652 patients were
identified with diabetes; 71% of 197 subjects taking oral hypoglycemic
agents and 39% of 212 taking insulin were able to discontinue their
medication. Overall, the combined effect of lifestyle modification on
diabetes over five studies (nb. see below) and 864 subjects is shown in
Fig. 3. These data suggest the need to emphasize lifestyle modification
early in the treatment of diabetes. It should be noted that these
studies were performed when diabetes was defined as fasting glucose
>140 mg/dl.
Barnard RJ, Jung T, and Inkeles SB. Diet and exercise in the treatment
of NIDDM. The need for early emphasis. Diabetes Care 17: 1469-1472,
1994.[Abstract]
Barnard RJ, Lattimore L, Holly RG, Cherny S, and Pritikin N. Response
of non-insulin-dependent diabetic patients to an intensive program of
diet and exercise. Diabetes Care 5: 370-374, 1982.[Abstract]
Barnard RJ, Martin DA, Ugianskis EJ, and Inkeles SB. The effects of an
intensive diet and exercise program on patients with NIDDM and
hypertension. J Cardpulm Rehabil 12: 194-201, 1992.
Barnard RJ, Massey MR, Cherny S, O'Brien LT, and Pritikin N.
Long-term use of a high-complex-carbohydrate, high-fiber, low-fat diet
and exercise in the treatment of NIDDM patients. Diabetes Care 6:
268-273, 1983.[Abstract]
Barnard RJ, Ugianskis EJ, Martin DA, and Inkeles SB. Role of diet and
exercise in the management of hyperinsulinemia and associated
atherosclerotic risk factors. Am J Cardiol 69: 440-444,
1992.[ISI][Medline]
Barnard RJ and Wen SJ. Exercise and diet in the prevention and control
of the metabolic syndrome. Sports Med 18: 218-228,
1994.[ISI][Medline]
>>>>
It should be noted that these studies were largely carried out with
people having very flagrant Type II diabetes (average fasting blood
sugars in the range of 180 - 200 at the time of admission to the
lifestyle intervention program.
I'll address the issue of the relative contributions of exercise and
diet in parts II and III of my little series on this.
- Larry W
runnswim@aol.com (Larry Weisenthal)
carb diets are appropriate for tight blood glucose control and
prevention and reversal of diabetic damage.<<
I'll get there.
- Larry W
runnswim@aol.com (Larry Weisenthal)
interventions studies with studies of people with long established,
advanced disease. Let's keep talking; keeping it objective, I'm
certain that we'll eventually arrive at a common understanding.
- Larry W
runnswim@aol.com (Larry Weisenthal)
Susan, I can't anticipate your questions and objections in advance; I
can only respond to them. Although I am willing to stick with the
subject until I've given my best answers to all questions and responded
to all objections, I have to do this in segments over time.
If you recall, my original statement was that diabetes-related
parameters improved on a high carb diet and exercise program. You've
morphed this into a full fledged debate over the best diet to give to
the average diabetic, when my whole point from the very beginning was
that diets (lke everything else in medicine) should be individualized
and that a high carb diet and exercise program was appropriate for some
(but certainly not all, as I from the beginning accepted your own
personal, anecdotal testimony) type II diabetics.
Now, I'm perfectly willing to stick with this and cover all the issues
over time. I can't sit down and anticipate every question you might
ask or objection you might raise.
For example, we are now (I think) discussing what the literature shows
about the effect of various diet/exercise programs on people who enter
the program with fasting blood sugars in the range of 180-200, despite
virtually all being on either oral agents or insulin upon entry to the
program. With the diet/exercise program not involving adding
additional pharmacologic agents but, in fact, removing such agents in
many cases.
Perhaps, for purposes of comparison, you could cite studies of similar
or superior quality of other diet/exercise programs which have achieved
superior results in this population of diabetic patients.
- Larry W
runnswim@aol.com (Larry Weisenthal)
cites to demonstrate my points, but at this point, you haven't made a
single valid one to refute. <<
I am presuming that you have no data with any other diet/exercise plan
to indicate that one can take a population of patients with fasting
blood sugars in the range of 180-200, with the vast majority being on
oral hypoglycemics or insulin and achieve the same results which were
achieved with the high carb diet and exercise program without the
addition of additional medications and with the subtraction of
medications in a large percentage of cases.
If we can agree on that point, I can move on to the next part of my
discussion. In the end, we'll have covered your objections.
- Larry W
runnswim@aol.com (Larry Weisenthal)
is notable as the only dietary intervention to move diabetics into
target glucose and lipid ranges, *current ones* even with reduction or
cessation of meds. Results that are better than the cutoffs, which are
way too high, for diabetes. <<
Before going on, I'd like to review the study(ies) to which you refer.
Pertaining to established diabetics with FBS 180-200 while on oral meds
or insulin.
I don't need an abstract. I have easy access to full text. Just the
citation(s) (as I provided to you).
- Larry W
runnswim@aol.com (Larry Weisenthal)
that a high fat diet improves diabetes-related parameters in
established, medication-dependent Type II diabetic patients with FBS in
the 180-200 mg% level without the addition of medications to a superior
extent to that which they were improved in the Pritikin studies.
So I infer that she has no such data and I shall proceed with my
presentation, on my own terms and on my own schedule. Those who are
interested may either continue to follow this thread or check back at a
later time, by Google Grouping "runnswim" on the sci.med.nutrition
group and sorting by date.
- Larry W
Matti Narkia
<1135117185.9...@g44g2000cwa.googlegroups.com> "runn...@aol.com
(Larry Weisenthal)" <runn...@aol.com> wrote:
>Susan refuses to back up her assertion that she has data which indicate
>that a high fat diet improves diabetes-related parameters in
>established, medication-dependent Type II diabetic patients with FBS in
>the 180-200 mg% level without the addition of medications to a superior
>extent to that which they were improved in the Pritikin studies.
>
Pritikin studies used combined exercise + diet regime. From other studies we
know that exercise helps in type 2 diabetes. Based on what you have so far
told about us about the Pritikin studies, there is no way we can draw a
conclusion that diet helped, at all.
There so many questions about these studies:
1) Why only combined regimen? Why not to have also diet only (and perhaps
also exercise only) group.
2) Why other kind of healthy anti-diabetic diets such low barb diet were not
included as a different group? Now we don't really know how the Pritikin
diet would have compared with the low carb diet (although from other studies
we can deduct it is worse). Hey, we don't even know, if it helped at all,
perhaps exercise covered its weaknesses?
3) What exactly were the results? Were they satisfactory according to the
current standards in the treatment of type 2 diabetes? Susan seems to think
that they weren't.
I think you have not told us even nearly enough about the Pritikin studies.
If you have access to them, how about posting here the essential parts of
the studies or alternatively making them temporarily visible on a web site
of your choice, so we could read them.
--
Matti Narkia
runnswim@aol.com (Larry Weisenthal)
fight between me and Susan.
If the reader scrolls down to the "<<<<<<<<<<<<<<<<" this will take
him/her to beyond the cat fighting to a discussion which is hopefully
pertinent and helpful to the subject of this thread ("low fat vs low
carb"):
First, the cat fight:
Susan quotes me:
runns...@aol.com (Larry Weisenthal) wrote:
> Susan refuses to back up her assertion that she has data which indicate
> that a high fat diet improves diabetes-related parameters in
> established, medication-dependent Type II diabetic patients with FBS in
> the 180-200 mg% level without the addition of medications to a superior
> extent to that which they were improved in the Pritikin studies.
Susan retorts:
>>First of all, to whom are you speaking, the masses your narcissm leads
you to believe are hanging on breathlessly?
>Second of all, that was not our discussion, and I will not play this
meaningless game with you.
Not our discussion? "Meaningless game?" I don't think so...
Let's first look at the way you quoted me:
runns...@aol.com (Larry Weisenthal) wrote:
> I am presuming that you have no data with any other diet/exercise plan
> to indicate that one can take a population of patients with fasting
> blood sugars in the range of 180-200, with the vast majority being on
> oral hypoglycemics or insulin and achieve the same results which were
> achieved with the high carb diet and exercise program without the
> addition of additional medications and with the subtraction of
> medications in a large percentage of cases.
> If we can agree on that point, I can move on to the next part of my
> discussion. In the end, we'll have covered your objections.
> - Larry W
You responded by saying:
>>No, I only have ones with much, much better results. <<
So this clearly WAS part of our discussion. You made a specific claim.
I asked, respectfully, for one or more references supporting this
claim; so that I might read them and perhaps learn something that I
didn't know. I've learned a lot by participating in Usenet discussion
groups. But you appear to be uninterested in participating in a
discussion. What you are interested in is difficult to say.
Discrediting me as a person (unlike you, I'm a real person, with a real
name, a real reputation, a real family, a real career, a real
business)?
Look, you made a direct statement (see above). When I ask for
references (note you say "ones" -- meaning plural, relating to studies,
meaning more than one study), you refuse -- twice -- to provide them
and instead continue to attack me on a personal level. How is this
helpful? Why do you make claims that you won't support? If you didn't
want to "go down a bunny trail," then why did you make the claim?
You also made the following statement:
>>My whole point that there is absolutely never an instance in which a
high carb diet is appropriate for a type 2 diabetic. <<
This statement is breathtaking in its scope and certitude. My own
claims were far more modest. I claimed that diet, as in the case of
virtually all other medical interventions, must be individualized.
For example, you state (above) that "there is absolutely never an
instance in which a high carb diet is appropriate for a type 2
diabetic."
Yet I provided data which I believe (until you are finally willing to
provide evidence which you claim to have, but are unwilling to cite)
are unprecedented, examining established, medication-dependent
diabetics, with fasting blood sugars averaging 180-200, showing
substantial improvements in blood sugar, serum insulin, blood pressure,
serum lipids, etc. I am unable to find studies in which exercise alone
produced these degrees of improvement in all of the above parameters in
these types of diabetics.
So it is possible to infer that the high carb diet, in the presence of
the exercise program (to be discussed in my response to the pertinent
and helpful questions of Matti, below) was indeed highly appropriate
for some of the people in the study (presuming that some people did not
benefit, possibly because of the same genetic or other factors shared
by Susan, then the magnitude of benefit for those who did benefit was
even more impressive).
So Susan's contention that high carb diets are NEVER appropriate for a
Type II diabetic would seem to be over-reaching. Susan has stated that
she favors the high fat diet approach. Even were it to be shown that a
high fat diet was superior, on average, to a low fat/high carb diet and
exercise program, there are simply a great many people who will not
follow a life-long high fat diet because they don't like it, or who
have a strong family history of cancer and are concerned about the long
term carcinogenic effects of such a diet, or who worry appropriately
about other unanswered questions about such a diet. So are they better
off with NCEP (or whatever) diets (which are "high carb," though less
"high carb" than Pritikin) or no diet at all, than they would be with a
Pritikin-type diet? Based on what?
<<<<<<<<<<<<<<<<
(end of cat fight: on to substance -->)
Let's say, for the sake of argument, that a high fat diet is
"perfection," and that low fat/high carb + exercise is only
"improvement?" But if "perfection" isn't an option for all diabetics,
for a variety of reasons (e.g. see above); then does this mean that
"improvement only" should be eschewed?
I've made a diligent effort to look at the head to head comparisons
between high fat vs high carb for years, and I've spent time in the
past several days looking to see if there's something I missed. Susan,
afterall, said that she has volumes of data and studies proving the
superiority of high fat over high carb. Yet how is it that I can't
find them? Am I really as stupid and inept as Susan makes me out to
be?
Just within the past year are two prospective, randomized studies which
indicate that I'm not so stupid or inept, afterall.
McAuley, et al (Diabetologia, 48:8-16, 2005) randomized
insulin-resistant, obese women to (1) the Atkins Diet, (2) the Zone
Diet, and (3) a high carbohydrate diet. All three diets improved body
mass index, triglycerides, and serum insulin. There were no
differences between the Atkins diet and the "high carb" diet with
respect to fasting glucose, serum insulin, or CRP (for post-prandial
glucose, considered the most important of the glucose-related
parameters in diabetes, see below).
The Atkins Diet produced a greater reduction in fasting triglycerides
(but see below) and a slightly greater reduction in BMI than the "high
carb" diet. On the other hand, the tend line for weight related
parameters was still downsloping for the "high carb" diet at 6 months
than for the Atkins diet, which exhibited more of a plateau by week 8.
ANd 25% of Atkins dieters had an increase in LDL cholesterol, compared
with 13% in the high carb group.
The authors noted that the "high carb" diet did not meet (the modest)
targets for fiber intakes and saturated fats were higher than
intended.The "high carb" group reduced fat intake from an average of
31% to 24% of daily calories by week 8, which increased to 28% by week
24. The Atkins group increased fat from a baseline of 34% to 57% by
week 8 and down to 47% by week 24. Carb intake in the "high carb"
group went from 45% to 49% back to 45%. In the Atkins group, the
corresponding numbers were 44% to 11% to 26%, reflecting the (similar)
results of most Atkins studies with a "real world" design, showing
marked fall off in compliance over time.
The "high carb" results of the McAuley study were certainly not as
dramatic as those in the Pritikin (and other) studies, which achieved
greater fat restriction, higher carbohydrate intake, and which (most
importantly) included an exercise intervention (more on this in my
response to Matti). But the point is that there were huge differences
between carbohydrate intake between the high carb group and the Atkins
group (see above), yet there were no advantages for Atkins between the
studied parameters of most concern to diabetics (serum insulin, fasting
glucose, and CRP). And then there were the findings relating to
post-prandial glucose levels...
Actually, the authors did NOT make mention of the following interesting
fact -- relating to the most important of all glucose-related diabetes
parameters, namely post-prandial serum glucose levels: But I dug it out
of their data (Table 3).
Let's look at the 49% carbohydrate by week 8 versus 11% carbohydrate by
week 8, at which time there was the greatest disparity between
carbohydrate intake between the high carb group and Akins group:
The high carb group consumed a 450% increase in carbs versus Atkins,
yet look at the following two hour post prandial glucose.
The 2 hr PP for the high carb was LOWER than for the Atkins
group...6.4+/- 1.7(SD), n=30 for Atkins vs 5.4+/- 1.4, n=30 for high
carb. The preceding glucose units were mm/liter.
**The authors did not make note of the following fact, but this is
actually a highly significant (2 sided P value of 0.013 by Student's T
test) advantage for high carb over Atkins! **
Being a diabetes expert, I am certain that Susan recognizes that
post-prandial glucose levels are considered to be more important
relating to diabetes control than the fasting levels (which were
EXACTLY the same in both groups). And yet the post-prandial glucose
levels were worst in the Atkins group at the time when their
carbohydrate consumption was the lowest (8 weeks, when they were still
mostly adherent with the diet and were consuming only an average of 11%
calories as fat). And this was the same time when the high carb group
had the highest carbohydrate consumption. And, at the time when each
diet was at it's "best," there was a clear advantage for the most
important diabetes related parameter for the high carb group.
Now, a brief word about triglyceride levels (which were more improved
by Atkins than by the high carb). In the first place, as mentioned,
this was a diet only study and, as I'll discuss later on with Matti,
high carb diets work best when combined with exercise. But even more
important is this: published triglyceride levels in studies like this
are always FASTING levels. It's analogous to a fasting versus
post-prandial glucose. With a high fat diet, triglyceride levels are
always highest post-prandially (makes sense; you are eating a lot of
fat and it gets absorbed into your bloodstream).. The triglycerides
fall during fasting periods (e.g. at night). With a high carb diet,
post-prandial triglyceride levels are much lower, but there is not
nearly as great a diurnal fluctuation.
But post-prandial triglyceride levels are probably much more important
than fasting levels for diabetics, just as post-prandial glucose levels
are more important than fasting levels. Fat infusions exacerbate
glucose intolerance, which probably accounts for the advantage of the
high carb diets.
Now, it is important to note that the above cited study was carried out
in overweight (BMI>27 kg/m2), but normoglycemic women with a reduced
insulin sensitivity score. These subjects were not the florid type II
diabetics of the Pritikin studies and were only insulin-resistant and
not yet overtly hyperglycemic. But this study certainly does indicate
that carbohydrates, even in the absence of an exercise program, are not
an overt threat to women at high risk to develop overt Type II
diabetes. Neither is a high fat/low carbohydrate diet an obviously
more attractive choice. Quite the contrary, it would appear.
I'll discuss the second of the very recent randomized "real world"
studies tomorrow. I'll also respond to Matti's excellent questions
tomorrow.
Several advance caution relating to all of the studies purporting to
show disadvantages with high carb diets:
1. To my knowledge, every single published study purporting to show a
disadvantage of high carb versus some other diet has used an
"isocaloric" design, in which, in effect, the high carb group is being
force fed (like a faux gras goose) to maintain isoenergetic balance
with the lower carb group. This has no relevance at all to the real
world of ad libitum food intake. So if you want to claim that high
carb diets are disadvantageous compared with other diets, you need to
restrict your analysis only to those studies where subjects are
consuming food in an ad libitum, real world setting.
2. There is no question that high carb diets work best when combined
with an exercise program (a point to be addressed in my answer to
Matti). I am not a proponent of the "one size fits all" or "lowest
common denominator" approach to diet. I'm a proponent of individuals
performing clinical trials on themselves to determine which approach
works best for them. Diabetes (or obesity or hypertension or heart
disease) is not like cancer, where you've only got one chance and a
short period of time to choose the "best" treatment. You've got time
to find out what works for you (as Susan apparently did for herself)
and you should be open to the possibility that you might do best with a
Pritikin-type diet/exercise approach.
3. I haven't finished presenting all the evidence supporting this point
of view, but I want to keep emphasizing that I'm advocating
individualizing diet and my point, in the context of my debate with
Susan, is that there is no reason whatsoever that a Pritikin-type
approach should be excluded from the mix of approaches to be
considered.
2:45 AM and I've got to be at work by 8. Time for zzz.
If you are reading this right now, Matti (on the other side of the
world), greetings and thanks again for your comments/questions, which
I'll do my best to answer next time.
- Larry W
runnswim@aol.com (Larry Weisenthal)
post-prandial glucose levels are considered to be more important
relating to diabetes control than the fasting levels <<
What I meant to say was that, "Being a diabetes expert, Susan (I'm
sure) recognizes that post-prandial glucose levels are considered to be
more important relating to diabetes control than are fasting levels."
Doug Freese
<runn...@aol.com> wrote in message
news:1135117185.9...@g44g2000cwa.googlegroups.com...
I could have, and maybe I did, tell you she was closed to any and all
discussions. I know you are not claiming everyone with T2 Diabetes will
respond will on high carb diet but she claims there in not a one, as if
this topic is a fact for world. Leave her head in the sand and please
continue. There are some of us that are willing to look a reasonable
discussion.
-DF