Glycemic index
Jonathan
the terminology...) here, in which case I'm sure those mentioned will
be quick to put me right, but here goes...
In the blue corner, we have the ninja of nice himself, Watson Davis,
claiming that the glycemic index is largely irrelevant unless you're
eating carbs by themselves, because- to use his example- the protein
and fat in a ham and cheese sandwich will slow the absorption of the
bread.
In the red corner, we have Mistress Krista, who during her recent
pork-off exertions, attempted to eliminate "empty" carbs, restricting
her intake to the unappetizing triptych of oatmeal, buckwheat and
barley.
What exactly is the deal here? Presumably Krista's strategy is based
on the idea that the complex carbs she chose are more slowly absorbed
and thus less likely to convert to fat? Is Watson claiming her
strategy is pointless (assuming she wasn't eating barley by itself,
which sounds distinctly unpalatable), or is there more to it than
that?
Jonathan
Lyle McDonald
>
> Now, I may be setting up a dispute between straw people (careful with
> the terminology...) here, in which case I'm sure those mentioned will
> be quick to put me right, but here goes...
>
> In the blue corner, we have the ninja of nice himself, Watson Davis,
> claiming that the glycemic index is largely irrelevant unless you're
> eating carbs by themselves, because- to use his example- the protein
> and fat in a ham and cheese sandwich will slow the absorption of the
> bread.
there is much truth to this. Adding protein, fat and fiber to carbs
slows gastric emptying and lowering the effective GI. This makes GI far
less critical. however, lower GI foods will still have a lower effect
on blood sugar, etc than higher GI carbs even as a part of a mixed meal.
At least they will in diabetics. Whether this applies to non-diabetic
individuals is debatable.
> In the red corner, we have Mistress Krista, who during her recent
> pork-off exertions, attempted to eliminate "empty" carbs, restricting
> her intake to the unappetizing triptych of oatmeal, buckwheat and
> barley.
>
> What exactly is the deal here? Presumably Krista's strategy is based
> on the idea that the complex carbs she chose are more slowly absorbed
> and thus less likely to convert to fat? Is Watson claiming her
> strategy is pointless (assuming she wasn't eating barley by itself,
> which sounds distinctly unpalatable), or is there more to it than
> that?
Yes.
1. Carb conversion to fat almost never happens. It is qualitatively
irrelevant to human physiology under all but the most extreme
conditions. The only exceptions I've seen are with massive
carbohydrate overfeeding (or glucose infusion). By massive we're
talking 700+ grams/day for multiple days. In one amusing model (the
Gura Walla overfeeding model which is a rite of passage for young males
in the Guru Walla tribe), fat synthesis from carbs does occur but they
are overfed truly absurd amounts of carbs every day for weeks on end.
By definition, carb overfeeding doesn't happen on a diet.
1a. So you ask, what's the deal with carbs and fat loss. While carb ->
fat conversion is quantatively irrelevant in humans under most
conditions, carbs do affect fat metabolism. Simply put, the more carbs
you eat, the more carbs you burn, and the less fat you burn. As well,
high insulin from carb intake (either high amounts or high GI, but see
note above) limits fat mobilization. However, total carb intake appears
to be a much larger player in this effect than type. Simply reducing
carbohydrate amount intake will increase fat oxidation.
2. Perhaps the bigger issue, wrt: dieting, between low and high GI foods
has to do with appetite and hunger control. Higher GI foods are higher
in fiber, bulkier (volume wise), slower digesting (although see note
above), which means you can eat more of them (again, volume wise) for
the same caloric content. Put differently, given that you were going to
eat 50 grams of (digestible) carbs at a given meal, you could eat a lot
more food volume wise choosing lower GI foods than choosing higher GI foods.
3. Except for perhaps the extreme levels of leanness, choice of GI is
unlikely to radiacally affect fat loss, at a given calorie level. that
is, given a deficit of XXX calories, whether you pick high GI or low GI
carbs (esp. within the context of a reduced carb, moderate protein,
moderate fat diet in the first place) is unlikely to affect fat loss per
se. However, this assume you have no problem with appetite/hunger
control. If hte diet with higher GI carbs doesn't control hunger as
well, and you eat more because of it, obviusly fat loss will be
hindered. But it's an effect of your eating more than the GI per se.
Rev Lyle
geek_girl
>
>Jonathan wrote:
>>
>> Now, I may be setting up a dispute between straw people (careful with
>> the terminology...) here, in which case I'm sure those mentioned will
>> be quick to put me right, but here goes...
>>
>> In the blue corner, we have the ninja of nice himself, Watson Davis,
>> claiming that the glycemic index is largely irrelevant unless you're
>> eating carbs by themselves, because- to use his example- the protein
>> and fat in a ham and cheese sandwich will slow the absorption of the
>> bread.
>
>there is much truth to this. Adding protein, fat and fiber to carbs
>slows gastric emptying and lowering the effective GI. This makes GI far
>less critical. however, lower GI foods will still have a lower effect
>on blood sugar, etc than higher GI carbs even as a part of a mixed meal.
> At least they will in diabetics. Whether this applies to non-diabetic
>individuals is debatable.
>
I maintain that my turkey, mayo and lettuce on Ezekiel bread has less effect on
my blood glucose than the same turkey, mayo and lettuce on mushy white bread
would, while of course the turkey, mayo and lettuce on mushy white bread would
have less effect than the mushy bread would by itself. I would test this theory
but mushy white bread makes me gag.
Lyle McDonald
>
> In article <3C3B68D0...@onr.com>, Lyle McDonald says...
> >
> >Jonathan wrote:
> >>
> >> Now, I may be setting up a dispute between straw people (careful with
> >> the terminology...) here, in which case I'm sure those mentioned will
> >> be quick to put me right, but here goes...
> >>
> >> In the blue corner, we have the ninja of nice himself, Watson Davis,
> >> claiming that the glycemic index is largely irrelevant unless you're
> >> eating carbs by themselves, because- to use his example- the protein
> >> and fat in a ham and cheese sandwich will slow the absorption of the
> >> bread.
> >
> >there is much truth to this. Adding protein, fat and fiber to carbs
> >slows gastric emptying and lowering the effective GI. This makes GI far
> >less critical. however, lower GI foods will still have a lower effect
> >on blood sugar, etc than higher GI carbs even as a part of a mixed meal.
> > At least they will in diabetics. Whether this applies to non-diabetic
> >individuals is debatable.
> >
>
> I maintain that my turkey, mayo and lettuce on Ezekiel bread has less effect on
> my blood glucose than the same turkey, mayo and lettuce on mushy white bread
> would,
And you're demonstrably hypoglycemic, tying into my comment about it
being important in diabetic folks. YOu're demonstrably a lot of other
things too.
> while of course the turkey, mayo and lettuce on mushy white bread would
> have less effect than the mushy bread would by itself. I would test this theory
> but mushy white bread makes me gag.
I presume you're able to control such a reflex when you're with Canadians.
Or maybe that's why he didn't call back.....
Rev Lyle
now a reverend, still a prick
Mistress Krista
"Lyle McDonald" <lyl...@onr.com> wrote in message
news:3C3B68D0...@onr.com...
>
> > In the red corner, we have Mistress Krista, who during her recent
> > pork-off exertions, attempted to eliminate "empty" carbs, restricting
> > her intake to the unappetizing triptych of oatmeal, buckwheat and
> > barley.
All of them are actually quite tasty, IMHO. I make a mean barley pilaf, and
buckwheat when cooked right is deelish. There's a trick to it. Coat the
grains in egg before cooking (just crack an egg into the dry grains and
squoosh it all around till grains are coated). Then saute in a little butter
for 3-5 minutes till egg is cooked and grains are dry. Add liquid, cook like
rice. After cooking, saute chopped mushrooms and bacon, mix into cooked
buckwheat. This stuff is the shiznit. Goes great with scrambled eggs for
breakfast and is a good side dish for dinner. Good Ukrainian food!
> >
> > What exactly is the deal here? Presumably Krista's strategy is based
> > on the idea that the complex carbs she chose are more slowly absorbed
> > and thus less likely to convert to fat?
No, that was not my reasoning. First off, my body doesn't seem to like a
lot of refined wheat products. They're OK in small quantities but I noticed
a big difference in the way I felt, digestion-wise, when I cut down on wheat
stuff like bread and pasta (regular and whole wheat). Second, I don't
really like a lot of that plain crap. I think wild rice tastes worlds better
than white rice, for example. It's a taste thing.
>
> 2. Perhaps the bigger issue, wrt: dieting, between low and high GI foods
> has to do with appetite and hunger control. <snip>
While Lyle's point 1a) contributed, point 2 was the important physiological
consideration in my choice. I don't believe in all that "carbs magically
make you fat in any amount" stuff that some people promote (not saying Lyle
does it, or really anyone here, but I wanted to be clear). In a sense both
Watson and I are on the same team here.
My choice was very pragmatic and based more on the day-to-day practicalities
of dieting, satiety, appetite, etc. I could eat a big plate of pasta, waste
500 calories, and be starving/sleepy 1/2 hour later, or I could have a
chicken breast and a huge salad and feel satisfied on 300 calories, as well
as get 20g of protein and lots of good fibrous carbs in the form of
fruit/veg. When the "easy filler" portion of starchy carbs is removed from
a meal composition, the gap has to be filled in. It gets filled in with lean
protein and fruit/veg. I am also prone to symptoms of blood sugar swings so
it is important that I do my best to keep things constant.
Basically with dieting there's lots of ways to skin a cat. As long as you
don't do anything fucked like drop fat to 5% or eat only rice cakes or
whatever, various things will work for various people. The ideal diet:
a) meets the psychological needs of the dieter (some people like routine,
some like variety)
b) provides adequate nutrition (I'm talking about vitamins and all that good
stuff)
c) provides adequate protein
d) provides adequate fat
e) can be incorporated into the dieter's regular routine
f) meets the energy requirements of the dieter's physical activities
(endurance athletes, for example, would have different needs than weight
trainers)
g) meets other physiological needs such as possible insulin resistance, etc.
So there are many individual factors to consider, and GI is relevant but
must be understood in context, as Watson says. Keto dieting was a disaster
for me, but it works really well for others.
Krista
--
-------------------------
www.stumptuous.com/weights.html
mistresskrista at rogers dot com
geek_girl
>
>geek_girl wrote:
>>
>> In article <3C3B68D0...@onr.com>, Lyle McDonald says...
>> >
>> >Jonathan wrote:
>> >>
>> >> Now, I may be setting up a dispute between straw people (careful with
>> >> the terminology...) here, in which case I'm sure those mentioned will
>> >> be quick to put me right, but here goes...
>> >>
>> >> In the blue corner, we have the ninja of nice himself, Watson Davis,
>> >> claiming that the glycemic index is largely irrelevant unless you're
>> >> eating carbs by themselves, because- to use his example- the protein
>> >> and fat in a ham and cheese sandwich will slow the absorption of the
>> >> bread.
>> >
>> >there is much truth to this. Adding protein, fat and fiber to carbs
>> >slows gastric emptying and lowering the effective GI. This makes GI far
>> >less critical. however, lower GI foods will still have a lower effect
>> >on blood sugar, etc than higher GI carbs even as a part of a mixed meal.
>> > At least they will in diabetics. Whether this applies to non-diabetic
>> >individuals is debatable.
>> >
>>
>> I maintain that my turkey, mayo and lettuce on Ezekiel bread has less effect on
>> my blood glucose than the same turkey, mayo and lettuce on mushy white bread
>> would,
>
>And you're demonstrably hypoglycemic, tying into my comment about it
>being important in diabetic folks.
Hypoglycemic != diabetic. Perhaps you should have said something like "in people
with abnormal glucose metabolism."
>YOu're demonstrably a lot of other
>things too.
Ummm, thank you? Fuck you, Rev Beyotch?
Perhaps you should be more specific about the "other things."
>> while of course the turkey, mayo and lettuce on mushy white bread would
>> have less effect than the mushy bread would by itself. I would test this theory
>> but mushy white bread makes me gag.
>
>I presume you're able to control such a reflex when you're with Canadians.
I controlled it, although it was difficult.
>Or maybe that's why he didn't call back.....
>
He did call back. Several times. I just haven't seen him again. Don't you listen
when I talk to you?
>Rev Beytoch
>now a reverend, still a prick
But probably too small a prick to trigger anyone's gag reflex
Lyle McDonald
rebound hypogyemia is typically due to insulin resistance which is a
pre-diabetic state. So bite me.
> >YOu're demonstrably a lot of other
> >things too.
>
> Ummm, thank you? Fuck you, Rev Beyotch?
>
> Perhaps you should be more specific about the "other things."
This is a family forum.
> >> while of course the turkey, mayo and lettuce on mushy white bread would
> >> have less effect than the mushy bread would by itself. I would test this theory
> >> but mushy white bread makes me gag.
> >
> >I presume you're able to control such a reflex when you're with Canadians.
>
> I controlled it, although it was difficult.
>
> >Or maybe that's why he didn't call back.....
> >
>
> He did call back. Several times. I just haven't seen him again. Don't you listen
> when I talk to you?
Not really.
> >Rev Beytoch
Wow, you must really like me to go to the trouble of changing that.
> >now a reverend, still a prick
>
> But probably too small a prick to trigger anyone's gag reflex
Which should be a good thing.
Rev Lyle
geek_girl
Ahhh, typically. But in what respects am I typical? Remember I was going to ask
you about hypoglycemia caused by insulin sensitivity v. hypoglycemia caused by
insulin resistance? We got all sidetracked the other night by your lovely fat
cell chart, but I still wanted to ask you about that at some point.
>So bite me.
You'd better be nice to me or I'll tell everyone I saw you working out on the
foo-foo machines. Oops, did I type that out loud?
>
>> >YOu're demonstrably a lot of other
>> >things too.
>>
>> Ummm, thank you? Fuck you, Rev Beyotch?
>>
>> Perhaps you should be more specific about the "other things."
>
>This is a family forum.
Since when?
>> >> while of course the turkey, mayo and lettuce on mushy white bread would
>> >> have less effect than the mushy bread would by itself. I would test this theory
>> >> but mushy white bread makes me gag.
>> >
>> >I presume you're able to control such a reflex when you're with Canadians.
>>
>> I controlled it, although it was difficult.
>>
>> >Or maybe that's why he didn't call back.....
>> >
>>
>> He did call back. Several times. I just haven't seen him again. Don't you listen
>> when I talk to you?
>
>Not really.
>
Hmm? Did you say something?
>> >Rev Beytoch
>
>Wow, you must really like me to go to the trouble of changing that.
>
You know I think of you as the little brother I never wanted.
>> >now a reverend, still a prick
>>
>> But probably too small a prick to trigger anyone's gag reflex
>
>Which should be a good thing.
>
Should be. But probably not.
>Rev Beyotch
Lyle McDonald
> >> >> I maintain that my turkey, mayo and lettuce on Ezekiel bread has less effect on
> >> >> my blood glucose than the same turkey, mayo and lettuce on mushy white bread
> >> >> would,
> >> >
> >> >And you're demonstrably hypoglycemic, tying into my comment about it
> >> >being important in diabetic folks.
> >>
> >> Hypoglycemic != diabetic.
> >
> >rebound hypogyemia is typically due to insulin resistance which is a
> >pre-diabetic state.
>
> Ahhh, typically. But in what respects am I typical?
Remember who said it.
> Remember I was going to ask
> you about hypoglycemia caused by insulin sensitivity v. hypoglycemia caused by
> insulin resistance? We got all sidetracked the other night by your lovely fat
> cell chart, but I still wanted to ask you about that at some point.
The former is going to occur a lot less frequently than the latter.
Considering some of your other 'issues', I would tend to suspect the latter.
> >So bite me.
>
> You'd better be nice to me or I'll tell everyone I saw you working out on the
> foo-foo machines. Oops, did I type that out loud?
Yeah, you also saw me DL and front squat on a different day.
> >> >Rev Beytoch
> >
> >Wow, you must really like me to go to the trouble of changing that.
> >
>
> You know I think of you as the little brother I never wanted.
My mom thinks of me as the son she never wanted.
> >> >now a reverend, still a prick
> >>
> >> But probably too small a prick to trigger anyone's gag reflex
> >
> >Which should be a good thing.
> >
>
> Should be. But probably not.
apparently not.
Rev Lyle
geek_girl
>
>geek_girl wrote:
>>
>> In article <3C3B70C5...@onr.com>, Lyle McDonald says...
>> >
>> >geek_girl wrote:
>
>> >> >> I maintain that my turkey, mayo and lettuce on Ezekiel bread has less effect on
>> >> >> my blood glucose than the same turkey, mayo and lettuce on mushy white bread
>> >> >> would,
>> >> >
>> >> >And you're demonstrably hypoglycemic, tying into my comment about it
>> >> >being important in diabetic folks.
>> >>
>> >> Hypoglycemic != diabetic.
>> >
>> >rebound hypogyemia is typically due to insulin resistance which is a
>> >pre-diabetic state.
>>
>> Ahhh, typically. But in what respects am I typical?
>
>Remember who said it.
I'll remember. I'm not the one who doesn't listen when I talk.
>> Remember I was going to ask
>> you about hypoglycemia caused by insulin sensitivity v. hypoglycemia caused by
>> insulin resistance? We got all sidetracked the other night by your lovely fat
>> cell chart, but I still wanted to ask you about that at some point.
>
>The former is going to occur a lot less frequently than the latter.
>Considering some of your other 'issues', I would tend to suspect the latter.
>
Yes, but remember I said it was a long freakin story? We'll have to talk about
it this weekend in between stripper stalking stories.
>> >So bite me.
>>
>> You'd better be nice to me or I'll tell everyone I saw you working out on the
>> foo-foo machines. Oops, did I type that out loud?
>
>Yeah, you also saw me DL and front squat on a different day.
Yup, and I loved the grunting.
>> >> >Rev Beytoch
>> >
>> >Wow, you must really like me to go to the trouble of changing that.
>> >
>>
>> You know I think of you as the little brother I never wanted.
>
>My mom thinks of me as the son she never wanted.
My father thinks of me as the son he always wanted.
Lyle McDonald
>
> In article <3C3B7504...@onr.com>, Lyle McDonald says...
> >
> >geek_girl wrote:
> >>
> >> In article <3C3B70C5...@onr.com>, Lyle McDonald says...
> >> >
> >> >geek_girl wrote:
> >> >rebound hypogyemia is typically due to insulin resistance which is a
> >> >pre-diabetic state.
> >>
> >> Ahhh, typically. But in what respects am I typical?
> >
> >Remember who said it.
>
> I'll remember. I'm not the one who doesn't listen when I talk.
What was that?
> >> Remember I was going to ask
> >> you about hypoglycemia caused by insulin sensitivity v. hypoglycemia caused by
> >> insulin resistance? We got all sidetracked the other night by your lovely fat
> >> cell chart, but I still wanted to ask you about that at some point.
> >
> >The former is going to occur a lot less frequently than the latter.
> >Considering some of your other 'issues', I would tend to suspect the latter.
> >
>
> Yes, but remember I said it was a long freakin story? We'll have to talk about
> it this weekend in between stripper stalking stories.
You'll have to hope I lose my voice. That's about the only way to shut
me up.
> >> >So bite me.
> >>
> >> You'd better be nice to me or I'll tell everyone I saw you working out on the
> >> foo-foo machines. Oops, did I type that out loud?
> >
> >Yeah, you also saw me DL and front squat on a different day.
>
> Yup, and I loved the grunting.
It made you get that funny feeling in your special place, didn't it?
> >> >> >Rev Beytoch
> >> >
> >> >Wow, you must really like me to go to the trouble of changing that.
> >> >
> >>
> >> You know I think of you as the little brother I never wanted.
> >
> >My mom thinks of me as the son she never wanted.
>
> My father thinks of me as the son he always wanted.
Remember who said it.
Rev Lyle
geek_girl
>
>geek_girl wrote:
>>
>> In article <3C3B7504...@onr.com>, Lyle McDonald says...
>> >
>> >geek_girl wrote:
>> >>
>> >> In article <3C3B70C5...@onr.com>, Lyle McDonald says...
>> >> >
>> >> >geek_girl wrote:
>
>> >> >rebound hypogyemia is typically due to insulin resistance which is a
>> >> >pre-diabetic state.
>> >>
>> >> Ahhh, typically. But in what respects am I typical?
>> >
>> >Remember who said it.
>>
>> I'll remember. I'm not the one who doesn't listen when I talk.
>
>What was that?
>
>> >> Remember I was going to ask
>> >> you about hypoglycemia caused by insulin sensitivity v. hypoglycemia caused by
>> >> insulin resistance? We got all sidetracked the other night by your lovely fat
>> >> cell chart, but I still wanted to ask you about that at some point.
>> >
>> >The former is going to occur a lot less frequently than the latter.
>> >Considering some of your other 'issues', I would tend to suspect the latter.
>> >
>>
>> Yes, but remember I said it was a long freakin story? We'll have to talk about
>> it this weekend in between stripper stalking stories.
>
>You'll have to hope I lose my voice. That's about the only way to shut
>me up.
>
But if you lose your voice, how will you answer my questions? Draw me some
convoluted flow chart that makes zero sense?
>> >> >So bite me.
>> >>
>> >> You'd better be nice to me or I'll tell everyone I saw you working out on the
>> >> foo-foo machines. Oops, did I type that out loud?
>> >
>> >Yeah, you also saw me DL and front squat on a different day.
>>
>> Yup, and I loved the grunting.
>
>It made you get that funny feeling in your special place, didn't it?
You mean it triggered my gag reflex?
Watson Davis
wrote:
What we're saying isn't mutually exclusive.
Watson (the ninja of nice) Davis
Wayne S. Hill
>
> In the blue corner, we have the ninja of nice himself, Watson Davis,
<snip>
> In the red corner, we have Mistress Krista, who during her recent
<snip>
Shouldn't Watson be in the red corner?
-Wayne
Mark Hartman
> irrelevant to human physiology under all but the most extreme
> conditions
So then how does someone who is eat a caloric surplus of low/no fat, minimum
protein, and the balance carbs gain weight?
Mark
Lyle McDonald
If you'd paid attention to the rest of what I posted, you'd have the
answer. So I'll be nice (this time) and repost it and comment further.
1. Carb conversion to fat almost never happens. It is qualitatively
irrelevant to human physiology under all but the most extreme
conditions. The only exceptions I've seen are with massive
carbohydrate overfeeding (or glucose infusion). By massive we're
talking 700+ grams/day for multiple days. In one amusing model (the
Gura Walla overfeeding model which is a rite of passage for young males
in the Guru Walla tribe), fat synthesis from carbs does occur but they
are overfed truly absurd amounts of carbs every day for weeks on end.
By definition, carb overfeeding doesn't happen on a diet.
1a. So you ask, what's the deal with carbs and fat loss. While carb ->
fat conversion is quantatively irrelevant in humans under most
conditions, carbs do affect fat metabolism. Simply put, the more carbs
you eat, the more carbs you burn, and the less fat you burn. As well,
high insulin from carb intake (either high amounts or high GI, but see
note above) limits fat mobilization. However, total carb intake appears
to be a much larger player in this effect than type. Simply reducing
carbohydrate amount intake will increase fat oxidation.
So, with that in mind.
1. On a lowfat diet, once carbs become excessive to a certain point
(i.e. you're eating above maintenance calorie levels), they will make up
basically the entirety of what you burn each day. Meaning any dietary
fat that is present in the diet gets stored.
2. A no fat diet is one of the few extreme situations where de novo
lipogenesis can occur. With a fat intake less than 10% of total
calories, DNL becomes more pronounced.
3. By definition, on even a zero fat diet, if you're eating so many
carbs/calories as to be ABOVE your maintenance calorie levels, you're
approaching extreme levels. That is, figure an average male with a
metabolic rate of ~2700 calories. Ignoring the contribution of protein
(which makes up 5-10% max of your total energy production each day),
even if he's on a zero fat diet (which isn't achievable in reality), if
he's eating above maintenance that means he's getting in excess of 2700
calories from carbs. Let's say 2800 calories to make the math easier.
At 4 cal/gram, 2800 calories from carbs is 700 grams/day. Assuming he's
eating that way every day, that's 700 g/day for multiple days. Well,
gee whiz, Beavis, that's what I posted in #1 originally.
Please pay better attention in the future. And knock off the selective
snipping shit ; I answered your question in what you snipped out.
Rev. Lyle
George G.
>
> 1. Carb conversion to fat almost never happens. It is qualitatively
> irrelevant to human physiology under all but the most extreme
> conditions. The only exceptions I've seen are with massive
> carbohydrate overfeeding (or glucose infusion). By massive we're
> talking 700+ grams/day for multiple days. In one amusing model (the
> Gura Walla overfeeding model which is a rite of passage for young
> males in the Guru Walla tribe), fat synthesis from carbs does occur
> but they are overfed truly absurd amounts of carbs every day for weeks
> on end. By definition, carb overfeeding doesn't happen on a diet.
>
> 1a. So you ask, what's the deal with carbs and fat loss. While carb
> -> fat conversion is quantatively irrelevant in humans under most
> conditions, carbs do affect fat metabolism. Simply put, the more
> carbs you eat, the more carbs you burn, and the less fat you burn. As
> well, high insulin from carb intake (either high amounts or high GI,
> but see note above) limits fat mobilization. However, total carb
> intake appears to be a much larger player in this effect than type.
> Simply reducing carbohydrate amount intake will increase fat
> oxidation.
>
What is the problem with insulin resitance then?
--
George.
-----------------------------------------------------------------------
"The wise lifter senses when it's time to stop, even if the schedule
doesn't say so, and often calls that the end of his cycle - he lives to
lift, injury-free, again."
-Steven Freides-
Mark Hartman
;)
It was an honesty question to provide clarification. I appreciate
your going above and beyond. I'll throw in an extra buck when the
virual collection plate is passed this weekend.
> Please pay better attention in the future. And knock off the selective
> snipping shit ; I answered your question in what you snipped out.
Only selective to minimize post size - not deliberate selectivity.
>
> Rev. Lyle
Lyle McDonald
>
> Lyle McDonald <lyl...@onr.com> wrote in news:3C3B68D0...@onr.com:
>
> >
> > 1. Carb conversion to fat almost never happens. It is qualitatively
> > irrelevant to human physiology under all but the most extreme
> > conditions. The only exceptions I've seen are with massive
> > carbohydrate overfeeding (or glucose infusion). By massive we're
> > talking 700+ grams/day for multiple days. In one amusing model (the
> > Gura Walla overfeeding model which is a rite of passage for young
> > males in the Guru Walla tribe), fat synthesis from carbs does occur
> > but they are overfed truly absurd amounts of carbs every day for weeks
> > on end. By definition, carb overfeeding doesn't happen on a diet.
> >
> > 1a. So you ask, what's the deal with carbs and fat loss. While carb
> > -> fat conversion is quantatively irrelevant in humans under most
> > conditions, carbs do affect fat metabolism. Simply put, the more
> > carbs you eat, the more carbs you burn, and the less fat you burn. As
> > well, high insulin from carb intake (either high amounts or high GI,
> > but see note above) limits fat mobilization. However, total carb
> > intake appears to be a much larger player in this effect than type.
> > Simply reducing carbohydrate amount intake will increase fat
> > oxidation.
> >
>
> What is the problem with insulin resitance then?
Dunno what you're asking here.
Lyle
George G.
>
> Dunno what you're asking here.
>
> Lyle
>
I suppose I need to elaborate. By "carb conversion to fat almost never
happens" do you mean to include what happens wrt to fat cells? I thought
the problem with insulin resistance was that the fat cells continue to be
receptive to glucose beyond other cells.
If I'm still not being clear enough I'll just have to repost in few days.
Re-entering ketosis after 4 weeks off has me enjoying some mental
fogginess.
Lyle McDonald
>
> Lyle McDonald <lyl...@onr.com> wrote in news:3C3C93DC...@onr.com:
>
> >
> > Dunno what you're asking here.
> >
> > Lyle
> >
>
> I suppose I need to elaborate. By "carb conversion to fat almost never
> happens" do you mean to include what happens wrt to fat cells?
For the most part. Glucose entry into fat cells IS important for
triglyceride synthesis as glucose is the only way that fat cells can get
glycerol, but actual biochemical conversion of glucose -> fat doesn't
occur under most conditions (again, there was one weird glucose infusion
study that suggested high levels of adipose glucose-fat conversion but
it's not really applicable).
> I thought
> the problem with insulin resistance was that the fat cells continue to be
> receptive to glucose beyond other cells.
That's one of the problems.
First realize taht insulin is involved in the disposal/deposition of
glucose, fat and protein to one degree or another. So if you're getting
decreased storage of glucose in muscle cells (meaning more storage in
fat cells), the same is happening to fat and protein (protein to the
least degree, mind you).
AS well, a state of muscular insulin resistance essentially means that
the muscle is 'full' and can't store incoming nutrients any further (one
cause of insulin resistance is maxing out glycoge and/or intramuscualr
triglyceride levels). Now, under normal circumstances you usually get
some percentage of incoming nutrients going to muscle cells, another
percentage going to fat cells (this is ignoring what the other tissues
in teh body are using). If the muscle can't hold anything else, that
means that any nutrients that would have been stored in the muscle is
going to be stored in fat cells.
Hope that makes sense,
Lyle
Lyle McDonald
>
> Lyle McDonald <lyl...@onr.com> wrote in news:3C3C93DC...@onr.com:
>
> >
> > Dunno what you're asking here.
> >
> > Lyle
> >
>
> I suppose I need to elaborate. By "carb conversion to fat almost never
> happens" do you mean to include what happens wrt to fat cells?
For the most part. Glucose entry into fat cells IS important for
triglyceride synthesis as glucose is the only way that fat cells can get
glycerol, but actual biochemical conversion of glucose -> fat doesn't
occur under most conditions (again, there was one weird glucose infusion
study that suggested high levels of adipose glucose-fat conversion but
it's not really applicable).
> I thought
> the problem with insulin resistance was that the fat cells continue to be
> receptive to glucose beyond other cells.
That's one of the problems.
First realize taht insulin is involved in the disposal/deposition of
glucose, fat and protein to one degree or another. So if you're getting
decreased storage of glucose in muscle cells (meaning more storage in
fat cells), the same is happening to fat and protein (protein to the
least degree, mind you).
AS well, a state of muscular insulin resistance essentially means that
the muscle is 'full' and can't store incoming nutrients any further (one
cause of insulin resistance is maxing out glycoge and/or intramuscualr
triglyceride levels). Now, under normal circumstances you usually get
some percentage of incoming nutrients going to muscle cells, another
percentage going to fat cells (this is ignoring what the other tissues
in teh body are using). If the muscle can't hold anything else, that
means that any nutrients that would have been stored in the muscle is
going to be stored in fat cells.
Hope that makes sense,
Lyle
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George G.
> "George G." wrote:
>> I suppose I need to elaborate. By "carb conversion to fat almost
>> never happens" do you mean to include what happens wrt to fat cells?
>
> For the most part. Glucose entry into fat cells IS important for
> triglyceride synthesis as glucose is the only way that fat cells can
> get glycerol, but actual biochemical conversion of glucose -> fat
> doesn't occur under most conditions (again, there was one weird
> glucose infusion study that suggested high levels of adipose
> glucose-fat conversion but it's not really applicable).
I must be missing something here. What is the difference between
triglyceride synthethis from glucose in fat cells and "actual biochemical
conversion glucose -> fat"?
>
>> I thought
>> the problem with insulin resistance was that the fat cells continue
>> to be receptive to glucose beyond other cells.
>
> That's one of the problems.
> First realize taht insulin is involved in the disposal/deposition of
> glucose, fat and protein to one degree or another. So if you're
> getting decreased storage of glucose in muscle cells (meaning more
> storage in fat cells), the same is happening to fat and protein
> (protein to the least degree, mind you).
>
This I understood.
> AS well, a state of muscular insulin resistance essentially means that
> the muscle is 'full' and can't store incoming nutrients any further
> (one cause of insulin resistance is maxing out glycoge and/or
> intramuscualr triglyceride levels). Now, under normal circumstances
> you usually get some percentage of incoming nutrients going to muscle
> cells, another percentage going to fat cells (this is ignoring what
> the other tissues in teh body are using). If the muscle can't hold
> anything else, that means that any nutrients that would have been
> stored in the muscle is going to be stored in fat cells.
>
....and so insulin rises even more to attempt to clear the nutrients,
primarily glucose, from the blood. Leading to downregulation of the
receptors on muscle cells first. And yet more insulin, etc, etc. Correct?
George.
Lyle McDonald
>
> Lyle McDonald <lyl...@onr.com> wrote in news:3C3DC2F9...@onr.com:
>
> > "George G." wrote:
> >> I suppose I need to elaborate. By "carb conversion to fat almost
> >> never happens" do you mean to include what happens wrt to fat cells?
> >
> > For the most part. Glucose entry into fat cells IS important for
> > triglyceride synthesis as glucose is the only way that fat cells can
> > get glycerol, but actual biochemical conversion of glucose -> fat
> > doesn't occur under most conditions (again, there was one weird
> > glucose infusion study that suggested high levels of adipose
> > glucose-fat conversion but it's not really applicable).
>
> I must be missing something here. What is the difference between
> triglyceride synthethis from glucose in fat cells and "actual biochemical
> conversion glucose -> fat"?
Oh, sorry about the confusion.
1. Triglyceride synthesis refers to the combination of glycerol (the
backbone of a triglyceride molecule) and three free fatty acids (FFA).
The primary role of glucose in terms of TG synthesis in the fat cell is
to provide the glycerol backbone . Basically, you have a molecule of
glycerol and a three molecules of free fatty acids which are simply
attached to one another via the necessary enzymes. But outside of the
conversion of glucose to glycerol in the fat cell, no other real
biochemical conversions occur.
2. Conversion of glucose -> fat refers to the actual biochemical
conversion (a process called de novo lipogenesis) by which a glucose
molecule is converted to a free fatty acid molecule. In this process,
glucose goes through a ton of different biochemical conversions to end
up as a fatty acid.
> > AS well, a state of muscular insulin resistance essentially means that
> > the muscle is 'full' and can't store incoming nutrients any further
> > (one cause of insulin resistance is maxing out glycoge and/or
> > intramuscualr triglyceride levels). Now, under normal circumstances
> > you usually get some percentage of incoming nutrients going to muscle
> > cells, another percentage going to fat cells (this is ignoring what
> > the other tissues in teh body are using). If the muscle can't hold
> > anything else, that means that any nutrients that would have been
> > stored in the muscle is going to be stored in fat cells.
> >
>
> ....and so insulin rises even more to attempt to clear the nutrients,
> primarily glucose, from the blood. Leading to downregulation of the
> receptors on muscle cells first. And yet more insulin, etc, etc. Correct?
The current though is that, by the time you're starting to get increased
nutrient storage in the fat cells, the muscle is already insensitive for
teh most part.
That is, the usual pattern of events is:
1. muscle becomes insulin resistant, as a function of being full of
nutrients (glycogen and triglyceride) as well as constant pounding from
the high insulin associated with crappy diets (not to mention genetic
issues).
2. nutrients start to get preferentially deposited in fat cells, causing
them to expand (in size first, in number after they reach a certain
critical size) at which point they start becoming insulin resistant too
(due to increased levels of substances such as leptin, TNF-alpha,
resistin). This is an attempt by the body to limit further fat gain, by
preventing further nutrient storage in the fat cells.
3. At that point, with nowhere to go, nutrients sit in the bloodstream
and you get hyperglycemia and hypertriglyceridemia (high blood glucose
and TG levels).
Lyle
George G.
Ah, so both glucose and fatty acids are generally needed to store "fat".
Insulin resistance is normally the conclusion to chronic hypercaloric
diets, correct? Is it possible that the muscle cells become insulin
resistant even if they aren't full of nutrients?
Lyle McDonald
Yes, and some research suggests that it is the availability of the
former (glucose) that is the limiting step in TG synthesis.
> >> ....and so insulin rises even more to attempt to clear the nutrients,
> >> primarily glucose, from the blood. Leading to downregulation of the
> >> receptors on muscle cells first. And yet more insulin, etc, etc.
> >> Correct?
> >
> > The current though is that, by the time you're starting to get
> > increased nutrient storage in the fat cells, the muscle is already
> > insensitive for teh most part.
> >
> > That is, the usual pattern of events is:
> > 1. muscle becomes insulin resistant, as a function of being full of
> > nutrients (glycogen and triglyceride) as well as constant pounding
> > from the high insulin associated with crappy diets (not to mention
> > genetic issues).
>
> Insulin resistance is normally the conclusion to chronic hypercaloric
> diets, correct? Is it possible that the muscle cells become insulin
> resistant even if they aren't full of nutrients?
Was poking around on Medline just last night and found a paper to this
effect. So yes. They showed that three days of chronically high
insulin decreased insulin sensitivity without increasing muscle glycogen
above normal.
The reason being that insulin sensitivity in the muscle is actually
being controlled by several different pathways, all of which I'm lumping
together because I'm lazy.
the issue of insulin levels causing insulin receptor downregulation is
different than the issue of the muscle being 'full' of nutrients from a
physiological standpoint. And there are other factors involved as well.
The simple picture of what happens in terms of glucose uptake into
muscle is this.
Insulin latches onto the receptor, causing a bunch of 'stuff' to happen
inside the cell. Basically it triggers a cascade of different second
messengers which have a bunch of effects in the cell. One of those
effects is to stimulate GLUT-4 transporters (GLUT = glucose transporter)
to migrate from the inside of the cell to the cell membrane (at this
point it gets more complicated but Elzi is the GLUT-4 expert, not me so
I'll stop before I fuck anything up), and those GLUT-4 carry glucose
into the cell.
So right there we have three distinct pathways (and that's considering
the second messenger system as a single pathway) where things can get
screwy. There are probably more that are involved.
Chronically high insulin levels cause actual downregulation of insulin
receptor number on the cell membrane. With decreased insulin receptor
number, you can get less of a 'signal' sent inside the cell in response
to insulin. It's a lot more complicated than this (has to do with how
many receptors there are relative to how much insulin, as well as how
many receptors are needed to generate a maximum response inside the
cell) so just take it at face value.
I consider the second messenger system to be a 'black box' so I've
ignored it for the time being. There can be defects (which are probably
part of the cause of the genetic aspect of insulin resistance) and
that's as far a I've gotten. Elzi can expound if she wants, that's her
baby. Since I can't do much to affect it, I ignore it.
Chronically high nutrient levels in muscle 'tell' the muscle that it's
full (via a neato system called the hexosamine nutrient sensing system
which is just a metabolic pathway that tells the cell what its level of
nutrients are) which causes a decrease in GLUT-4 levels.
So insulin and high levels of nutrients are affecting two different
pathways that work together. If either insulin receptor number OR GLUT-4
levels are decreased, you will see a decrease in glucose transport into
the muscle cell.
Aren't you glad you asked? ;)
Lyle