Re: Sugar and Insulin Resistance

[Guest guest]

In a message dated 1/9/04 1:32:52 PM Eastern Standard Time,

mhysmith@... writes:

> The results underscore

> the importance of glycosylation - attachment of a sugar to a protein --

The fasting/feasting mice studies found that without reducing calories,

carbs, or sugars, periodic fasting combined with periodic overeating had a

dramatic

reduction of fasting blood glucose levels, which leads to decreased rates of

glycosylation.

Chris

[Guest guest]

http://www.sciencedaily.com/releases/2002/04/020416073449.htm

Source: s Hopkins Medical Institutions

Date:

2002-04-16

Scientists Close In On Trigger Of Insulin Resistance; Extra Sugar Can Cause

Insulin Resistance In Cells

In experiments with fat cells, s Hopkins scientists have discovered

direct evidence that a build-up of sugar on proteins triggers insulin

resistance, a key feature of most cases of diabetes. The results underscore

the importance of glycosylation - attachment of a sugar to a protein -- as a

way cells control proteins' activities, the scientists report in the April

16 issue of the Proceedings of the National Academy of Sciences. The

scientists found that at least two proteins involved in passing along

insulin's message were unlikely to work properly when coated in extra sugar.

What's Related

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Researchers Report

Stanford Study Shows Drug For Treating Type-2 Diabetes May Limit Heart

Disease Risk

Type 1 Diabetics Can Get 'Double Diabetes' From Insulin Resistance,

Says University Of Pittsburgh

> more related stories

--------------------------------------------------------------------------

Related section: Health & Medicine

Type 2 diabetes, the most common form in adults, occurs when muscle, fat and

other tissues stop responding to insulin's signals to mop up sugar from the

blood. The resulting high blood sugar, if uncontrolled, can lead to

blindness, amputation and death. Understanding sugar's precise influence on

insulin's activity may help improve treatment and prevention, scientists

hope.

" Cells don't respond to insulin itself. Instead, a whole cascade of events,

set in motion by insulin, eventually causes cells to take in sugar, "

explains Gerald Hart, Ph.D., professor and director of biological chemistry

in the school's Institute for Basic Biomedical Sciences. " We now have an

explanation of how sugar can affect these signals, and even a hypothesis for

how high blood sugar could cause tissue damage in diabetes -- by improperly

modifying proteins. "

Hart's lab discovered 18 years ago that sugar is used routinely inside cells

to modify proteins, turning them on and off. The more commonly known

protein-controller, phosphate, actually binds to some of the same building

blocks of proteins as sugar does. If proteins have too many sugars on them,

they can't be controlled properly by the cell and are unlikely to work

correctly, suggests Hart.

" We think we've come across a major mechanistic reason for insulin

resistance, " says Hart. " These cells developed insulin resistance simply

because their proteins, and specific proteins in fact, had more than the

normal number of sugar tags. "

If key proteins laden with sugar are present in patients with diabetes, the

findings may provide a target for developing new strategies to deal with

this growing public health threat, says Hart. While diabetes can be fairly

well controlled by diet and carefully monitoring one's blood sugar levels,

finding a way to remove extra sugar tags may help treat or prevent diabetes

someday, the researchers suggest.

" Textbooks frequently and incorrectly show glycosylation only happening to

proteins on the cell surface, " says Hart. " Complex sugars are added only to

proteins outside the cell, but simple sugars are used all the time in the

nucleus and cytoplasm to modify proteins. It's this glycosylation that

happens inside the cell, involving simple sugars, that is the key in insulin

resistance. "

The " simple sugar " to which he refers is O-linked beta-N-acetylglucosamine,

a complex name that condenses to a difficult acronym -- O-GlcNAc -- with an

ugly pronunciation -- " oh-gluck-nack. " But in many ways, O-GlcNAc is a

beautiful and mysterious thing, says Hart.

" O-GlcNAc is a modifier on many proteins, but if you didn't know to look for

it, you'd never find it, " he says. " Instruments and the usual laboratory

methods have a hard time measuring it, so we developed the techniques to

detect it. "

O-GlcNAc is added to proteins by one enzyme and removed from proteins by

another. By selectively blocking that removal, the scientists hoped to load

up proteins with sugar without adding extra sugar (the way other scientists

have created insulin resistance). " We wanted to see the effect of

glycosylation itself, so we used a molecular sledgehammer to increase the

amount of sugar bound to proteins, " says Hart, whose lab proved the ability

of the blocker, a molecule called PUGNAc.

Not only did the blocker increase the amount of O-GlcNAc bound to proteins,

but that increase caused the cells to stop responding to insulin, say

co-first authors and postdoctoral fellows Lance Wells and Vosseller.

Looking for proteins in the insulin-signaling pathway that were more

glycosylated than normal, Vosseller and Wells found two: beta-catenin and

insulin receptor substrate-1 (IRS-1). The crucial role these proteins play

in passing along insulin's messages is likely to be adversely affected by

the extra sugars they carry, the researchers say.

" Our experiments show that increasing O-GlcNAc on proteins is, by itself, a

cause of insulin resistance, rather than an effect or a coincidence, " says

Vosseller.

In the body, sugar (glucose) is changed into glucosamine, which is changed

into O-GlcNAc. Other scientists have shown that giving cells or animals

excessive amounts of sugar or glucosamine, along with extra insulin, leads

to insulin resistance. The new findings provide an explanation for others'

experience with animal and laboratory models of insulin resistance.

There has been little study of glucosamine, a commonly used dietary

supplement, in people. It is suggested that people taking glucosamine

consult their doctors if they are concerned about the possibility of

increasing their risk of developing diabetes.

### Funding was provided by grants and National Research Service Awards from

the National Institutes of Health. Professor of biological chemistry

Lane, Ph.D., is also an author.

Under a licensing agreement between Covance Research Products and The s

Hopkins University, Hart is entitled to a share of royalty received by the

university on sales of the antibody used to detect O-GlcNAc on proteins. The

terms of this arrangement are being managed by The s Hopkins University

in accordance with its conflict of interest policies.

----------------------------------------------------------------------------

----

This story has been adapted from a news release issued by s Hopkins

Medical Institutions.

[Guest guest]

Excellent article, !

Wanita

> http://www.sciencedaily.com/releases/2002/04/020416073449.htm

>

> Source: s Hopkins Medical Institutions

> Date:

> 2002-04-16

>

> Scientists Close In On Trigger Of Insulin Resistance; Extra Sugar Can

Cause

> Insulin Resistance In Cells

> In experiments with fat cells, s Hopkins scientists have discovered

> direct evidence that a build-up of sugar on proteins triggers insulin

> resistance, a key feature of most cases of diabetes. The results

underscore

> the importance of glycosylation - attachment of a sugar to a protein -- as

a

> way cells control proteins' activities, the scientists report in the April

> 16 issue of the Proceedings of the National Academy of Sciences. The

> scientists found that at least two proteins involved in passing along

> insulin's message were unlikely to work properly when coated in extra

sugar.

[Guest guest]

Re: Sugar and Insulin Resistance

> In a message dated 1/9/04 1:32:52 PM Eastern Standard Time,

> mhysmith@... writes:

>

> > The results underscore

> > the importance of glycosylation - attachment of a sugar to a protein --

>

> The fasting/feasting mice studies found that without reducing calories,

> carbs, or sugars, periodic fasting combined with periodic overeating had a

dramatic

> reduction of fasting blood glucose levels, which leads to decreased rates

of

> glycosylation.

>

> Chris

How can an insulin dependant type II fast if they have to have three

injections of insulin a day before each meal? Do they take it upon themself

to combine 3 doses in one for the feasting or divvy it around? If they're

controlling with the oral medication 1X day there's possibilities or they're

controlling with one injection a day. Doctors tend to use 1 X to begin both

oral and injections, doesn't work even with following the prescribed ADA

recipe for continued insulin resistance diet, so the doctor then divvys the

dosage up, down, between and to different meds to try to get control. Low

carb, higher fat, protein, Atkins type- better less processed, Schwartzbein

diet is the " only " choice and hope then for the 3 X day diabetic.

Wanita

[Guest guest]

>How can an insulin dependant type II fast if they have to have three

>injections of insulin a day before each meal? Do they take it upon themself

>to combine 3 doses in one for the feasting or divvy it around? If they're

>controlling with the oral medication 1X day there's possibilities or they're

>controlling with one injection a day. Doctors tend to use 1 X to begin both

>oral and injections, doesn't work even with following the prescribed ADA

>recipe for continued insulin resistance diet, so the doctor then divvys the

>dosage up, down, between and to different meds to try to get control. Low

>carb, higher fat, protein, Atkins type- better less processed, Schwartzbein

>diet is the " only " choice and hope then for the 3 X day diabetic.

>

>Wanita

May be, for now, because that's the only protocol they've tested. If

the feast/fast thing works as well as it seems to, in a few years

they'll have a protocol for it and will be able to say how

many shots to take. Right now it's all in the lab ...

-- Heidi

[Guest guest]

>> periodic fasting combined with periodic overeating had a dramatic

reduction of fasting blood glucose levels <<

Now, why does this matter? You have to be pretty well beyond insulin resistance

and into diabetes before your *fasting* blood glucose is elevated. Mine never

was. It was the post-prandial blood glucose level that was more revealing at a

much earlier stage. In fact, most of us with insulin resistance tended to have

LOW fasting blood glucose (hypoglycemia).

Christie

[Guest guest]

In a message dated 1/10/04 2:46:04 AM Eastern Standard Time,

christiekeith@... writes:

> Now, why does this matter? You have to be pretty well beyond insulin

> resistance and into diabetes before your *fasting* blood glucose is elevated.

Mine

> never was. It was the post-prandial blood glucose level that was more

> revealing at a much earlier stage. In fact, most of us with insulin resistance

> tended to have LOW fasting blood glucose (hypoglycemia).

Christie,

I don't know, except the calorie-restricted mice and fasting-feasting mice

both had lower BG levels than the other groups.

Chris

[Guest guest]

> >How can an insulin dependant type II fast if they have to have three

> >injections of insulin a day before each meal? Do they take it upon

themself

> >to combine 3 doses in one for the feasting or divvy it around? If they're

> >controlling with the oral medication 1X day there's possibilities or

they're

> >controlling with one injection a day. Doctors tend to use 1 X to begin

both

> >oral and injections, doesn't work even with following the prescribed ADA

> >recipe for continued insulin resistance diet, so the doctor then divvys

the

> >dosage up, down, between and to different meds to try to get control. Low

> >carb, higher fat, protein, Atkins type- better less processed,

Schwartzbein

> >diet is the " only " choice and hope then for the 3 X day diabetic.

> >

> >Wanita

>

> May be, for now, because that's the only protocol they've tested. If

> the feast/fast thing works as well as it seems to, in a few years

> they'll have a protocol for it and will be able to say how

> many shots to take. Right now it's all in the lab ...

>

> -- Heidi

Not going to hold my breath till the scientists, doctors and food industry

mutually agree to implement such a threat to their pockets. More in the

meantime will stop breathing as a result of the ugly complications of this

disease. All because of self and society given authority rightness that

amounts to little but foolish,blind greed. Are scientists finding whats

needed to work from. Its like hydrogen energy, if there's no big profit for

everyone marketing along the way to the consumer its not going to happen. If

it implicates they were wrong and change of too much has to happen it'll

stay a finding.

Wanita

[Guest guest]

In a message dated 1/10/04 2:46:04 AM Eastern Standard Time,

christiekeith@... writes:

> Now, why does this matter? You have to be pretty well beyond insulin

> resistance and into diabetes before your *fasting* blood glucose is elevated.

Mine

> never was. It was the post-prandial blood glucose level that was more

> revealing at a much earlier stage. In fact, most of us with insulin resistance

> tended to have LOW fasting blood glucose (hypoglycemia).

Christie,

I responded earlier without being able to think of a flaw in your reasoning,

but I think I can give a better response now.

First, I don't understand these details and I don't think anyone does as of

yet, but since insulin sensitivity had a direct correlation to blood glucose

levels, there *has* to be a flaw in your argument somewhere.

Here's one possible flaw: hypoglycemia is not necessarily an indication of

low fasting blood glucose levels. As Heidi's pointed out in the past,

hypoglycemic symptoms are often confounded with high cortisol symptoms.

Moreover,

when your blood sugar goes low, this usually produces not a constant state of

low

blood sugar, but hypoglycemic-high cortisol swings. It's natural for the

body to secrete glucagon and cortisol when blood sugar becomes low, causing high

blood sugar.

So, hypoglycemia after a carb rich meal or a skipped meal, is not necessarily

an indication that after 18 hours of fasting ones BG levels will be low.

That said, I don't think anyone really fully understands all the intricate

workings here. For some reason, fast/feasting mice have the best overall

markers of health out of all categories testing, with dramatic results in

increased

insulin sensitivity, increased life span, increased resistance to

excitotoxins, lowered blood glucose levels, heightened IGF-1 levels with a

simultaneous

*decrease* in cancer, etc. The lower BG levels are correlated for whatever

reason, and the researchers throw out the possibility that glycosylation is the

mechanism by which this correlation exists.

Chris

[Guest guest]

>> but since insulin sensitivity had a direct correlation to blood glucose

levels, there *has* to be a flaw in your argument somewhere. <<

I didn't say it doesn't have a direct correlation to blood glucose levels, I

said FASTING blood glucose levels (which is specifically what you referred to

being lower in feast/famine and CR mice). My feeling is that overall blood

glucose levels - fasting, postprandial, etc. - would be more useful to look at

than just fasting blood glucose levels, when discussing insulin resistance as

opposed to diabetes.

However, the body will keep blood sugar as normal as possible as long as it

possibly can, even long after you have become insulin resistant. So the problem

can be there even when blood sugar levels at all times are normal.

>> As Heidi's pointed out in the past,

hypoglycemic symptoms are often confounded with high cortisol symptoms. <<

Absolutely - and also, with blood sugar levels that are falling rapidly, but are

not absolutely LOW, so won't register as " low blood sugar " if you check it. I

did use an Accucheck to monitor my blood sugar, I didn't just base it on

symptoms.

However, I don't think that we should posit an either/or for insulin, blood

sugar, and cortisol symptoms, because they are all closely inter-related.

Let me also say, that even if it's shown that feasting/fasting and calorie

restriction control insulin resistance, I'd much rather do it by low carbing,

which also does, because feasting/fasting and calorie restriction don't appeal

to me at all, and no matter how good they made me feel, they'd have to be my

only option before I'd consider them.

Christie

[Guest guest]

In a message dated 1/10/04 4:56:44 PM Eastern Standard Time,

christiekeith@... writes:

> I didn't say it doesn't have a direct correlation to blood glucose levels,

> I said FASTING blood glucose levels (which is specifically what you referred

> to being lower in feast/famine and CR mice). My feeling is that overall blood

> glucose levels - fasting, postprandial, etc. - would be more useful to look

> at than just fasting blood glucose levels, when discussing insulin resistance

> as opposed to diabetes.

But fasting BG levels have direct correlation to insulin sensativity. I

don't know *why*, but nevertheless, to the degree mice get benefits of insulin

sensitivity, they have lowered BG levels.

>

> However, the body will keep blood sugar as normal as possible as long as it

> possibly can, even long after you have become insulin resistant. So the

> problem can be there even when blood sugar levels at all times are normal.

I wonder if what is " normal " is fixed or not. Does blood sugar need to be as

high if one is in a state of ketosis?

>

> >>As Heidi's pointed out in the past,

> hypoglycemic symptoms are often confounded with high cortisol symptoms. <<

>

> Absolutely - and also, with blood sugar levels that are falling rapidly, but

> are not absolutely LOW, so won't register as " low blood sugar " if you check

> it. I did use an Accucheck to monitor my blood sugar, I didn't just base it

> on symptoms.

>

> However, I don't think that we should posit an either/or for insulin, blood

> sugar, and cortisol symptoms, because they are all closely inter-related.

>

> Let me also say, that even if it's shown that feasting/fasting and calorie

> restriction control insulin resistance, I'd much rather do it by low carbing,

> which also does, because feasting/fasting and calorie restriction don't

> appeal to me at all, and no matter how good they made me feel, they'd have to

be

> my only option before I'd consider them.

Fair enough. I'd like to see low-carb thrown in the mix in these studies.

F-F has far greater benefits than calorie restriction in these studies, and it

would be interesting to compare low-carb. I suspect low-carb would come up

more like calorie restriction than f-f in some ways, such as IGF-1 levels, but

don't know, and have no idea how it would affect excitotoxin vulnerability.

Since F-f and calorie restriction have different degrees of effect on insulin

sensitivity, I'd like to see how low-carb compares.

Chris

[Guest guest]

>> Let me also say, that even if it's shown that feasting/fasting and calorie

>> restriction control insulin resistance, I'd much rather do it by low carbing,

>> which also does, because feasting/fasting and calorie restriction don't

>> appeal to me at all, and no matter how good they made me feel, they'd have to

be

>> my only option before I'd consider them.

>

>Fair enough. I'd like to see low-carb thrown in the mix in these studies.

>F-F has far greater benefits than calorie restriction in these studies, and it

>would be interesting to compare low-carb. I suspect low-carb would come up

>more like calorie restriction than f-f in some ways, such as IGF-1 levels, but

>don't know, and have no idea how it would affect excitotoxin vulnerability.

>Since F-f and calorie restriction have different degrees of effect on insulin

>sensitivity, I'd like to see how low-carb compares.

>

>Chris

I've been looking and looking for studies on low-carb mice. I did find

some on tumors (low carb inhibits tumor development) and seizures.

http://charm.cs.uiuc.edu/users/jyelon/lowcarb.med/topic8.html

An interesting one though, is that they reversed T2 diabetes

on a LOW FAT diet:

http://dukemednews.duke.edu/news/article.php?id=519

While doctors have long known that weight loss can control diabetes, the new

research is the first scientific study to show that type 2 diabetes can be

completely reversed in animals by lowering dietary fat, said Dr. Surwit,

professor and vice chairman in the department of psychiatry at Duke. Moreover,

the findings suggest that reducing fat, not just weight, is a primary mechanism

behind the reversal, Surwit said.

Now that doesn't fit ...

I haven't found anything that low-carb diets make mice live longer

though. Only FF and low-cal mice.

-- Heidi

[Guest guest]

In a message dated 1/12/04 2:18:36 AM Eastern Standard Time,

heidis@... writes:

> 519

>

> While doctors have long known that weight loss can control diabetes, the new

> research is the first scientific study to show that type 2 diabetes can be

> completely reversed in animals by lowering dietary fat, said Dr.

> Surwit, professor and vice chairman in the department of psychiatry at Duke.

> Moreover, the findings suggest that reducing fat, not just weight, is a

primary

> mechanism behind the reversal, Surwit said.

>

>

> Now that doesn't fit ...

Maybe the problem is large amounts of fat with significant amounts of

carbohydrate? Some theorize that high blood triglycerides (which are generally

pronounced postprandially with a high-fat meal) interfere with the action of

insulin by " crowding out " the insulin from the cells. They at least *claim* a

lot

of evidence for this.

Perhaps low-carb diets succeed because they are lots of fat, but there isn't

enough carb to get " blocked, " and the problem comes when there is a lot of

both fat and carbohydrate?

I have no idea.

Chris

[Guest guest]

When they say " reducing fat " , are they talking about reducing the

amount of fat in the meals (contrary to what Schwarzbein recommends),

or are they talking about reducing the amount of fat in the person's

body?

Perhaps if it's the latter, then having less fat already in the

body's cells can abate insulin resistance.

If they're talking about reducing the amount of fat in meals, I am

inclined to write them off.

> In a message dated 1/12/04 2:18:36 AM Eastern Standard Time,

> heidis@t... writes:

>

> > 519

> >

> > While doctors have long known that weight loss can control

diabetes, the new

> > research is the first scientific study to show that type 2

diabetes can be

> > completely reversed in animals by lowering dietary fat, said Dr.

> > Surwit, professor and vice chairman in the department of

psychiatry at Duke.

> > Moreover, the findings suggest that reducing fat, not just

weight, is a primary

> > mechanism behind the reversal, Surwit said.

> >

> >

> > Now that doesn't fit ...

>

> Maybe the problem is large amounts of fat with significant amounts

of

> carbohydrate? Some theorize that high blood triglycerides (which

are generally

> pronounced postprandially with a high-fat meal) interfere with the

action of

> insulin by " crowding out " the insulin from the cells. They at

least *claim* a lot

> of evidence for this.

>

> Perhaps low-carb diets succeed because they are lots of fat, but

there isn't

> enough carb to get " blocked, " and the problem comes when there is a

lot of

> both fat and carbohydrate?

>

> I have no idea.

>

> Chris

>

>

>

[Guest guest]

>Perhaps low-carb diets succeed because they are lots of fat, but there isn't

>enough carb to get " blocked, " and the problem comes when there is a lot of

>both fat and carbohydrate?

>

>I have no idea.

>

>Chris

I have no idea either. It also doesn't fit with the healthy Mediterranean

folks, who seem to have a diet pretty high in fat (olive oil) and

carbs (bread at that!).

I still think it turns on the idea of eating TOO MUCH.

They found that rats overeat when fed certain

foods (I think they were using fast food as an

experiment). If your carb stores are " empty " they'd

be more apt to accept extra carbs for storage.

But the Mediterranean folks don't seem to overeat ...

whatever they are eating, they don't eat so much of it

as to make them fat.

-- Heidi

[Guest guest]

My first skeptism to this research comes from the fact it was done in the

department of psychiatry - bad sign for any research, even more questionable

when they are trying to present as experts on endocrine problems and

nutrition. Second would be to look at the study. Most likely it is a

clinical study using only statistics which are easily manipulated. Next you

would look at who paid for the studies. It most likely was the sugar

industry who is pumping out the dollars for any substantiation they can buy

to get the focus off of themselves for all the health problems their sugar

is being blamed for. You cannot believe any research study at face value.

Many of them are not worth the time reading.

Re: Sugar and Insulin Resistance

In a message dated 1/12/04 2:18:36 AM Eastern Standard Time,

heidis@... writes:

> 519

>

> While doctors have long known that weight loss can control diabetes, the

new

> research is the first scientific study to show that type 2 diabetes can

be

> completely reversed in animals by lowering dietary fat, said Dr.

> Surwit, professor and vice chairman in the department of psychiatry at

Duke.

> Moreover, the findings suggest that reducing fat, not just weight, is a

primary

> mechanism behind the reversal, Surwit said.

>

>

> Now that doesn't fit ...

Maybe the problem is large amounts of fat with significant amounts of

carbohydrate? Some theorize that high blood triglycerides (which are

generally

pronounced postprandially with a high-fat meal) interfere with the action

of

insulin by " crowding out " the insulin from the cells. They at least

*claim* a lot

of evidence for this.

Perhaps low-carb diets succeed because they are lots of fat, but there

isn't

enough carb to get " blocked, " and the problem comes when there is a lot of

both fat and carbohydrate?

I have no idea.

Chris

[Guest guest]

This falls into the chicken or egg coming first question. But this is

actually trick thinking. It's overconsumption of carbs that cause insulin

resistance problems as well as weight gain. That is to say, neither diabetes

or excess weight cause each other but rather go together. It is the over

consumption of carbs that cause both.

Losing the weight, whatever diet it is, will require a reduction of the

intake of carbs and will thus, reduce the problems of over production of

insulin. In other words, it is not the weight loss but rather the

improvement in diet that will help control diabetes.

Re: Sugar and Insulin Resistance

When they say " reducing fat " , are they talking about reducing the

amount of fat in the meals (contrary to what Schwarzbein recommends),

or are they talking about reducing the amount of fat in the person's

body?

Perhaps if it's the latter, then having less fat already in the

body's cells can abate insulin resistance.

If they're talking about reducing the amount of fat in meals, I am

inclined to write them off.

> In a message dated 1/12/04 2:18:36 AM Eastern Standard Time,

> heidis@t... writes:

>

> > 519

> >

> > While doctors have long known that weight loss can control

diabetes, the new

> > research is the first scientific study to show that type 2

diabetes can be

> > completely reversed in animals by lowering dietary fat, said Dr.

> > Surwit, professor and vice chairman in the department of

psychiatry at Duke.

> > Moreover, the findings suggest that reducing fat, not just

weight, is a primary

> > mechanism behind the reversal, Surwit said.

> >

> >

> > Now that doesn't fit ...

>

> Maybe the problem is large amounts of fat with significant amounts

of

> carbohydrate? Some theorize that high blood triglycerides (which

are generally

> pronounced postprandially with a high-fat meal) interfere with the

action of

> insulin by " crowding out " the insulin from the cells. They at

least *claim* a lot

> of evidence for this.

>

> Perhaps low-carb diets succeed because they are lots of fat, but

there isn't

> enough carb to get " blocked, " and the problem comes when there is a

lot of

> both fat and carbohydrate?

>

> I have no idea.

>

> Chris

>

>

>

[Guest guest]

>> Since F-f and calorie restriction have different degrees of effect on insulin

sensitivity, I'd like to see how low-carb compares. <<

I agree, I'd love to see that! Of course, we also need to get a definition of

" low carb " in place. <G>

Christie

[Guest guest]

In a message dated 1/12/04 9:56:56 PM Eastern Standard Time,

jaltak@... writes:

> It may be as you say, the diabetic gene has been just lying in wait for

> major adherence to a very poor diet.

Or, a very poor diet in relation to the genetics. I tend to think that

high-animal food diet is inherently a better diet. However, some peoples seems

to

be genetically adapted to a higher carb and lower fat diet. I wonder if these

people have the same potential, on their same diet, to achieve the kind of

health Price's subjects had, since they are essentially adapted to a less

nutrient dense diet?

In any case, I think most of us seem to agree, and it seems pretty obvious to

me, that it is a combination of genetics and environmental factors that

produces EVERY genetic expression, to some degree or other.

Insulin and a variety of other chemicals can have very different effects on a

cell depending on the type of receptor present on the cells surface. This

could, in part, be responsible for genetic predispositions to react a certain

way, perhaps positive or negative, to a certain diet.

People like the Inuit in cold diets would presumably have a genetic

predisposition to have fat cells more receptive to insulin's inhbition of

lypolysis,

and less receptive to adrenalins stimulation of lypolysis, in order to maintain

high body fat. So if their insulin levels are higher than what their 75% fat

diet produced, their going to get fat fast, which might have lots of negative

effects on their physiology.

Chris

[Guest guest]

We have to remember that lab rats and mice are fed artificial food, similar

to commercial dog food, only formulated for them. Their " natural diet " is

far from natural. So when studies are done we need to know if the results

are from the test diet or getting away from the " natural " one.

Judith Alta

-----Original Message-----

>Perhaps low-carb diets succeed because they are lots of fat, but there

isn't

>enough carb to get " blocked, " and the problem comes when there is a lot of

>both fat and carbohydrate?

>

>I have no idea.

>

>Chris

I have no idea either. It also doesn't fit with the healthy Mediterranean

folks, who seem to have a diet pretty high in fat (olive oil) and

carbs (bread at that!).

I still think it turns on the idea of eating TOO MUCH.

They found that rats overeat when fed certain

foods (I think they were using fast food as an

experiment). If your carb stores are " empty " they'd

be more apt to accept extra carbs for storage.

But the Mediterranean folks don't seem to overeat ...

whatever they are eating, they don't eat so much of it

as to make them fat.

-- Heidi

[Guest guest]

Well said, .

Anyone notice how many physical problems are " genetic " these days?

I've thought for a long time that diabetes, etc. look genetic because it

seems to run in families. But the members of those families all eat the same

high carb foods. How does the establishment know that it is genetic and not

diet?

They don't. They just throw out whatever smokescreen they can to cover up

their own greed and incompetence.

Judith Alta

Re: Sugar and Insulin Resistance

When they say " reducing fat " , are they talking about reducing the

amount of fat in the meals (contrary to what Schwarzbein recommends),

or are they talking about reducing the amount of fat in the person's

body?

Perhaps if it's the latter, then having less fat already in the

body's cells can abate insulin resistance.

If they're talking about reducing the amount of fat in meals, I am

inclined to write them off.

> In a message dated 1/12/04 2:18:36 AM Eastern Standard Time,

> heidis@t... writes:

>

> > 519

> >

> > While doctors have long known that weight loss can control

diabetes, the new

> > research is the first scientific study to show that type 2

diabetes can be

> > completely reversed in animals by lowering dietary fat, said Dr.

> > Surwit, professor and vice chairman in the department of

psychiatry at Duke.

> > Moreover, the findings suggest that reducing fat, not just

weight, is a primary

> > mechanism behind the reversal, Surwit said.

> >

> >

> > Now that doesn't fit ...

>

> Maybe the problem is large amounts of fat with significant amounts

of

> carbohydrate? Some theorize that high blood triglycerides (which

are generally

> pronounced postprandially with a high-fat meal) interfere with the

action of

> insulin by " crowding out " the insulin from the cells. They at

least *claim* a lot

> of evidence for this.

>

> Perhaps low-carb diets succeed because they are lots of fat, but

there isn't

> enough carb to get " blocked, " and the problem comes when there is a

lot of

> both fat and carbohydrate?

>

> I have no idea.

>

> Chris

>

>

>

[Guest guest]

Judith-

I've noticed exactly that problem. They don't adequately account for

familial practices, and it seems they never consider the inevitable

interaction of genes with environment. The " gene for diabetes " might cause

or contribute to diabetes under certain conditions (such as, oh, say, a

low-fat high-carb diet) but might have completely different, likely

positive, effects under others.

>Anyone notice how many physical problems are " genetic " these days?

>

>I've thought for a long time that diabetes, etc. look genetic because it

>seems to run in families. But the members of those families all eat the same

>high carb foods. How does the establishment know that it is genetic and not

>diet?

-

[Guest guest]

>> I've noticed exactly that problem. They don't adequately account for

familial practices, and it seems they never consider the inevitable

interaction of genes with environment. The " gene for diabetes " might cause

or contribute to diabetes under certain conditions (such as, oh, say, a

low-fat high-carb diet) but might have completely different, likely

positive, effects under others. <<

I have mixed feelings about this.

I breed dogs. I was indoctrinated like everyone else who breeds dogs that

genetics is all, and then I threw that bit of " conventional wisdom " out the

window in the mid 80s when I discovered the holistic path. No, husbandry was

all! Raw diet, no vaccines, herbal medicine, homeopathy, clean air and water...

this is all you need to have healthy dogs in most cases!

But you know.... now that 18 years have passed, I've come to realize that the

truth lies in between those two extremes. There really ARE many genetic issues

that affect dogs, and also humans. In many human studies they control for

familial practices in a variety of ways, including looking at twins raised since

birth in different families. In dogs, whenever something is more common the more

affected animals are in a pedigree, you have pretty compelling evidence that

genetics are in play.

There is a condition in dogs known as canine hip dysplasia. This is a genetic

disorder that is heavily influenced by diet and environment. You can influence

its expression in susceptible dogs but cannot induce it in breeds who aren't

susceptible. Incidence varies by breed, with the more greyhound-like dogs having

the lowest incidence (or even zero, as in my breed, the ish Deerhound).

It's clear there is a genetic component to this condition, BUT....

Breeders and vets took this to mean that they could completely eliminate CHD

only by breeding practices, and all kinds of breeding programs and testing

schemes came into play in different countries. The incidence of CHD can be

reduced by rigid adherence to these protocols (although often at the cost of

other traits), which does demonstrate that the condition is basically genetic.

But so many people have such an incredibly simplistic (or just plain incorrect)

understanding of how genes work, that any multi-factorial trait, or any genetic

trait that can be affected by environment, stops being " genetic " to them. The

fact that its expression can be influenced by husbandry has led many breeders to

insist that there is NO genetic component to the condition, and to simply breed

whatever dogs they want, ignoring their hip status, or the status of the hips of

the dogs in the pedigree, claiming that raw diets or not vaccinating or not

raising your puppies on hard surfaces or giving vitamin C or whatever their

favorite " cure " was, would prevent CHD, because CHD was NOT genetic. No, it was

a disease of nutritional deficiency or.... fill in the blanks with your pet

theory.

I always say in breeding I make my husbandry decisions as if husbandry were

everything, and my breeding decisions as if genetics were everything. I don't

know any other way to do it. But I think we get into trouble in dog breeding

when we hang our hat on EITHER theory too hard. So I tend to be very wary with

humans, too, in rejecting genetics as the cause of a lot of health problems. I

think there is a definite genetic suspectibility to type 2 diabetes, although

it's obviously highly influenced by diet and other environmental factors. But

that doesn't mean that genes don't come into play.

Christie

[Guest guest]

Having been a small time dog breeder in the distant past, I relate to what

you are saying.

My comment was only about diabetes in humans and was not intended to imply

that genetic diseases and/or conditions do not exist.

It may be as you say, the diabetic gene has been just lying in wait for

major adherence to a very poor diet.

Judith Alta

-----Original Message-----

>> I've noticed exactly that problem. They don't adequately account for

familial practices, and it seems they never consider the inevitable

interaction of genes with environment. The " gene for diabetes " might cause

or contribute to diabetes under certain conditions (such as, oh, say, a

low-fat high-carb diet) but might have completely different, likely

positive, effects under others. <<

I have mixed feelings about this.

I breed dogs. I was indoctrinated like everyone else who breeds dogs that

genetics is all, and then I threw that bit of " conventional wisdom " out the

window in the mid 80s when I discovered the holistic path. No, husbandry was

all! Raw diet, no vaccines, herbal medicine, homeopathy, clean air and

water... this is all you need to have healthy dogs in most cases!

But you know.... now that 18 years have passed, I've come to realize that

the truth lies in between those two extremes. There really ARE many genetic

issues that affect dogs, and also humans. In many human studies they control

for familial practices in a variety of ways, including looking at twins

raised since birth in different families. In dogs, whenever something is

more common the more affected animals are in a pedigree, you have pretty

compelling evidence that genetics are in play.

There is a condition in dogs known as canine hip dysplasia. This is a

genetic disorder that is heavily influenced by diet and environment. You can

influence its expression in susceptible dogs but cannot induce it in breeds

who aren't susceptible. Incidence varies by breed, with the more

greyhound-like dogs having the lowest incidence (or even zero, as in my

breed, the ish Deerhound). It's clear there is a genetic component to

this condition, BUT....

Breeders and vets took this to mean that they could completely eliminate CHD

only by breeding practices, and all kinds of breeding programs and testing

schemes came into play in different countries. The incidence of CHD can be

reduced by rigid adherence to these protocols (although often at the cost of

other traits), which does demonstrate that the condition is basically

genetic. But so many people have such an incredibly simplistic (or just

plain incorrect) understanding of how genes work, that any multi-factorial

trait, or any genetic trait that can be affected by environment, stops being

" genetic " to them. The fact that its expression can be influenced by

husbandry has led many breeders to insist that there is NO genetic component

to the condition, and to simply breed whatever dogs they want, ignoring

their hip status, or the status of the hips of the dogs in the pedigree,

claiming that raw diets or not vaccinating or not raising your puppies on

hard surfaces or giving vitamin C or whatever their favorite " cure " was,

would prevent CHD, because CHD was NOT genetic. No, it was a disease of

nutritional deficiency or.... fill in the blanks with your pet theory.

I always say in breeding I make my husbandry decisions as if husbandry were

everything, and my breeding decisions as if genetics were everything. I

don't know any other way to do it. But I think we get into trouble in dog

breeding when we hang our hat on EITHER theory too hard. So I tend to be

very wary with humans, too, in rejecting genetics as the cause of a lot of

health problems. I think there is a definite genetic suspectibility to type

2 diabetes, although it's obviously highly influenced by diet and other

environmental factors. But that doesn't mean that genes don't come into

play.

Christie

[Guest guest]

Christie,

As I read it, this is exactly the difference in diabetes I and diabetes II.

They know that diabetes I is genetic - they've identified the absence of a

particular pancreatic gene. It's not in a precedant, and it is not in the

baby when born.

With diabetes II, there is no problem gene. It is induced by diet and can

be induced by diet when wanted in a lab.