Re: Re: Setting CRON Objectives

[Guest guest]

I don't know how useful to us, but my recollection is the Ob/Ob genetic variant  mice were ones who were heavier on same energy intake as other mice. Since this seems fall under genetic control rather than behavior there is little we can do besides hope to be Ob-Ob humans.There may have been speculation that overweight humans were Ob-Ob but it seems the vast majority of humans share the overweight gene.. :-)My suggestion was to search Ob/Ob.. from one link The ob/ob homozygous mouse is leptin deficient, hyper-insulinemic and becomes extremely obese.http://www.google.com/search?hl=en & client=safari & rls=en & q=ob%2Fob & btnG=SearchJROn Jul 30, 2008, at 6:02 AM, Rodney wrote:Hi JR:I do not remember the details.  It must have been posted three to five years ago.  So if anyone knows which study it was, that would be very helpful.  As would other papers relevant to the issue.Rodney.> > >> > Hi folks:> >> > For some reason a comment in one of Warren 's posts here, > > long ago, has always stuck in my mind. It was a finding that, > > among the restricted mice, those that lived the absolute longest > > were the ones which, while fed the identical very restricted diet, > > somehow managed to maintain the greatest body fat, compared with > > the other restricted mice.> >> > (If anyone can recall the paper which found this, please post it.)> >> > There is a number of possible explanations for this. One I > > particularly like is that perhaps the longest-lived mice were those > > which managed to avoid any exercise over and above the threshold > > amount absolutely necessary for health, thereby storing the > > calories as fat that the others were burning in exercise ; ^ ))). > > Another possibility is that the longest-lived mice had a lower > > 'metabolic rate', or an especially low body temperature. Or they > > could have been the more diminutive mice, using up fewer calories > > while fed the same as the others.> >> > In any event, whatever the explanation, if it is true, then > > focussing on body fat percentage as a measure of compliance with > > CRON, which is what I have been thinking is appropriate up until > > now, may be mistaken. Rather, perhaps the emphasis should be on > > attaining excellent typical CRON biomarkers** while MAINTAINING THE > > HIGHEST BODY FAT.> >> > In this case, perhaps it may not be helpful to squeeze the last few > > decimals out of some of the biomarkers past the point of > > diminishing returns, by dropping caloric intake appreciably further > > to get a comparatively small additional improvement in biomarker > > values.> >> > Instead, maybe it would be better for longevity (based on the > > Warren quote) to maintain a somewhat higher body fat, if the > > biomarkers are already very good? (I am expecting Tony to agree > > with this!)> >> > Of course arguing against this is the fact that one study found 60% > > restriction produced longer lifespans than 40% restriction. The > > 60% restricted animals couldn't have had a lot of spare body fat! > > But perhaps the longest lived among them were also those with the > > highest traces of body fat?> >> > Any thoughts? Even better, any papers that might help to clarify > > this issue?> >> > ** lipids, BP, CRP, glucose, insulin, T3 .......... perhaps using > > the WUSTL study subjects' data as a benchmark for 'excellent'.> >> > Rodney.> >> >> >>

[Guest guest]

On Sun, Aug 3, 2008 at 6:35 AM, Rodney <perspect1111@...> wrote:

I sure would like to see definitive clarification of whether regular fructose is hazardous. HFCS is avoidable. Fruit is avoidable. But from where I sit the conventional wisdom seems to be that HFCS definitely should be avoided, while fruit definitely should not be. It will be an eye-opener to all of us, I think, if consumption of fructose chemically identical to that in fruit is convincingly shown to be deleterious to health.

My Granny says, and she is never wrong, that glucose is the foundation carbohydrate, perhaps as much as 3 billion years old. Fructose, is a johnny-come-lately, evolving with the flowering plants and selected for because it tastes sweeter than glucose. Glucose can be metabolised by a wide variety of cells, fructose is handled largely by the liver.

Our ancestors of eons ago may only have had large glycemic loads of fructose in the fall, when there was abundant ripe fruit ......

The Finns very recently (damn them) devised methods to enzymatically convert corn starch to fructose at a cost lower than the prior cheap sweetener, sucrose. Therefore the vast array of fructose loaded foods and drinks in any of our supermarkets.

My Granny is 4' 10 " , 90 lbs, is asthmatic, but has a clear mind. She will answer any and all of your questionsOupa with a grin

[Guest guest]

I assume you mean hazardous as in lifespan, because certainly HFCS is

" nutritious " , ie, too much so. It's the excess perhaps that increases weight

in some people - certainly not all.

But you go on as if " being " obese is life shortening. Perhaps it is, but I

don't see it as a premise.

It is more likely higher risk in mortality, which can be overcome with

better medical practices.

HFCS is probably a great agent for athletes who consume maybe 6000 kcals per

day in their training, but not for me walking 3 miles per day.

In any case it seems that vegetarians maybe have more training using a

" good " diet.

Realizing that people are different in their capacity to absorb or reject

nutrients, exercise, grow or reduce weight, the choice of a " standard " diet

for CRON seems to me silly.

It is still my belief that humans can eat anything, as long as they control

their growth which they should have started at 20 yo. If they grew too large

that is a different medical requirement altogether.

The stats we continue to look at are people who are not us. The centenarians

are not CRONers, not vegans, not 7th Day Adventists or Mormons, ie, not

anything in particular.

We have an advantage with drugs that control our systems that evolution

created but didn't necessarily design for >120 yrs.

The best thing for a CRON objective is to make sure we don't do something

silly and result in something like osteoporosis, eg. I don't want to be one

of those " 150 yo " mice that in autopsy bones were easily cut with the

scalpel.

Each person's FX has an effect on their objective. I for example, have

little concern with CVD or cancer or diabetes, rather dementia. Maybe kidney

disease or stroke, at age.

So my diet is least fat, and lower protein than average. Maybe not the diet

for a diabetic.

IOW, you wouldn't like my rice, fruit and ffmilk emphasis, but that for one

reason or another remains.

Regards

[ ] Re: Setting CRON Objectives

Hi Jeff:

I suppose one of the things that may come out of this paper is an

explanation of the data we have discussed before - that vegetarians, and

especially vegans, are no healthier as a group than HEALTH-CONSCIOUS

omnivores.

Perhaps the explanation is that some vegetarians consume as much or more

(methionine and) fructose than omnivores, thereby skewing the health

attributes of the entire group. Some of them are substantially overweight

also, of course.

As you keep reminding us: " Saying they are vegetarian does not tell us what

they eat ................ . "

I sure would like to see definitive clarification of whether regular

fructose is hazardous. HFCS is avoidable.

[Guest guest]

Hi Rodney

1) i think you are putting too much weight into this one paper on

vegetarians. If you read the paper, the author is not very clear on how

he evaluated the diet, but that he didnt count all food consumed. It is

really a poorly done study. In addition, the difference in AGEs was 9.91

to 13.07 which are both extremely low. So, while the " relative " value

was higher (32% which sounds HUGE) , the absolute value was still

extremely low and in regard to total AGE content as discussed in other

papers, irrelevant. And, the above amount can easily be explained by the

3x intake of honey in the vegetarian group.

2) This is the summary review from a recent journal that was dedicated

to a great debate around the issue of AGEs. I highlighted the relevant

comments

Mol. Nutr. Food Res. 2007, 51, 1075 – 1078

Review

Dietary advanced glycation end products – a risk to

human health? A call for an interdisciplinary debate

Henle

3 Biological activity of dietary AGEs – two

sides of a medal?

Starting with reports in the mid 1980s of the 20th century,

the formation ofAGEswas linked to consequences of diabetes

[22] and later on to biological disorders such as cataract

or diabetic nephropathy [23, 24]. Artificially prepared

“AGE-proteins” were found to initiate a range of cellular

responses in vitro, including stimulation of monocyte chemotaxis,

secretion of cytokines and growth factors from

macrophages and endothelial cells, and proliferation of

smooth muscle cells [15]. Concerning molecular mechanisms

responsible for cell activation by AGEs, a specific

receptor designated “RAGE” (”receptor for AGEs”) gained

particular interest [36]. Since its first description, a myriad

of papers has been published showing that binding of ligands

to RAGE results in activation of the proinflammatory transcription

factor nuclear factor-kappaB (NF-jB) and subsequent

expression of NF-jB-regulated cytokines [37, 38].

RAGE-AGE interaction thus may trigger cellular dysfunction

in inflammatory disorders. Based on this findings,

RAGE is discussed as a target for drug development [39],

although the structures of possible RAGE-ligands still have

not been identified. Nowadays, it is generally accepted that

AGEs are an important class of uremic toxins, although there

is virtually no information about defined structure-activity

relationships documenting the “toxic” effect of individual

compounds in physiological concentrations [15, 25].

In line with this discussion, it was not a surprise that

questions arose concerning the intake of dietary AGEs via

the daily food and their possible (patho)physiological role

[26]. From the quantitative point of view, the amount of specific

amino acid derivatives ingested with meals from certain

heated foods farly exceed the total amount of AGEs in

the human body. In this context, it was proposed that serum

AGE levels can be influenced by a diet containing AGEs,

and the term “glycotoxins” was created in order to express

that dietary glycation products may represent a risk factor

in diabetic and uremic patients [27]. Indeed, spectacular

reports showed that a high-AGE diet may lead to an

increase in inflammatory markers [28], and concrete dietary

recommendations were published in order to minimize

health risks by avoiding heated foods [29]. On the other

hand, however, these studies must be discussed carefully

due to considerable limitations in the analytical techniques

used. Furthermore, several recent reports argue against

adverse effects and even discuss positive aspects resulting

from consumption of browned foods. In a cross-sectional

study with hemodialysis patients, it was found that

increased AGEs are not linked to mortality [30]. On a cellular

level, it was found that defined AGEs do not bind to

RAGE, the prominent receptor for AGEs, and do not induce

inflammatory signals, thus arguing against a uniformly role

of AGEs in cellular activation [31, 32]. Furthermore, there

may even be a “chemoprotective” role of individual dietary

AGES due to antioxidative properties or by inhibiting

tumor cell growth [33–35].

4 Conclusion

Physiological consequences resulting from protein-bound

Maillard compounds in foods must be discussed carefully.

This was the idea behind the debate, which is put for discussion

by the papers by Sebekova and Somoza, who argued

for the motion that dietary AGEs are a health risk, and by

Ames, who provided evidence against the motion. In this

two excellent reviews, numerous arguments based on

papers published in high-impact journals are given for each

of the opinions. The fact that no final conclusion can be

drawn, may reflect the need for a more comprehensive

examination of this issue in the future. For a deeper understanding

of biological consequences resulting from heated

foods, the relationships between well-defined biological

effects and well-characterized chemical structures must be

studied. Prerequisite for this is profound chemistry – pure

compounds, exact concentrations, and unambiguous analytical

techniques. A real “risk assessment” is much too complex

than to leave it up to one discipline alone. It must be a

comprehensive and interdisciplinary approach, joining the

resources of biology, medicine, and chemistry.

Regards

*Jeff*

Rodney wrote:

>

> Hi JW:

>

> My argument I think is this:

>

> 1. AGEs are generally agreed to be deleterious to health.

>

> 2. Vegetarians have been shown to have levels of AGEs that are higher

> than those of omnivores. And that is odd because AGEs are usually

> associated with the consumption of high fat animal products and food

> preparation at high temperatures, neither of which are expected

> characteristics of vegetarian diets.

>

> 3. Some are suggesting the explanation for the apparently higher

> levels of AGEs in vegetarians may be the conversion of fructose in

> foods eaten to AGEs internally after consumption. (PMID: 12234125 )

>

> 4. If this is really true, and if low levels of AGEs are desirable,

> then it has some pretty interesting implications as regards the type

> of diet most likely to be associated with lower levels of AGE

> biomarkers. Like: " avoid foods containing unusually large quantities

> of fructose. "

>

> Now of course there may well be a flaw in the above logic. And if

> someone knows what it is, please explain. But if not, how many of us

> (not me for a start) have, up to this point, been actively pursuing a

> diet that, among many other characteristics, is low in fructose?

>

> Should we be?

>

> Rodney.

>

>

> >

> > I assume you mean hazardous as in lifespan, because certainly HFCS is

> > " nutritious " , ie, too much so. It's the excess perhaps that

> increases weight

> > in some people - certainly not all.

> >

> > But you go on as if " being " obese is life shortening. Perhaps it is,

> but I

> > don't see it as a premise.

> > It is more likely higher risk in mortality, which can be overcome with

> > better medical practices.

> >

> > HFCS is probably a great agent for athletes who consume maybe 6000

> kcals per

> > day in their training, but not for me walking 3 miles per day.

> > In any case it seems that vegetarians maybe have more training using a

> > " good " diet.

> >

> > Realizing that people are different in their capacity to absorb or

> reject

> > nutrients, exercise, grow or reduce weight, the choice of a

> " standard " diet

> > for CRON seems to me silly.

> >

> > It is still my belief that humans can eat anything, as long as they

> control

> > their growth which they should have started at 20 yo. If they grew

> too large

> > that is a different medical requirement altogether.

> >

> > The stats we continue to look at are people who are not us. The

> centenarians

> > are not CRONers, not vegans, not 7th Day Adventists or Mormons, ie, not

> > anything in particular.

> > We have an advantage with drugs that control our systems that evolution

> > created but didn't necessarily design for >120 yrs.

> >

> > The best thing for a CRON objective is to make sure we don't do

> something

> > silly and result in something like osteoporosis, eg. I don't want to

> be one

> > of those " 150 yo " mice that in autopsy bones were easily cut with the

> > scalpel.

> >

> > Each person's FX has an effect on their objective. I for example, have

> > little concern with CVD or cancer or diabetes, rather dementia.

> Maybe kidney

> > disease or stroke, at age.

> > So my diet is least fat, and lower protein than average. Maybe not

> the diet

> > for a diabetic.

> >

> > IOW, you wouldn't like my rice, fruit and ffmilk emphasis, but that

> for one

> > reason or another remains.

> >

> > Regards

> >

> >

> >

> >

> >

> > [ ] Re: Setting CRON Objectives

> >

> >

> > Hi Jeff:

> > I suppose one of the things that may come out of this paper is an

> > explanation of the data we have discussed before - that vegetarians, and

> > especially vegans, are no healthier as a group than HEALTH-CONSCIOUS

> > omnivores.

> > Perhaps the explanation is that some vegetarians consume as much or more

> > (methionine and) fructose than omnivores, thereby skewing the health

> > attributes of the entire group. Some of them are substantially

> overweight

> > also, of course.

> > As you keep reminding us: " Saying they are vegetarian does not tell

> us what

> > they eat ................ . "

> > I sure would like to see definitive clarification of whether regular

> > fructose is hazardous. HFCS is avoidable.

> >

>

>

[Guest guest]

Per MNHD,1999, pg 1815:

" Foods that undergo Maillard browning include bread and other baked items,

dried fruits, gravy mixes, maple syrup, dried milk, cocoa and extruded

products ( eg, cereals). "

I assume it could include coffee, peanut butter, roasted peanuts, cookies,

maybe popcorn.

I think also that it maybe doesn't have to be the color of " brown " .

" ...However, in the presence of glucose this reactivity changed, and

compound 1/glucose mixtures showed a positive synergism (synergism factor =

1.6), which was observed neither in methyl stearate/glucose mixtures nor in

the presence of antioxidants. This synergism is proposed to be a consequence

of the formation of free radicals during the asparagine/glucose Maillard

reaction, which oxidized the lipid and facilitated its reaction with the

amino acid. These results suggest that both unoxidized and oxidized lipids

are able to contribute to the conversion of asparagine into acrylamide, but

unoxidized lipids need to be oxidized as a preliminary step. PMID: 18624449

Regards.

[ ] Re: Setting CRON Objectives

Hi JW:

My argument I think is this:

1. AGEs are generally agreed to be deleterious to health.

2. Vegetarians have been shown to have levels of AGEs that are higher than

those of omnivores. And that is odd because AGEs are usually associated

with the consumption of high fat animal products and food preparation at

high temperatures, neither of which are expected characteristics of

vegetarian diets.

3. Some are suggesting the explanation for the apparently higher levels of

AGEs in vegetarians may be the conversion of fructose in foods eaten to AGEs

internally after consumption. (PMID: 12234125 )

4. If this is really true, and if low levels of AGEs are desirable, then

it has some pretty interesting implications as regards the type of diet most

likely to be associated with lower levels of AGE biomarkers. Like: " avoid

foods containing unusually large quantities of fructose. "

Now of course there may well be a flaw in the above logic. And if someone

knows what it is, please explain. But if not, how many of us (not me for a

start) have, up to this point, been actively pursuing a diet that, among

many other characteristics, is low in fructose?

Should we be?

Rodney.

[Guest guest]

I notice that Granny’s age was not revealed. (Not that anecdotal evidence is worth much anyway).

From: jwwright <jwwright@...>

Reply-< >

Date: Mon, 4 Aug 2008 08:49:04 -0700

< >

Subject: Re: [ ] Re: Setting CRON Objectives

Just questions.

Ask her what our ancestors ate when they lived in trees 26 mill years ago.

Weren't those trees flowering?

Was the " fruit " like a pear or a nut? Did it not contain fructose or

glucose(dextrose)?

Why did plants evolve the technique of feeding the animal to spread the

seed?

Regards

Re: [ ] Re: Setting CRON Objectives

My Granny says, and she is never wrong, that glucose is the foundation

carbohydrate, perhaps as much as 3 billion years old. Fructose, is a

johnny-come-lately, evolving with the flowering plants and selected for

because it tastes sweeter than glucose. Glucose can be metabolised by a wide

variety of cells, fructose is handled largely by the liver.

Our ancestors of eons ago may only have had large glycemic loads of fructose

in the fall, when there was abundant ripe fruit ......

The Finns very recently (damn them) devised methods to enzymatically convert

corn starch to fructose at a cost lower than the prior cheap sweetener,

sucrose. Therefore the vast array of fructose loaded foods and drinks in any

of our supermarkets.

My Granny is 4' 10 " , 90 lbs, is asthmatic, but has a clear mind. She will

answer any and all of your questions

Oupa with a grin

[Guest guest]

Just questions.

Ask her what our ancestors ate when they lived in trees 26 mill years ago.

Weren't those trees flowering?

Was the " fruit " like a pear or a nut? Did it not contain fructose or

glucose(dextrose)?

Why did plants evolve the technique of feeding the animal to spread the

seed?

Regards

Re: [ ] Re: Setting CRON Objectives

My Granny says, and she is never wrong, that glucose is the foundation

carbohydrate, perhaps as much as 3 billion years old. Fructose, is a

johnny-come-lately, evolving with the flowering plants and selected for

because it tastes sweeter than glucose. Glucose can be metabolised by a wide

variety of cells, fructose is handled largely by the liver.

Our ancestors of eons ago may only have had large glycemic loads of fructose

in the fall, when there was abundant ripe fruit ......

The Finns very recently (damn them) devised methods to enzymatically convert

corn starch to fructose at a cost lower than the prior cheap sweetener,

sucrose. Therefore the vast array of fructose loaded foods and drinks in any

of our supermarkets.

My Granny is 4' 10 " , 90 lbs, is asthmatic, but has a clear mind. She will

answer any and all of your questions

Oupa with a grin

[Guest guest]

No argument.

I think the comments were inre to understanding the biochemistry evolution.

I had just assumed that trees held the same kind of fruit.

Actually I doubt anyone knows. We don't have that produce in stores.

There are millions of things we were not evolved/adapted to eat and don't eat because they are toxic.

HFCS was never offered as a health food, rather the solution to a rising cost of sugar. In excess, it might easily be shown to cause something bad.

Regards

Re: [ ] Re: Setting CRON Objectives> > My Granny says, and she is never wrong, that glucose is the foundation> carbohydrate, perhaps as much as 3 billion years old. Fructose, is a> johnny-come-lately, evolving with the flowering plants and selected for> because it tastes sweeter than glucose. Glucose can be metabolisedby a wide> variety of cells, fructose is handled largely by the liver.> Our ancestors of eons ago may only have had large glycemic loads offructose> in the fall, when there was abundant ripe fruit ......> The Finns very recently (damn them) devised methods to enzymaticallyconvert> corn starch to fructose at a cost lower than the prior cheap sweetener,> sucrose. Therefore the vast array of fructose loaded foods anddrinks in any> of our supermarkets.> My Granny is 4' 10", 90 lbs, is asthmatic, but has a clear mind. Shewill> answer any and all of your questions> Oupa with a grin>