• Log in with Facebook Log in with Twitter Log In with Google      Sign In    
  • Create Account
  LongeCity
              Advocacy & Research for Unlimited Lifespans

Photo
* * * * * 3 votes

Carbs = aging


  • Please log in to reply
335 replies to this topic

#241 Dmitri

  • Guest
  • 841 posts
  • 33
  • Location:Houston and Chicago

Posted 06 February 2009 - 01:17 AM

proving a lack of something is impossible. You want me to show you a bunch of papers that aren't there? The burden of proof is with those who claim there is a program, and they haven't done it.

Human aging is best explained by outlasting our warranty period. If there were an aging program there would be people walking around with that program broken just like there are people with every developmental program you can imagine broken.


I thought aging was part of evolution or programmed as a way to prevent overpopulation or competition for future generations since evolution is all about survival of the fittest and reproduction is it not?

#242 Prometheus

  • Guest
  • 592 posts
  • -3
  • Location:right behind you

Posted 06 February 2009 - 04:37 AM

proving a lack of something is impossible. You want me to show you a bunch of papers that aren't there? The burden of proof is with those who claim there is a program, and they haven't done it.

Human aging is best explained by outlasting our warranty period. If there were an aging program there would be people walking around with that program broken just like there are people with every developmental program you can imagine broken.


I thought aging was part of evolution or programmed as a way to prevent overpopulation or competition for future generations since evolution is all about survival of the fittest and reproduction is it not?


Yep.

sponsored ad

  • Advert
Click HERE to rent this advertising spot for NUTRITION to support LongeCity (this will replace the google ad above).

#243 JLL

  • Guest
  • 2,192 posts
  • 161

Posted 06 February 2009 - 09:30 AM

Using prevention of overpopulation as an answer only raises the question of why would we need to pass our genes on in the first place if we did not age? It would make more sense that we reproduce because we die, not the other way around.

#244 nowayout

  • Guest
  • 2,946 posts
  • 439
  • Location:Earth

Posted 06 February 2009 - 11:48 AM

proving a lack of something is impossible. You want me to show you a bunch of papers that aren't there? The burden of proof is with those who claim there is a program, and they haven't done it.

Human aging is best explained by outlasting our warranty period. If there were an aging program there would be people walking around with that program broken just like there are people with every developmental program you can imagine broken.


I thought aging was part of evolution or programmed as a way to prevent overpopulation or competition for future generations since evolution is all about survival of the fittest and reproduction is it not?



I believe that theory, proposed by Weismann in the 18th century, has largely fallen by the wayside in evolutionary circles. Weismann himself rejected this theory later on.

#245 Prometheus

  • Guest
  • 592 posts
  • -3
  • Location:right behind you

Posted 06 February 2009 - 02:46 PM

Evolution..? Consider the consequence of non-aging organisms.. An aging trait would be selected for..

#246 nowayout

  • Guest
  • 2,946 posts
  • 439
  • Location:Earth

Posted 06 February 2009 - 03:50 PM

Evolution..? Consider the consequence of non-aging organisms.. An aging trait would be selected for..


What you say sounds reasonable, except that there is pretty strong evidence against it. A good review of this can be found in the article at http://longevity-sci...g/Evolution.htm. Quoting from that article:

Evolutionary Theories of
Aging and Longevity
Leonid A. Gavrilov* and Natalia S. Gavrilova Center on Aging, NORC/University of Chicago, 1155 East 60th Street, Chicago, IL 60637

[....]

Subsequent studies confirmed that Weismann's decision to abandon the initial idea of programmed death was a wise one. Many scientific tests of the programmed death hypothesis were made since Weismann proposed his theory, and some of them are summarized here (for more details[2]). One way of testing the programmed death hypothesis is based on a comparison of lifespan data for individuals of a single species in natural (wild) and protected (laboratory, domestic, civilized) environments. If the hypothesis is correct, there should not be very large differences in the lifetimes of adult individuals across compared environments. Indeed, for a self-destruction program to arise, take hold, and be maintained in the course of evolution, it must at least have some opportunity, however small, of expression in natural conditions. Consequently, the age at which such a program is "switched on"cannot be too high. Otherwise, because of the high mortality in the wild from predators, hunger, infections, and harsh natural conditions, no one would live to the fateful age, and the self-destruction mechanism could not be expressed. It follows from this that lifespans in even the most favorable conditions cannot significantly exceed the ages reached by the most robust individuals in the wild, if, of course, the tested concept is correct. Analysis of the actual data reveals, however, a picture completely opposite to what would be expected from the programmed death theory: the lifespans of organisms in protected environments greatly exceed the lifespans observed in natural conditions.

For example, the chaffinch (Fringilla coelebs) can live for 29 years in captivity[70]. However, in the wild this is practically impossible, since about half of all birds perish in the course of a year from hunger, cold, disease, and attack by predators, and the mean life span is only 1.4 to 1.5 years[71]. As a result of this high mortality, only 0.1% of the initial number of chaffinches survives to age 11.

Similar observations have been made for field voles (Microtus arvalis Pall). In protected laboratory conditions, the average lifespan of voles is about 7 to 8 months while individual specimens survive to 25 months[72]. In the wild, however, the average lifespan of voles is only 1.2 months while only 0.1% of the original number of voles survives to 10 months[72].

As for primates, the median lifespan (age at 50% survival) of chimpanzees (Pan troglodytes) living in captivity is between 23 years (males) and 30 years (females), and almost 20% of captive female chimpanzees survive to age 50[73,74]. However, in the wild "natural" conditions the median lifespan is only 8 years, and almost nobody survives to age 50[74].

Observations like these are common for many biological species. Thus, if one attempts to estimate the age of programmed death on the basis of lifespans in laboratory conditions, it becomes clear that no death program could arise or be maintained in evolution if only because it would not be able to come into operation in natural conditions where practically no individual lives to the required age.




The same conclusion is reached from an analysis of data on the human lifespan. At present, the mean life expectancy in developed countries is about 70 to 80 years while the documented record for longevity is 122 years[75,76]. If we take these figures as an estimate for age range in which the death program is switched on, we are forced to admit that such a program could not have arisen in human evolution since, according to palaeodemographic data, virtually nobody survived to such an age. For example, only half of those born in the Late Palaeolithic (30,000 to 10,000 B.C.) reached 8 to 9 years, and only half of those born in the Neolithic (6,000 to 2,000 B.C.) reached 26 years[77]. Moreover, even in the Middle Ages (9th to 12th centuries), life expectancy at birth was no greater than 27 to 29 years. Investigations of the skeletons of American Indians have shown that only 4% of the population survived to age 50 even as late as in the 18th century[78]. Note for comparison that the probability of surviving to this age in the developed countries is 94 to 96%. If these facts are compared, it is difficult to refrain from posing the following question: Can the guaranteed destruction of a few old people who are chance survivors and doomed in the wild be a sufficient evolutionary basis for the formation and preservation of a special self-destruction program in the human genome? Viewed in this light, the inconsistency of the programmed death hypothesis becomes clear.

The second way to test the programmed death hypothesis is to study the dependence of death rates on an animal's age. If this theory is correct, then the age-dependence of death rates should change dramatically (explode) after some critical age later in life when the alleged death program comes into action. There should be a breaking point in the dependence of death rates on an animal's age, and this breaking point should be particularly evident in genetically homogeneous stocks of animals kept in standard laboratory conditions. This prediction was carefully tested by studying hundreds of published life tables compiled for many dozens of different biological species, including humans[2]. This study found that the age-dependence of death rates is very smooth and monotonic without any signs of some critical age or breaking point later in life corresponding to an expected mortality explosion[2]. For example, in humans the death rates start to increase with age as early as age 20, and the mortality trajectory follows a simple monotonic Gompertz-Makeham curve[2]. Moreover, the actual death rates at extreme old ages are even lower than expected according to the monotonic Gompertz-Makeham model[79], which is completely opposite to the prediction of the programmed death theory[2].

Finally, if the question whether death is programmed is approached from the evolutionary point of view, it becomes obvious that special mechanisms for the termination of life could hardly help the individual to fight successfully for his survival and the survival of his progeny. On the contrary, those individuals in whom the action of such a program of self-destruction had been impaired by some spontaneous mutation would quickly displace all the remaining individuals. This is because they would produce more offspring in their longer lifespan, or at least they could increase the survival of their offspring by providing longer parental support.

In 1957 George Williams[11], the author of another evolutionary theory of aging (see discussion later) summarized critical arguments against the programmed death theory (called Weismann's theory for historical reasons). Here is the partial list of his most forceful critical arguments that have now gained even more strength and support:

  • "The extreme rarity, in natural populations, of individuals that would be old enough to die of the postulated death-mechanism"."The failure of several decades [now a century! L.A.G. & N.S.G.] of gerontological research to uncover any death-mechanism"; (Note that the later discovery of apoptosis, programmed cell death [80,81], is irrelevant to this discussion focusing on the death-mechanism for the whole organism rather than for some of its somatic cells. It is also important to note that apoptosis is mainly at play during early development and thus is not specific to aging.) "The difficulties involved in visualizing how such a feature [program for death] could be produced by natural selection".
[...]





#247 Shepard

  • Member, Director, Moderator
  • 6,360 posts
  • 932
  • Location:Auburn, AL

Posted 06 February 2009 - 11:57 PM

Well it was my thinking that insulinogenic proteins have a concomittment rise in glucagon, this doesnt happen to the same extent with carbohydrates. So if we have insulin rising, which increases fat storage, along with glucagon rising which helps burn fat then we have blunted fat storage activity compared to carbohydrates which exhibit mostly a rise in insulin without the glucagon.


Could you elaborate on this idea? Glucagon doesn't have anything directly to do with fat tissue. By lowering liver glycogen, it would set into motion a situation where ketone concentrations would increase, but in the above setting, provided energy was balanced, the newfound glucose would just be restored in the liver.

And, this fat storage idea needs to be reapproached. Dietary fat makes a pass through adipose before being oxidized. One should worry about FA oxidation and/or lipolysis (whichever is the limiting factor, depending on situation).

Depends on how much fat you eat.

Could you elaborate?


Meaning that chylomicron concentration scales linearly with the amount of ingested fat.

#248 Prometheus

  • Guest
  • 592 posts
  • -3
  • Location:right behind you

Posted 07 February 2009 - 12:04 AM

From an evolutionary perspective, there would be a negative selection force that would support an aging program that Weismann and Gavrilov et al did not account for - the advantage of a non-aging individual over an aging one. In order to understand why this would be so, let's define non-aging as a trait that can be selected for, or against. Also, lets be reminded that evolution is driven by changes in DNA that arise by mutation events and recombination, and that these changes in DNA become manifest only with each new generation.

Individuals with the non-aging trait, as they become older (not in frailty but in experience), will have the benefit of additional knowledge about their environment as compared to younger individuals and will have a survival advantage. In time, non-aging individuals would displace aging individuals due to this survival advantage until the population is dominated by non-aging individuals. Given limited resources, in a non-aging population the amount of progeny surviving to reproduce would decrease and therefore have a negative impact on the rate of evolution for that population. Over time, and particularly with changing environmental conditions (climate, predation, pathogen evolution, etc), the individuals that are capable of evolution would be selected for.

#249 Lazarus Long

  • Life Member, Guardian
  • 8,116 posts
  • 242
  • Location:Northern, Western Hemisphere of Earth, Usually of late, New York

Posted 07 February 2009 - 12:15 AM

From an evolutionary perspective, there would be a negative selection force that would support an aging program that Weismann and Gavrilov et al did not account for - the advantage of a non-aging individual over an aging one. In order to understand why this would be so, let's define non-aging as a trait that can be selected for, or against. Also, lets be reminded that evolution is driven by changes in DNA that arise by mutation events and recombination, and that these changes in DNA become manifest only with each new generation.


Actually this is not true because of the selective pressure throughout human evolution to have children and raise them while relatively young. This means that even if an aging gene exists there is no selection advantage.

What you are describing would require a selective pressure away from this common evolutionary experience to one where the age of parenting trends older and younger parenting was selected against.

Ironically while that never occurred naturally throughout human evolution we are now making that event occur due to socioeconomic pressure as we adapt to a new environment of our own creation.

Individuals with the non-aging trait, as they become older (not in frailty but in experience), will have the benefit of additional knowledge about their environment as compared to younger individuals and will have a survival advantage. In time, non-aging individuals would displace aging individuals due to this survival advantage until the population is dominated by non-aging individuals. Given limited resources, in a non-aging population the amount of progeny surviving to reproduce would decrease and therefore have a negative impact on the rate of evolution for that population. Over time, and particularly with changing environmental conditions (climate, predation, pathogen evolution, etc), the individuals that are capable of evolution would be selected for.


This is not an example of Darwinian selection and is more like Lamarck. I am afraid you are confusing the advantages of learning associated with longevity for its genetic selection characteristics. The traits you are describing are not really transmittable generation to generation through genetics but are transmittable through memetics.

#250 nowayout

  • Guest
  • 2,946 posts
  • 439
  • Location:Earth

Posted 07 February 2009 - 01:34 PM

From an evolutionary perspective, there would be a negative selection force that would support an aging program that Weismann and Gavrilov et al did not account for - the advantage of a non-aging individual over an aging one.


The point is that under natural conditions for most species there is no difference between an aging and a non-aging individual, because animals overwhelmingly die of environmental conditions, predation, etc., not of age. To take the first of their examples, even physiologically immortal chaffinches in nature would still have very short lives. Physiological immortality would make absolutely no difference to their lifespan (and might even shorten it because of the extra resources needed for DNA repair, etc.). The same can probably be said for early humans (see the survival figures in the piece I quoted).

So the point was, no, the evidence shows no significant advantage for a non-aging individual over an aging one in a number of species.

Your negative selection force, on the other hand, probably has something to do with the longer lifespans of species that do not die so early of environmental causes. It probably partially explains why humans have a longer maximal lifespan than other primates. But it only seems to be active up until the point where environmental causes of death again cancel out any advantage, which is probably why humans don't live forever.

Edited by andre, 07 February 2009 - 01:43 PM.


#251 Prometheus

  • Guest
  • 592 posts
  • -3
  • Location:right behind you

Posted 07 February 2009 - 11:05 PM

(incidentally, Lamarckian evolution has been proven to exist - its known as epigenetics)

A non-aging trait would confer increased individual survivability provided the organism is capable of learning from experience. With humans we have come to think of experience as a trade-off for vigor due to aging, but if aging did not exist then those who survived initial adversities would become increasingly adept at survival due to learning. For example, compare a human at age 80 who has the physical vigor of a 18-year old with an actual 18-year old who is less 'informed' about their environment. Who do you think is most likely to survive and pass on their genes? Given that evolution is mediated by changes in DNA whose suitability can only be tested once an organism has grown to reproductive age, it follows that if you have more 80-year olds passing on their genes than 18-year olds that the rate of evolution would decrease.

As previously stated, such a scenario would lead to dominance of the gene pool by - for illustrative purposes - great, great, great grandfathers who are becoming increasing older and therefore more survival-adept yet have no accompanying age-associated frailty. In human societies, an 'elder' is typically rendered some leadership role within the group. Now imagine an elder that does not age. If its a he, its very likely that he would have greater access to the reproductive females and his genes would dominate the group. Given limited resources, if death by aging is no longer a factor the population increase would require a commensurate decrease in births..

#252 Mind

  • Life Member, Director, Moderator, Treasurer
  • 19,077 posts
  • 2,000
  • Location:Wausau, WI

Posted 08 February 2009 - 02:24 AM

Sorry to break from the great discussion about evolved aging (or not) but I found this relevant to the thread at hand: Alzheimers linked with diabetes. For everyone who understands the carbs/insulin/diabetes connection it is not hard to make the connection to Alzheimer's as well.

cross-posted here as well.

#253 RoadToAwe

  • Guest
  • 60 posts
  • 8

Posted 09 February 2009 - 12:08 AM

I'm pretty sure you're talking about the Pima, a well studied tribe that at one time was thin and healthy, but then along came the white man's high-grain diet and fattened them up within a decade or two. Carbs are pinpointed as the exact reason for this tribe's obesity problem.


Duke, what is your source?

Traditional Pima Indian diet was heavy on carbohydrates(70-80%). 

http://www.ncbi.nlm..../pubmed/8422813

Modern Pima Indian diet is heavy on fat.

Deterioration in carbohydrate metabolism and lipoprotein changes induced by modern, high fat diet in Pima Indians and Caucasians.

http://www.ncbi.nlm..../pubmed/2045466

Edited by RoadToAwe, 09 February 2009 - 12:09 AM.


#254 mike250

  • Guest
  • 981 posts
  • 9

Posted 11 February 2009 - 12:08 AM

I'm pretty sure you're talking about the Pima, a well studied tribe that at one time was thin and healthy, but then along came the white man's high-grain diet and fattened them up within a decade or two. Carbs are pinpointed as the exact reason for this tribe's obesity problem.


Duke, what is your source?

Traditional Pima Indian diet was heavy on carbohydrates(70-80%). 

http://www.ncbi.nlm..../pubmed/8422813

Modern Pima Indian diet is heavy on fat.

Deterioration in carbohydrate metabolism and lipoprotein changes induced by modern, high fat diet in Pima Indians and Caucasians.

http://www.ncbi.nlm..../pubmed/2045466


I'd be curious if they were healthy on 80% carbohydrates. That had to have been corn. I guess nixtamalizing corn is effective at reducing lectins. The specific fats they switched to are relevant. It was no doubt industrial vegetable oils. However I dont buy the "thrifty gene" hypothesis. Using white flour and corn oil are probably why american indians started getting diabetes.

#255 nowayout

  • Guest
  • 2,946 posts
  • 439
  • Location:Earth

Posted 11 February 2009 - 12:48 AM

I'd be curious if they were healthy on 80% carbohydrates. That had to have been corn. I guess nixtamalizing corn is effective at reducing lectins. The specific fats they switched to are relevant. It was no doubt industrial vegetable oils. However I dont buy the "thrifty gene" hypothesis. Using white flour and corn oil are probably why american indians started getting diabetes.


Well, the fat may very well be the main culprit.

The effects of diet differing in fat, carbohydrate, and fiber on carbohydrate and lipid metabolism in type II diabetes.
O'Dea K, Traianedes K, Ireland P, Niall M, Sadler J, Hopper J, De Luise M. Department of Medicine (University of Melbourne) Repatriation General Hospital, Heidelberg, Victoria, Australia.

This study was designed to determine the effects of varying the proportions of carbohydrate, fiber, and fat on metabolic control in Type II diabetes. Ten men, aged 50 to 69 years, with Type II diabetes participated. Four isocaloric diets were consumed for 2 weeks each, with a break of 6 to 14 weeks between diets to ensure no carryover effects. Two of the diets were high in carbohydrate (63% to 65% energy) and low in fat (10% to 12% energy) but differed in their fiber contents (20 vs. 45 gm/day). The other two diets were low in carbohydrate (23% to 27% energy) with either a low or a high fat content (15% vs. 55% energy) and a high or normal protein content (62% vs. 18% energy). The composition of the subjects' usual diets in the week before each of the experimental diets did not vary significantly: carbohydrate 47% to 50% energy, protein 22% to 25% energy, fat 27% to 31% energy, and fiber 24 to 25 gm/day. A 75-gm oral glucose tolerance test and a 12-hour metabolic profile in response to 3 meals typical of the particular diet were conducted before and at the conclusion of each 2-week dietary period. The most significant improvements in metabolic control (as assessed by the effects of the diets on fasting glucose and on lipids, and on the glucose and insulin responses to oral glucose and the mixed meals) were obtained with the high-fiber, high-carbohydrate, low-fat diet and with the low-carbohydrate, high-protein, low-fat diet. Metabolic control was not significantly affected by the low-fiber, high-carbohydrate, low-fat diet, but it deteriorated significantly on the low-carbohydrate, high-fat diet. The results of this study confirmed the importance of high fiber and low fat in improving metabolic control in Type II diabetes. In conclusion, if high-carbohydrate, low-fat diets are to be recommended to patients with diabetes, it is essential that the type of carbohydrate recommended be unrefined and high in fiber


Edited by andre, 11 February 2009 - 12:49 AM.


#256 JLL

  • Guest
  • 2,192 posts
  • 161

Posted 11 February 2009 - 09:53 AM

So is that what shepard was talking about in another thread? That what's good for a healthy person (low-carb) is not good for a type II diabetes patient? Otherwise that seems like a strange result.

#257 mike250

  • Guest
  • 981 posts
  • 9

Posted 12 February 2009 - 01:20 AM

I'd be curious if they were healthy on 80% carbohydrates. That had to have been corn. I guess nixtamalizing corn is effective at reducing lectins. The specific fats they switched to are relevant. It was no doubt industrial vegetable oils. However I dont buy the "thrifty gene" hypothesis. Using white flour and corn oil are probably why american indians started getting diabetes.


Well, the fat may very well be the main culprit.

The effects of diet differing in fat, carbohydrate, and fiber on carbohydrate and lipid metabolism in type II diabetes.
O'Dea K, Traianedes K, Ireland P, Niall M, Sadler J, Hopper J, De Luise M. Department of Medicine (University of Melbourne) Repatriation General Hospital, Heidelberg, Victoria, Australia.

This study was designed to determine the effects of varying the proportions of carbohydrate, fiber, and fat on metabolic control in Type II diabetes. Ten men, aged 50 to 69 years, with Type II diabetes participated. Four isocaloric diets were consumed for 2 weeks each, with a break of 6 to 14 weeks between diets to ensure no carryover effects. Two of the diets were high in carbohydrate (63% to 65% energy) and low in fat (10% to 12% energy) but differed in their fiber contents (20 vs. 45 gm/day). The other two diets were low in carbohydrate (23% to 27% energy) with either a low or a high fat content (15% vs. 55% energy) and a high or normal protein content (62% vs. 18% energy). The composition of the subjects' usual diets in the week before each of the experimental diets did not vary significantly: carbohydrate 47% to 50% energy, protein 22% to 25% energy, fat 27% to 31% energy, and fiber 24 to 25 gm/day. A 75-gm oral glucose tolerance test and a 12-hour metabolic profile in response to 3 meals typical of the particular diet were conducted before and at the conclusion of each 2-week dietary period. The most significant improvements in metabolic control (as assessed by the effects of the diets on fasting glucose and on lipids, and on the glucose and insulin responses to oral glucose and the mixed meals) were obtained with the high-fiber, high-carbohydrate, low-fat diet and with the low-carbohydrate, high-protein, low-fat diet. Metabolic control was not significantly affected by the low-fiber, high-carbohydrate, low-fat diet, but it deteriorated significantly on the low-carbohydrate, high-fat diet. The results of this study confirmed the importance of high fiber and low fat in improving metabolic control in Type II diabetes. In conclusion, if high-carbohydrate, low-fat diets are to be recommended to patients with diabetes, it is essential that the type of carbohydrate recommended be unrefined and high in fiber


lol, 25% calories from carbs as low-carb. these guys are jokers. I'm going to disregard the abstract unless you can bring up the paper.

Edited by mike250, 12 February 2009 - 01:21 AM.


#258 DukeNukem

  • Topic Starter
  • Guest
  • 2,008 posts
  • 141
  • Location:Dallas, Texas

Posted 12 February 2009 - 04:08 AM

I'm pretty sure you're talking about the Pima, a well studied tribe that at one time was thin and healthy, but then along came the white man's high-grain diet and fattened them up within a decade or two. Carbs are pinpointed as the exact reason for this tribe's obesity problem.


Duke, what is your source?

Traditional Pima Indian diet was heavy on carbohydrates(70-80%). 

http://www.ncbi.nlm..../pubmed/8422813

Modern Pima Indian diet is heavy on fat.

Deterioration in carbohydrate metabolism and lipoprotein changes induced by modern, high fat diet in Pima Indians and Caucasians.

http://www.ncbi.nlm..../pubmed/2045466


Good Calorie, Bad Calorie used the Pima as an example, plus I had read about them in other books (can't remember which ones currently).

#259 wydell

  • Guest
  • 503 posts
  • -1

Posted 14 February 2009 - 04:48 PM

I was browsing around and saw that this reference indicated that beef produced the same or similar insulin secretion response as brown rice. So perhaps the "whole grains stimulate insulin" argument is bogus at least with respect to the idea of substituting meat to obtain better insulin response.


http://www.ajcn.org/...print/66/5/1264

#260 woly

  • Guest, F@H
  • 279 posts
  • 11

Posted 15 February 2009 - 08:17 AM

1. while some low carb foods such as meat exhibit a high insulin response, i beleive that the rise in insulin is met with a glucagon which blunts the fat storage effects. however to what extent, i am unsure


How would it blunt any fat storage effects (not that I'm on the insulin = fat bandwagon)? Glucagon is also used to help maintain glucose homeostasis. More insulinogenic proteins should elicit greater glucagon responses since insulin would drive down the glucose (created via gluconeogenesis) more than optimal.

c) while ASP rises during a high fat meal, it seems that it is most potently activated by chylomicrons. this point seems important to me because chylomicrons have a half life of about 5 minutes in the blood which gives me the impression that while ASP would rise after eating a high fat meal, the rise would be short lived.


Depends on how much fat you eat.


1. Doesnt glucagon influence lipolysis?

2. Absolutely it depends on how fat you eat. I am not saying that you cannot get fat on a low carb but rather it is more difficult to.

#261 Shepard

  • Member, Director, Moderator
  • 6,360 posts
  • 932
  • Location:Auburn, AL

Posted 15 February 2009 - 06:01 PM

1. Doesnt glucagon influence lipolysis?



It seems to act directly on lipolysis in vitro and at pharmacological doses in vivo, but not at physiological doses. In normal scenarios where glucagon is raised, such as carbohydrate restriction or between meals, this is all semantics as the glucagon-induced rise of cAMP and the increase in AMPK (from the shift in AMP:ATP ratio) increase lipolysis on their own. The only point WRT protein ingestion, is that unless the end result is a liver with less stored glycogen (for whatever reason), the rise in glucagon should be seen as nothing more than an attempt to maintain glucose homeostasis from the rise in insulin.

#262 Jay

  • Guest
  • 406 posts
  • 22
  • Location:New York

Posted 24 February 2009 - 03:38 PM

What about the methylglyoxal issue? I'm sure you low carbers are familiar with it. If not: http://mfoundation.o...t=methylglyoxal

Do the benefits outweigh the risks?


I've been wondering about that too. This is what Michael Eades (responding to a comment) says about the issue:

"I was surprised, however, with his [Aubrey] one page attack on ketogenic diets as causing an increase in methylglycoxal as being a driving force in protein cross linking. I though Aubrey was smarter than that. He first states that high blood sugar is a potent AGE-producing force (as are increased levels of blood fats) then says that if you follow a ketogenic diet to reduce blood sugar and triglycerides you will be increasing the levels of methylglycoxal, which is a more potent AGE promoter. He bases this supposition on the paper you link to above [http://www.blackwell...ournalCode=nyas]. Altough methylglcoxal is a more potent AGE promoter, its concentration - even when elevated - is so abysmally low compared to that of the less potent blood sugar that it makes very little difference. A reduction in blood sugar (even if accompanied by an increase in methylglycoxal) brings about a reduction of AGE formation that is orders of magnitude greater than the increase engendered by even a doubling of methylglycoxal levels (which is about what most papers report). In addition, most other papers demonstrate that methylglycoxal levels track WITH blood sugar levels and not in the opposite direction."

BTW, he also (later in the comments) states he questions the study itself.

Edited by Jay, 24 February 2009 - 03:56 PM.


#263 FunkOdyssey

  • Guest
  • 3,443 posts
  • 166
  • Location:Manchester, CT USA

Posted 24 February 2009 - 03:44 PM

What about the methylglyoxal issue? I'm sure you low carbers are familiar with it. If not: http://mfoundation.o...t=methylglyoxal

Do the benefits outweigh the risks?


I've been wondering about that too. This is what Michael Eades (responding to a comment) says about the issue:

"I was surprised, however, with his [Aubrey] one page attack on ketogenic diets as causing an increase in methylglycoxal as being a driving force in protein cross linking. I though Aubrey was smarter than that. He first states that high blood sugar is a potent AGE-producing force (as are increased levels of blood fats) then says that if you follow a ketogenic diet to reduce blood sugar and triglycerides you will be increasing the levels of methylglycoxal, which is a more potent AGE promoter. He bases this supposition on the paper you link to above [http://www.blackwell...ournalCode=nyas]. Altough methylglcoxal is a more potent AGE promoter, its concentration - even when elevated - is so abysmally low compared to that of the less potent blood sugar that it makes very little difference. A reduction in blood sugar (even if accompanied by an increase in methylglycoxal) brings about a reduction of AGE formation that is orders of magnitude greater than the increase engendered by even a doubling of methylglycoxal levels (which is about what most papers report). In addition, most other papers demonstrate that methylglycoxal levels track WITH blood sugar levels and not in the opposite direction."


Sounds good to me.

#264 wydell

  • Guest
  • 503 posts
  • -1

Posted 25 February 2009 - 12:56 AM

As I look into this issue more, it seems to me that a diet high in animal products is not the best. The link below states that primitive cultures (masai and intuits) that eat a diet high in animal products have a short life span. I have yet to see any evidence that a hunter gatherer diet high in animal products leads to a long life span. I jumped on my own version of the paleo bandwagon (less meat and more veggies) for about three weeks, but I think I am jumping off.


http://www.diseasepr...ive-longer.html

Edited by wydell, 25 February 2009 - 01:16 AM.


#265 kismet

  • Guest
  • 2,984 posts
  • 424
  • Location:Austria, Vienna

Posted 25 February 2009 - 01:21 AM

What about the methylglyoxal issue? I'm sure you low carbers are familiar with it. If not: http://mfoundation.o...t=methylglyoxal

Do the benefits outweigh the risks?


I've been wondering about that too. This is what Michael Eades (responding to a comment) says about the issue:

"I was surprised, however, with his [Aubrey] one page attack on ketogenic diets as causing an increase in methylglycoxal as being a driving force in protein cross linking. I though Aubrey was smarter than that. He first states that high blood sugar is a potent AGE-producing force (as are increased levels of blood fats) then says that if you follow a ketogenic diet to reduce blood sugar and triglycerides you will be increasing the levels of methylglycoxal, which is a more potent AGE promoter. He bases this supposition on the paper you link to above [http://www.blackwell...ournalCode=nyas]. Altough methylglcoxal is a more potent AGE promoter, its concentration - even when elevated - is so abysmally low compared to that of the less potent blood sugar that it makes very little difference. A reduction in blood sugar (even if accompanied by an increase in methylglycoxal) brings about a reduction of AGE formation that is orders of magnitude greater than the increase engendered by even a doubling of methylglycoxal levels (which is about what most papers report). In addition, most other papers demonstrate that methylglycoxal levels track WITH blood sugar levels and not in the opposite direction."


Sounds good to me.

Good post Jay, although you sound almost offended by the very possiblity of low carb being detrimental (I hope this does not stem from some kind of pro-keto bias); Firstly it was Michael (we're talking about my URL right? Aubrey de Grey is someone else) and it was hardly perceivable as an "attack". Neither does it sound completely off-base -- but who am I to judge, I don't know..
If the methylglyoxal production is a metabolic byproduct of ketosis the levels probably won't track with your blood sugar if you are in ketosis. That might explain the study data.
So how should we put it? Choose between "up to 40% lowered and constant blood sugar vs. doubled methylglyoxal concentrations (which in absolute terms is not much?)"

Edited by kismet, 25 February 2009 - 01:23 AM.


#266 Jay

  • Guest
  • 406 posts
  • 22
  • Location:New York

Posted 25 February 2009 - 08:20 PM

What about the methylglyoxal issue? I'm sure you low carbers are familiar with it. If not: http://mfoundation.o...t=methylglyoxal

Do the benefits outweigh the risks?


I've been wondering about that too. This is what Michael Eades (responding to a comment) says about the issue:

"I was surprised, however, with his [Aubrey] one page attack on ketogenic diets as causing an increase in methylglycoxal as being a driving force in protein cross linking. I though Aubrey was smarter than that. He first states that high blood sugar is a potent AGE-producing force (as are increased levels of blood fats) then says that if you follow a ketogenic diet to reduce blood sugar and triglycerides you will be increasing the levels of methylglycoxal, which is a more potent AGE promoter. He bases this supposition on the paper you link to above [http://www.blackwell...ournalCode=nyas]. Altough methylglcoxal is a more potent AGE promoter, its concentration - even when elevated - is so abysmally low compared to that of the less potent blood sugar that it makes very little difference. A reduction in blood sugar (even if accompanied by an increase in methylglycoxal) brings about a reduction of AGE formation that is orders of magnitude greater than the increase engendered by even a doubling of methylglycoxal levels (which is about what most papers report). In addition, most other papers demonstrate that methylglycoxal levels track WITH blood sugar levels and not in the opposite direction."


Sounds good to me.

Good post Jay, although you sound almost offended by the very possiblity of low carb being detrimental (I hope this does not stem from some kind of pro-keto bias); Firstly it was Michael (we're talking about my URL right? Aubrey de Grey is someone else) and it was hardly perceivable as an "attack". Neither does it sound completely off-base -- but who am I to judge, I don't know..
If the methylglyoxal production is a metabolic byproduct of ketosis the levels probably won't track with your blood sugar if you are in ketosis. That might explain the study data.
So how should we put it? Choose between "up to 40% lowered and constant blood sugar vs. doubled methylglyoxal concentrations (which in absolute terms is not much?)"


I believe you've mistaken my quote from Michael Eades (http://www.proteinpower.com/drmike/) as my post. I was just passing on his response to the issue being discussed. It seems to answer the question if he is right about the numbers. As for whether Eades has a low-carb bias, it's hard to say when the rest of the world has had such a low-fat bias for so long. His blog is very thoughtful IMO.

#267 DukeNukem

  • Topic Starter
  • Guest
  • 2,008 posts
  • 141
  • Location:Dallas, Texas

Posted 11 March 2009 - 12:30 AM

Not So Sweet: Over-consumption Of Sugar Linked To Aging
"Thanks to this study, the link between the rise in age-related diseases and the over-consumption of sugar in today's diet is clearer. Our research opens a door to new therapeutic strategies for fighting age-related diseases," says Professor Rokeach.
http://www.scienceda...90305204328.htm

Note that many of today's most prevalent carbs are merely long chains of sugar that are easily and quickly cleaved into pure, simple glucose molecules.

#268 stephen_b

  • Guest
  • 1,735 posts
  • 231

Posted 13 March 2009 - 04:13 PM

Given that carnosine's anti-glycating properties may be an explanation for vegetarian's having higher AGE levels than omnivores (PMID 16804013), perhaps taking supplementary carnosine would be a good idea at those times, like breakfast with oatmeal, one's meal is low in carnosine.

StephenB

#269 TheFountain

  • Guest
  • 5,362 posts
  • 257

Posted 13 March 2009 - 04:19 PM

Not So Sweet: Over-consumption Of Sugar Linked To Aging
"Thanks to this study, the link between the rise in age-related diseases and the over-consumption of sugar in today's diet is clearer. Our research opens a door to new therapeutic strategies for fighting age-related diseases," says Professor Rokeach.
http://www.scienceda...90305204328.htm

Note that many of today's most prevalent carbs are merely long chains of sugar that are easily and quickly cleaved into pure, simple glucose molecules.


Then it makes no sense to me why some think whole grains are bad carbs, as they have anti-glycation isoflavones.

#270 stephen_b

  • Guest
  • 1,735 posts
  • 231

Posted 13 March 2009 - 04:41 PM

Then it makes no sense to me why some think whole grains are bad carbs, as they have anti-glycation isoflavones.

One argument against whole grains was made in this blog posting from the whole health source blog. Another factor to consider is gluten. Some people are quite intolerant to it, but perhaps quite a few more have a subclinical intolerance.

StephenB




0 user(s) are reading this topic

0 members, 0 guests, 0 anonymous users