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How giving up sugar can take 20 years off your looks

sugar glucose skin collagen elasticity aging

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#1 JBForrester

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Posted 02 December 2012 - 12:17 AM


Perhaps not the most reputable journal, but this report offers from insight on what sugar can do to skin and your aging process:

http://www.dailymail...ears-looks.html

"...for every 1mm/litre increase in blood sugar, the perceived age of that person rose by five months."

#2 rwac

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Posted 02 December 2012 - 04:10 AM

That study says reducing blood sugar will improve skin.
The title on the other hand claims that "giving up sugar can take 20 years off your looks".

But never actually makes that link between sugar consumption and elevated blood sugar.

In fact, the two haven't actually been connected except via body fatness.
http://wholehealthso...nce-part-v.html
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#3 maxwatt

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Posted 02 December 2012 - 04:25 AM

Dr. Cynthia Kenyon (PhD) might beg to differ with you:

http://www.more.com/...ed-eating-sugar

#4 rwac

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Posted 02 December 2012 - 06:41 AM

Dr. Cynthia Kenyon (PhD) might beg to differ with you:

http://www.more.com/...ed-eating-sugar


Sure, sugar may or may not be bad for you, but it probably doesn't contribute to diabetes.

Also, the study she talks about refers to glucose, not sucrose (table sugar) which just so happens to have a lower glycemic/insulin index (ref:http://www.ncbi.nlm.nih.gov/pubmed/9881888) than glucose. So maybe she was leaning that way and just used this study as an excuse?

#5 DAMI

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Posted 02 December 2012 - 05:32 PM

Sucrose may have a lower glycemic index but at the same time the fructose portion of it has 7 times the glycation potential of glucose. If you wanted to estimate the glycation caused by sucrose you would probably have to multiply the glycemic index by 3.5 ..
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#6 Turnbuckle

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Posted 02 December 2012 - 05:54 PM

From the picture of the 50 year-old Kirsty Price, I'd say she looks 55-60.
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#7 maxwatt

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Posted 02 December 2012 - 06:41 PM

Reducing sugar in your diet improves insulin sensitivity in turn reducing blood glucose.

Fructose bad. Sucrose is about half fructose, as is corn syrup. Dextrose/glucose, not so bad, in a matrix of other nutrients. Not to excess. A little fruit in the diet should be ok, two spoons of sugar in your coffee, maybe not. Other, complex carbs, maybe not so bad depending on one's genetic makeup. Some people thrive on low-carb, others on Mediterranean (relatively high in mono-unsaturated fat from olive oil), others require relatively high carb with fats in moderation.

What is clear is that high levels of fructose in the diet lead to obesity, in turn to insulin resistance and to diabetes. Sucrose is half fructose. We get too much of it. The liver can process only so much fructose at a time, the excess is turned to triglycerides in the blood leading to fatty deposits in the arteries and elsewhere. The so-called obesity epidemic correlates precisely with a region's increase in fructose consumption. Eliminating it from your diet is probably as good for you as taking any supplement you can name. Easier said than done. Read labels, and you soon realize you need to give up processed foods.

#8 rwac

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Posted 03 December 2012 - 12:24 AM

Reducing sugar in your diet improves insulin sensitivity in turn reducing blood glucose.

Do you have evidence for that? Here's some evidence to the contrary.
http://www.medicalne...eases/59111.php

Fructose bad. Sucrose is about half fructose, as is corn syrup. Dextrose/glucose, not so bad, in a matrix of other nutrients. Not to excess. A little fruit in the diet should be ok, two spoons of sugar in your coffee, maybe not. Other, complex carbs, maybe not so bad depending on one's genetic makeup. Some people thrive on low-carb, others on Mediterranean (relatively high in mono-unsaturated fat from olive oil), others require relatively high carb with fats in moderation.

That's almost a world-view. Do you have evidence for that?

What is clear is that high levels of fructose in the diet lead to obesity, in turn to insulin resistance and to diabetes. Sucrose is half fructose. We get too much of it. The liver can process only so much fructose at a time, the excess is turned to triglycerides in the blood leading to fatty deposits in the arteries and elsewhere. The so-called obesity epidemic correlates precisely with a region's increase in fructose consumption. Eliminating it from your diet is probably as good for you as taking any supplement you can name. Easier said than done. Read labels, and you soon realize you need to give up processed foods.

High levels of fructose do not necessarily lead to obesity. Think durianrider (or 80/10/10 diet). He may have lost a bunch of mass, but he's not getting obese.

There's lots of nasty stuff in processed foods, and plenty of reasons to give it up.

We're on different paths. You want to eliminate sugar, I eat 200-300g of sugar daily. You want to reduce metabolism, I want to raise it.

#9 niner

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Posted 03 December 2012 - 12:43 AM

Reducing sugar in your diet improves insulin sensitivity in turn reducing blood glucose.

Do you have evidence for that? Here's some evidence to the contrary.
http://www.medicalne...eases/59111.php


But in this study, they compared equi-caloric diets with different sucrose fractions. Not only that, but the "low sugar" arm got 10% of their calories from sucrose. In the real world, the high sugar diet is inevitably higher calorie, and all that fructose ends up getting turned into fat. It's a ticket to obesity.

I eat 200-300g of sugar daily. You want to reduce metabolism, I want to raise it.


Yikes! I guess you have your reasons, but I don't think this would work well for me. Why exactly do you want to do this? Does it really raise your metabolism? What are the consequences of that?

#10 rwac

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Posted 03 December 2012 - 02:11 AM

I eat 200-300g of sugar daily. You want to reduce metabolism, I want to raise it.


Yikes! I guess you have your reasons, but I don't think this would work well for me. Why exactly do you want to do this? Does it really raise your metabolism? What are the consequences of that?


It's hard to find exactly equivalent studies unfortunately ...

Well, you don't gain much weight if you keep your metabolism high.

First of all low-carb doesn't really work for me, and I'm pretty sure most people can't workout/think nearly as well on a low-carb diet. I suspect most people notice that but ignore it to some extent. Next, starches usually cause a big insulin surge, and feed gut bacteria. That leaves sugar as a source of carbs. I feel a *lot* better on high sugar, better than I've ever been in my whole life.

Btw, my weight holds steady between 160-165 lb even with most of my carbs coming from sugar.

#11 maxwatt

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Posted 03 December 2012 - 02:39 AM

If you are burning them as fast as you're eating them you'll maintain stable weight ("sufficient" means intense exercise whilst consuming them) but the triglycerides can still be a problem if you don't burn them up before they stick to your arteries. Suggest 10% fructose, 20% glucose/dextrose, the rest long chain carbs like maltodextrin. This is the combination in an 'ideal' energy drink, something I'll consume on a 2 to 5 hour bike ride (>17 mph, 21 in a group). More time, real food, protein and a little fat. But never without exercise.

Edited by maxwatt, 03 December 2012 - 03:27 AM.


#12 maxwatt

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Posted 03 December 2012 - 02:57 AM

Reducing sugar in your diet improves insulin sensitivity in turn reducing blood glucose.

Do you have evidence for that? Here's some evidence to the contrary.
http://www.medicalne...eases/59111.php

Fructose bad. Sucrose is about half fructose, as is corn syrup. Dextrose/glucose, not so bad, in a matrix of other nutrients. Not to excess. A little fruit in the diet should be ok, two spoons of sugar in your coffee, maybe not. Other, complex carbs, maybe not so bad depending on one's genetic makeup. Some people thrive on low-carb, others on Mediterranean (relatively high in mono-unsaturated fat from olive oil), others require relatively high carb with fats in moderation.

That's almost a world-view. Do you have evidence for that?
...


These studies, among others:

Razquin C et al. (2009) . “The Mediterranean diet protects against waist circumference enlargement in 12Ala carriers for the PPARgamma gene: 2 years' follow-up of 774 subjects at high cardiovascular risk.” Br J Nutr 102(5):672-9.
Memisoglu A et al. (2003) . “Interaction between a peroxisome proliferator-activated receptor gamma gene polymorphism and dietary fat intake in relation to body mass.” Hum Mol Genet 12(22):2923-9.
Corella D et al. (2009) . “APOA2, dietary fat, and body mass index: replication of a gene-diet interaction in 3 independent populations.” Arch Intern Med169(20):1897-906.
Corella D et al. (2007) . “APOA5 gene variation modulates the effects of dietary fat intake on body mass index and obesity risk in the Framingham Heart Study.”J Mol Med 85(2):119-28.

Edited by maxwatt, 03 December 2012 - 02:58 AM.


#13 rwac

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Posted 03 December 2012 - 05:35 AM

If you are burning them as fast as you're eating them you'll maintain stable weight ("sufficient" means intense exercise whilst consuming them) but the triglycerides can still be a problem if you don't burn them up before they stick to your arteries. Suggest 10% fructose, 20% glucose/dextrose, the rest long chain carbs like maltodextrin. This is the combination in an 'ideal' energy drink, something I'll consume on a 2 to 5 hour bike ride (>17 mph, 21 in a group). More time, real food, protein and a little fat. But never without exercise.


Well, I'm maintaining stable weight with next to no exercise.
Besides, maltodextrin is absorbed as quickly as glucose, and creates a larger insulin spike than glucose.
What difference does a longer chain make?

#14 JBForrester

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Posted 03 December 2012 - 07:06 AM

High levels of fructose do not necessarily lead to obesity. Think durianrider (or 80/10/10 diet). He may have lost a bunch of mass, but he's not getting obese.



I'm sorry, but Durianrider looks like he's on meth. He may be in shape, but his face has taken a beatin'. I think you unintentionally gave a prime example that proves the main point of the article.

Edited by JBForrester, 03 December 2012 - 07:08 AM.


#15 rwac

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Posted 03 December 2012 - 07:33 AM

High levels of fructose do not necessarily lead to obesity. Think durianrider (or 80/10/10 diet). He may have lost a bunch of mass, but he's not getting obese.


I'm sorry, but Durianrider looks like he's on meth. He may be in shape, but his face has taken a beatin'. I think you unintentionally gave a prime example that proves the main point of the article.


DR has other issues like probably too little protein, etc. That statement was made to show specifically that you can't blame sugar/fructose alone for obesity, which is a necessary step in the chain

sugar -> obesity ->diabetes

There's not very much evidence that shows that consumption of sugar is directly responsible for diabetes otherwise.
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#16 maxwatt

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Posted 03 December 2012 - 01:49 PM

Epidemiologically you can blame sugar; most people in a large group will fatten up with increased consumption, some will not. Fidgiters tend to remain thinner. Also, around age thirty, give or take, metabolic changes make it much harder to keep the carb weight off.

Re: maltodextrins - True, their glucemic index is the same as glucose, but osmality is different. The are absorbed more slowly when competing with other sugars, such as glucose, fructose. Though the science is not yet settled, they do appear to stretch out the absorption time, so the spike in blood sugar is stretched out giving a more steady energy source during exercise.

#17 sthira

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Posted 03 December 2012 - 02:17 PM

We're on different paths. You want to eliminate sugar, I eat 200-300g of sugar daily. You want to reduce metabolism, I want to raise it.


Do you mean you eat a lot of (whole, untampered) fruit?

#18 rwac

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Posted 03 December 2012 - 08:09 PM

We're on different paths. You want to eliminate sugar, I eat 200-300g of sugar daily. You want to reduce metabolism, I want to raise it.


Do you mean you eat a lot of (whole, untampered) fruit?


Ideally that would be the case. But given the cost/lack of ripe fruit in the supermarkets, It mostly comes from OJ, white sugar, non-HFCS soda.

#19 nowayout

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Posted 03 December 2012 - 08:35 PM

Btw, my weight holds steady between 160-165 lb even with most of my carbs coming from sugar.


Even so, you may be missing the point regarding aging. The real problem with sugars is glycation. Even if, like me, you don't gain weight (I actually lose weight when I eat lots of sugar), I think it may still be a good idea to avoid too much sugar because too much glycation can play havoc with your skin, blood vessels, and organs.
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#20 rwac

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Posted 03 December 2012 - 09:32 PM

Btw, my weight holds steady between 160-165 lb even with most of my carbs coming from sugar.


Even so, you may be missing the point regarding aging. The real problem with sugars is glycation. Even if, like me, you don't gain weight (I actually lose weight when I eat lots of sugar), I think it may still be a good idea to avoid too much sugar because too much glycation can play havoc with your skin, blood vessels, and organs.


I would say that the term "glycation" is something of a misnomer. The oxidation of PUFAs in the presence of a protein results in higher concentration of the same products.

The advanced glycation end product, Nepsilon-(carboxymethyl)lysine, is a product of both lipid peroxidation and glycoxidation reactions.


Source

Department of Chemistry and Biochemistry and School of Medicine, University of South Carolina, Columbia, South Carolina 29208, USA.

Abstract

Nepsilon-(Carboxymethyl)lysine (CML) is an advanced glycation end product formed on protein by combined nonenzymatic glycation and oxidation (glycoxidation) reactions. We now report that CML is also formed during metal-catalyzed oxidation of polyunsaturated fatty acids in the presence of protein. During copper-catalyzed oxidation in vitro, the CML content of low density lipoprotein increased in concert with conjugated dienes but was independent of the presence of the Amadori compound, fructoselysine, on the protein. CML was also formed in a time-dependent manner in RNase incubated under aerobic conditions in phosphate buffer containing arachidonate or linoleate; only trace amounts of CML were formed from oleate. After 6 days of incubation the yield of CML in RNase from arachidonate was approximately 0.7 mmol/mol lysine compared with only 0.03 mmol/mol lysine for protein incubated under the same conditions with glucose. Glyoxal, a known precursor of CML, was also formed during incubation of RNase with arachidonate. These results suggest that lipid peroxidation, as well as glycoxidation, may be an important source of CML in tissue proteins in vivo and that CML may be a general marker of oxidative stress and long term damage to protein in aging, atherosclerosis, and diabetes.


http://www.ncbi.nlm..../pubmed/8626637

#21 JBForrester

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Posted 03 December 2012 - 10:28 PM

Again, not the best source, but interesting:

http://www.msnbc.msn...s/#.ULvXO4W9Wq1

#22 niner

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Posted 04 December 2012 - 12:42 AM

I would say that the term "glycation" is something of a misnomer. The oxidation of PUFAs in the presence of a protein results in higher concentration of the same products.

The advanced glycation end product, Nepsilon-(carboxymethyl)lysine, is a product of both lipid peroxidation and glycoxidation reactions.

Nepsilon-(Carboxymethyl)lysine (CML) is an advanced glycation end product formed on protein by combined nonenzymatic glycation and oxidation (glycoxidation) reactions. We now report that CML is also formed during metal-catalyzed oxidation of polyunsaturated fatty acids in the presence of protein. During copper-catalyzed oxidation in vitro, the CML content of low density lipoprotein increased in concert with conjugated dienes but was independent of the presence of the Amadori compound, fructoselysine, on the protein. CML was also formed in a time-dependent manner in RNase incubated under aerobic conditions in phosphate buffer containing arachidonate or linoleate; only trace amounts of CML were formed from oleate. After 6 days of incubation the yield of CML in RNase from arachidonate was approximately 0.7 mmol/mol lysine compared with only 0.03 mmol/mol lysine for protein incubated under the same conditions with glucose. Glyoxal, a known precursor of CML, was also formed during incubation of RNase with arachidonate. These results suggest that lipid peroxidation, as well as glycoxidation, may be an important source of CML in tissue proteins in vivo and that CML may be a general marker of oxidative stress and long term damage to protein in aging, atherosclerosis, and diabetes.


This is a pretty interesting paper. More fuel for the PUFA = toxins fire. I have to wonder about the relative level of damage done by PUFAs versus glycation, though, as this was an in vitro study, so it may or may not be relevant to the in vivo case. They might have had an unnaturally high level of free copper, for example, where in the body a lot of it is safely bound so it won't engage in damaging chemistry. It was also looked at under aerobic conditions, which wouldn't be the case in vivo, for the most part.

#23 rwac

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Posted 04 December 2012 - 04:17 AM

This is a pretty interesting paper. More fuel for the PUFA = toxins fire. I have to wonder about the relative level of damage done by PUFAs versus glycation, though, as this was an in vitro study, so it may or may not be relevant to the in vivo case. They might have had an unnaturally high level of free copper, for example, where in the body a lot of it is safely bound so it won't engage in damaging chemistry. It was also looked at under aerobic conditions, which wouldn't be the case in vivo, for the most part.


From the end of that paper

To distinguish carbohydrate- from lipid-mediated damage and assess the relative importance of oxidation of these two substrates in the development of diabetic complications, it will be necessary to identify unique products derived from each of these precursors. In the meantime, since CML has been identified as a major AGE antigen in tissue proteins and a product of both carbohydrate and lipid peroxidation reactions, our results suggest that CML may be more useful as a general biomarker of oxidative stress and damage in tissue proteins.

http://www.jbc.org/content/271/17/9982.long

I wonder if that's doable with information we have right now.

#24 nowayout

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Posted 04 December 2012 - 03:43 PM

Btw, my weight holds steady between 160-165 lb even with most of my carbs coming from sugar.


Even so, you may be missing the point regarding aging. The real problem with sugars is glycation. Even if, like me, you don't gain weight (I actually lose weight when I eat lots of sugar), I think it may still be a good idea to avoid too much sugar because too much glycation can play havoc with your skin, blood vessels, and organs.


I would say that the term "glycation" is something of a misnomer. The oxidation of PUFAs in the presence of a protein results in higher concentration of the same products.


I mention apples and you write a non sequitur about oranges.
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#25 rwac

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Posted 04 December 2012 - 08:43 PM

Btw, my weight holds steady between 160-165 lb even with most of my carbs coming from sugar.


Even so, you may be missing the point regarding aging. The real problem with sugars is glycation. Even if, like me, you don't gain weight (I actually lose weight when I eat lots of sugar), I think it may still be a good idea to avoid too much sugar because too much glycation can play havoc with your skin, blood vessels, and organs.


I would say that the term "glycation" is something of a misnomer. The oxidation of PUFAs in the presence of a protein results in higher concentration of the same products.


I mention apples and you write a non sequitur about oranges.


You're right. I hope this is a more reasonable response: Glycation probably isn't the biggest source of glycation products, it's not the significant cause of glycation. For instance blood a1c does not accurately measure blood glucose levels. If the previous link holds in vivo, then glycation damage from sugar is far outweighed by damage from PUFAs. I realize that it's not a complete response, but it seems to be rather hard to distinguish between the two effects.

http://www.scienceda...11121151552.htm

Lipid peroxidation increases cross-linkage of glycated proteins.
http://www.ncbi.nlm..../pubmed/2492180

Immunochemical crossreactivity of antibodies specific for "advanced glycation endproducts" with "advanced lipoxidation endproducts".
http://www.ncbi.nlm....pubmed/15653175
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#26 JohnD60

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Posted 05 December 2012 - 03:59 PM

From the picture of the 50 year-old Kirsty Price, I'd say she looks 55-60.

Agreed!
She does have a good figure though, I can imagine someone looking at her from behind mistaking her for much younger. But from the front, no.... yikes, what did she look like before stopping sugar consumption?

#27 rwac

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Posted 06 December 2012 - 04:58 AM

Yikes! I guess you have your reasons, but I don't think this would work well for me. Why exactly do you want to do this? Does it really raise your metabolism? What are the consequences of that?


I don't see why it wouldn't. Most people doing it are veterans of the low-carb world, and have figured out that they feel better on a high carb/sugar diet. Although some people do gain weigh in the beginning just from stopping a stressful low carb diet.

#28 niner

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Posted 07 December 2012 - 01:16 PM

just from stopping a stressful low carb diet.


LoL....

#29 Shepard

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Posted 07 December 2012 - 02:02 PM

just from stopping a stressful low carb diet.


LoL....


I assume this is meant in the literal form of increased catecholamine concentration and not in the popular notion of stress.

#30 maxwatt

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Posted 07 December 2012 - 02:47 PM

complex carbs = good, at least not so bad, but
fructose and sucrose (dextrose+fructose) = bad
PUFA = bad
MUFA = bad, neutral or good, depends on your genetically determined metabolism

moderation in all things - Herodotus
all generalities are false, including this one - Voltaire

I do still think 200g of sucrose will be detrimental in the long run. because another substance also causes glycation, does not mean the first is harmless.

Edited by maxwatt, 07 December 2012 - 02:48 PM.

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