http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1865572/

Either way it is a great argument for adopting a low carb or ketogenic diet.

In my experience, such a diet does not lead to a “healthy” appearance or high quality of life.

It would be tragically ironic if these folks were actually shortening their lifespans.

As an aside- a picture of Mr. de Grey on wikipedia suggest that he is not aging well (http://en.wikipedia.org/wiki/Aubrey_de_Grey)

“After muscle samples were obtained, subjects consumed a single high-fat meal (35% daily kcal intake; >60% kcal from fat), and a second muscle biopsy was taken 4 hours later. Subjects then consumed a high-fat diet (isocaloric; >60% kcal from fat) for 5 days and returned 12-hour fasted on the morning of the sixth day, when a final muscle biopsy was obtained.”

60% fat. Not 100%. Big difference. Why blame the fat?

Because fat is the whipping boy for most academicians.

Here is a link to the actual study:

Re the double comment: it’s more than just the moderating queue: when I posted the second comment above, it appeared on the screen, with the note that it was awaiting moderation; the original post didn’t appear at all …

Re the study, you wrote:
I’ll wait for the in vivo studies instead of the in vitro ones. . Well, of course, there was an in vivo study: that’s how this thread got started . I agree, however, that it would be good to see it repeated, and perhaps with more subjects (although 10 is a fairly common study size for metabolic studies of this kind) and without the accursed ITT analysis .

I wondered at the time how fructose could have a 3.9 fold increase and glucose a 3.5 fold increase in MG production when sucrose, which is half fructose and half glucose had only a 2.3 fold increase.
Being in vitro, the acidity and digestive enzymes of the mouth and GI aren’t available to hydrolyze it, and I’m guessing that it just wasn’t metabolized by the cells into methylglyoxal or much of anything else.

In vivo, of course, this is rather a moot point: with the possible exception of in the upper jejunum, cells would very rarely be exposed to unhydrolyzed sucrose as such, and even their constituent fructose would not reach many cells in that chemical form, having first been metabolized into glucose in the liver (although I certainly don’t have to tell you or most of your readers that this process is itself metabolically deleterious). By contrast, cells routinely encounter and metabolize glucose, fructose (plasma concentration 35 µmol/L, formed endogenously from glucose through the aldose reductase pathway, vs ~5 mmol/L for glucose), and ketone bodies. Very low-carb diets substantially increase ketone body formation, shifting the substrate mix for cellular fuel and metabolic byproducts, as the Beisswenger study suggests.

I’m trying to post a study that I’ve just discovered that updates and informs the issues we discussed here. I posted last night, and nothing happened; I came back this morning, tried to post again (I’d saved a draft in an email), and was told “Duplicate comment detected; it looks as though you’ve already said that!”

Do you have some sort of blocking or hold-for-approval system? Any tricks I can try or snares into which I may’ve fallen?

Thanks!

No, I’m just chronically woefully behind on moderating comments.

Following up on our previous discussion: the below is an in vitro study, but it does provide a mechanism that might explain the finding of higher methylglyoxal in Atkins dieters, despite lower levels of “usual-suspect” AGE precursors. Note that (a) as they say, it was already known that high glucose levels could form methylglyoxal, through overloading the glycolytic machinery and generating triosephosphates, and (b) they did specifically monitor ketosis in the Atkins dieters in the study. This of course wouldn’t apply to a less strict low-carb regime, probably even including Atkins’ own “Ongoing Weight Loss” (OWL) plan.

Metabolism. 2008 Sep;57(9):1211-20.Click here to read Links
Methylglyoxal production in vascular smooth muscle cells from different metabolic precursors.
Dhar A, Desai K, Kazachmov M, Yu P, Wu L.

PMID: 18702946

“High protein intake,” of course, wouldn’t be the issue, but very low carb intake.

Maybe, but I seriously doubt it. I’ll wait for the in vivo studies instead of the in vitro ones. I read this study when it came out, and I wondered at the time how fructose could have a 3.9 fold increase and glucose a 3.5 fold increase in MG production when sucrose, which is half fructose and half glucose had only a 2.3 fold increase.

The reason I am just babbling on about this is I have noticed a good reduction of gray hair.I have always thought that my low carb lifestyle had something to do with it and I believe that I made a comment about this somewhere deep in your archives. I also recently sprouted a gray hair in my eye brow. I just checked in the mirror and now it is gone. This is making me insane doctor…What does it all mean???

I’ve never heard this theory, but if it works, great.

I’m sorry to post a little off-topic, but I wished to point out an article in the New York Times to you – http://www.nytimes.com/2009/05/12/health/research/12exer.html. It outlines an argument against taking antioxidant supplements when using exercise to improve insulin response. I wonder if you could treat us all to a brief excursus on the processes and relationships that they are describing here?

With thanks from a very regular reader – Alison