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Welcome all seeking refuge from low carb dogma!

“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
~ Charles Darwin (it's evolutionary baybeee!)

Sunday, November 28, 2010

Lipogenesis v. Adipose Mass Gain ~ Fructose

A while back I posted a summary of lipid vocabulary:  Lip-ocabulary.  I had hoped to address this sooner than now.

Another topic on my (rather long) list of how Taubes either misunderstands or misrepresents lipid metabolism and storage involves his use of terms related to "lipogenesis"  (e.g. fructose is the most lipogenic of carbs) to imply that it leads to fat accumulation.  

In his defense, there are any number of scholarly articles and texts that use the term lipogenesis to describe the "genesis" of fat stores.  However they do so in the context of discussions of adipose tissue and do not conflate de novo lipogenesis and fat storage.  Adipogenesis may not be exactly appropriate either, as this term is most correctly attributed to the formation of new fat cells.  But at least the "adipo" implies fat tissue, thus it might loosely apply to the genesis of adipose tissue (whether by proliferation or filling of existing cells) rather than the synthesis of lipids per se.

Where obesity is concerned, we're interested in what causes changes in adipose tissue mass: increases or decreases.

In the past few years, fructose has become the new "saturated fat", to where fructophobes will avoid even carrots!  This is due in large part to Lustig's alarmism, but Taubes weaves this into his lectures as well.   We are to equate fructose with alcohol because it is processed in the liver and consider it particularly fattening because fructose elicits the highest rate of DNL of any carbohydrate.  But just as carbohydrate per se is not uniquely fattening, neither is fructose per se.  It is the processed tasty vehicles either in liquid form and/or packing a caloric whollop that are.  Can you say ice cream?!

But back to the vocabulary, I've posted before demonstrating that lipogenesis does not contribute much to adipogenesis.  See:  Nutrient Fates after Absorption and Excess carbs converted to fat?   But lipogenesis -- the synthesis of larger lipid molecules from smaller molecules -- is not only an energy consuming process, it may also be thermogenic as I posted about here:  Fat Futile Cycling from Carb Excess (or more lay-friendly).

Bottom line, it is misleading to equate lipogenesis with fat accumulation in adipose tissue.


6 comments:

Sanjeev said...

Dr. Lustig tries to have things both ways.

On Alan Aragon's critique, the Dr. posted that he said in his famous presentation it's all about dose. And he did.

But so many people showed up on Alan's blog proclaiming the "Fructose=teh 3vil p0iz0nz" that it was obvious what message Dr. Lustig actually sent.

And aside from all that, just after proclaiming "it's all about dose" Dr. Lustig immediately fell back to making the "Fructose=teh 3vil p0iz0nz" case, reinforcing the idea that he's just saying that other stuff "for the lawyers" or some such, but he really doesn't believe it.

Sanjeev said...

>> But so many people showed up on Alan's blog
>> proclaiming the "Fructose=teh 3vil p0iz0nz"

this was unclear above - those posters made this claim, AND attributed the belief directly to Dr. Lustig's presentation.

dietconcepts said...

In one of his recent Research Review newsletters, Alan comments on a paper that looks at the effect of consuming wast amounts of grapefruit on a daily basis. The respondents drank about half a liter every day, which amounts to something like 45-55 grams of fructose. While weight gain/loss wasn't the focus of the study, it's interesting to note that none of the respondents gained any weight during the study.

I think it's as simple as this: fruit won't make you gain weight if your diet is at or below maintenance levels, and while the fructose in fruit may or may not lead to weight gain if your diet is above maintenance level - does it really matter from whence the calories come?

The need to demonize certain foods is quite surreal. Even transfats can be consumed on a healthy diet, as long as you're sensible about it (ie. consuming small amounts of natural transfats in dairy versus large amounts of industrial transfats from storebought cookies).

CarbSane said...

I read Alan's piece on Lustig and Lustig's contribution there. He did not outfit himself (Lustig) very well IMO. His mention of YouTube hits was laughable. He had a recent interview with Jimmy Moore where I somewhat changed my mind about him as he sounded much more reasonable. I just remember in his lecture he got all conspiracy theory over Coke adding some miniscule amount of salt to their soda ... presumably so they could add more HFCS and get us all addicted.

The whole 50g/day average thing really blows my mind as that would be 100g sucrose/HFCS. I'm sure there are some who may eat that way on a chronic basis, but I think there are those 2L+/day soda habit folks who skew this. The average person though??

I just don't see whole fruit, even pineapples and bananas, making anyone fat unless one is deliberately gorging themselves on it.

I do think some of us need to re-sensitize ourselves to sweet taste. I recall adding AS to apple slices years ago, now I find some of the apples out there almost too sweet to eat.

Dietconcepts: Funny how it seems to come back to everything in moderation!!

Sanjeev said...

So if I have the story right up to now,

dietary fat cannot be used for energy immediately after ingestion[0] because digestion packages that fat up as chylomicrons and adipose tissue preferentially grabs chylomicrons out of the blood

but fat from lipogenesis may be immediately used for energy, if needed

[0] except maybe by the digestive tract's tissues

CarbSane said...

That DNL derived lipids are used right away might be explained by the fact that these fatty acids are already inside cells? That's just an educated guess on my part, but the direction of transport for the most part is a one-way street (in) for most cells/tissues. We already expended the energy to move the original substrate into the cell so it would seem wasteful to move it back out to send it to a remote depot when it could also be esterified and stored locally in a lipid droplet. Perhaps this is how non-alcoholic fatty liver disease develops?

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