Tag Archives: carbs

Are carbs stored as fat?

Hint: “no”

DNL proper.

Lots of metabolism talk below, but first a brief intro.  My “muse,” if you will.

Taubes’ recent article in the BMJ (Taubes, 2013full text) generated some interesting feedback.

In the original article, Taubes basically re-states his philosophy on obesity.  Nothing new.  But one rebuttal by Cottrell got under my skin (Cottrell, 2013), and Taubes’ response was woefully inadequate.

Cottrell [sic]: “A third incorrect assertion is that obesity can be attributed to the conversion of carbohydrate to fat. This is an unsatisfactory explanation of obesity, because this route is a minor pathway to depot fat in humans, even under conditions of substantial overfeeding of sugars to obese subjects.  An unproved assumption is that the hypothetical diversion of carbohydrate energy into fat storage leaves the subject hungry, thus stimulating overeating.”

strawman

Cottrell set up a straw man and handily took it down.  The primary mechanism whereby excess carbs contribute to obesity is via insulin’s effects on adipose tissue.  Even if you’re eating very little fat, insulin will cause it to get stored.  Insulin is very good at this – it is actually far more potent at stimulating fat storage than it is at stimulating glucose uptake (eg, Insulin vs. fat metabolism FTW).  Cottrell’s straw man is that excess carbs themselves are stored as fat.  This does not occur to any appreciable extent in humans.  Here is why I believe that to be true, from one of most insightful and informative studies on the topic IMHO.

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MOA of MCTs – black magic or something less?

MCTs provide a respectable boost in diet-induced thermogenesis (in some studies [eg, Kasai 2002  & Clegg 2012], but not others [Alexandrou 2007]), but I don’t think that’s what does it.

The alternative?  MCTs aren’t “linoleate.” (sorry for lack of suspense)

Alcohol + MCTs vs. corn oil (from Kirpich 2013):

Kirpich

Further, feed rats a diet rich in either coconut oil, olive oil, safflower oil, evening primrose oil, or menhaden oil… and eventually the fat stored in their bodies reflect those fats – eg, linoleate only accumulated in the tissues of those fed safflower & evening primrose oils (Yaqoob 1995) (expect similar results with soybean & corn oils).

Researchers constantly refer to MCTs & coconut oil as “saturated fats,” but I always thought the chain length should be recognized.  Perhaps.  But with regard to certain benefits (eg, hepatoprotection), perhaps not.

Cacao butter has a lot of stearate (a fully saturated 18-carbon fatty acid) but not much linoleate or MCTs.  This linoleate may very well be more of a detriment than stearate or MCTs are a benefit… (with regard to certain benefits [eg, hepatoprotection])Beef and chocolate

(Leslie Roberts, 1988) (she’s talking about stearate)

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Liver is evil but need not be punished. SFAs.

What to serve with a liquid lunch, and a recipe for chocolate.

It’s like a feed forward downward spiral.  If you don’t eat saturated fat & MCTs prior to imbibing, then liver intentionally makes more PUFAs for the alcohol-induced burning ROS to molest.  Liver is evil but need not be punished.  SFAs.

Brief background: (Kirpich et al., 2011 & 2013)

Researchers studying alcohol in rodents know where they’re going and like to get there fast.  70 drinks per day fast.  Granted, rats metabolize faster than humans so it’s likely a little less… but a little less than 70 is still a lot of sauce.

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salt makes you thirsty, soda makes you hungry.

As previously discussed, DRINK was a randomized intervention study that gave children either regular or diet soda for a year and surprise surprise, the regular soda drinkers gained about more body fat than the diet soda drinkers (de Ruyter et al., 2012).  And in the follow-up, with an opposite study design, overweight & obese children who continued to drink regular soda gained twice as much weight as those who cut their intake (Ebbeling et al., 2012).  There was no apparent black box in the latter study as the kids who stopped drinking soda also decreased their intake of other foods…

-does not compute-fructose

wait a minute … By switching from regular soda to diet, you just end up compensating by eating more of something else, right?  My initial response to that has always been that it doesn’t matter – ANYTHING else is better than a straight shot of 100% HFCS (+ some other chemicals).  But those kids didn’t do that.  they ate less of other foods.

 

Does HFCS soda make you eat more?

A recent study has put a little more fuel on this fire.  Similar to the abovementioned two, it’s not a sophisticated study designed to accurately assess the impact of regular soda on appetite, satiety, hunger, etc., but it supports the theory that diet soda negative calories are NOT compensated for by eating more of something else.


Food and beverages associated with higher intake of sugar-sweetened beverages (Mathias et al., 2013)

It was another big cross-sectional NHANES study that simply asked how much regular soda, diet soda, and other foods kids were eating.Mathias data 1

They showed that as soda intake increased, so did total calories, which could simply mean the soda was adding calories to their diets.  This would indirectly support the opposite of the above mentioned theory, namely, that soda calories aren’t compensated for.  But it gets better (or worse, depending how you look at it):Mathias data 2

soda didn’t simply add to the total calorie intake.  More often than not, calorie intake increased above and beyond that contributed by the soda.  And it wasn’t just that bigger kids were drinking more soda and eating more food – these data were controlled for body weight.  The authors estimated that for every 100 kcal of soda drank, an additional 36 – 86 kcal of food was eaten.

salt makes you thirsty, and now soda makes you hungry?

 

calories proper

 

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Obesity is not permanent

Take a group of obese people (> 250 lbs) and put them on a massive calorie restricted diet.  They lose weight and metabolic rate plummets.  Weight loss fail?  In most cases, yes.  But a recent study showed that the decrepit post-weight loss metabolic rate gradually improves in parallel with an increase in dietary fat ingestion to such a degree that even after two long years: totally food intake was almost back to normal, energy expenditure improved, and all this happened despite continual weight loss.  In other words, obesity is not permanent. 

creme brulee

Decreased energy density and changes in food selection following Roux-en-Y gastric bypass (Laurenius et al., 2013)

Statistically speaking, no diet on Earth comes close to RYGB in terms of weight loss success.  Long term.  Seemingly permanent.  It’s the closest thing to a cure we’ve got.

Laurenius

Body weight is down by 30%, and energy expenditure is rising faster than a speeding bullet.  because food intake is increasing while body weight is dropping – they’re probably more active too ** weight loss than more exercise –

But there’s a more mystical aspect to RYGB that warrants attention.  (it could be the increasing fat intake, but for now let’s just say it’s RYGB per se).  According to this pearl, weight loss of only 10% via diet alone causes energy expenditure crash by 394-500 kcal/d, and physiological replacement of leptin via subcutaneous injection can increase this by 234-454 kcal/d (Rosenbaum, Murphy, Heymsfield, Matthews, and Leibel, 2002).

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How to define a “healthy” diet. Period.

Whether you’re strictly adhering to a diet or just doing your own thing, if year after year your GP is prescribing more and more medications to stave off morbidity and keep you intact, then the diet you’re following is most likely Fail.  The same is true if your body weight is creeping upward or your quality of life is creeping downward.lunchables

The glaring Fail of all 3 diets in the recent Mediterranean Diet Study for the medications criteria threw up a huge red flag.  As a brief refresher, at baseline and 5 years later, prescription medication usage was as follows:

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Mediterranean Diet Fail – Nutrition Disinformation, Part I.

Do not get your hopes up, do not pass GO!  do not collect $200.  The Mediterranean Diet.  Fail.

Primary Prevention of Cardiovascular Disease with a Mediterranean Diet (Estruch et al., 2013)

This is one of the biggest diet studies we’ve seen in a while, and no doubt it was a very good one.  It very effectively put the Mediterranean Diet to the test.

I felt compelled to write about this study out of fear for the nutrition disinformation that it would likely inspire.  The Mediterranean Diet is associated with all good things, happiness, red wine and olive oil; whereas the Atkins Diet is associated with artery clogging bacon-wrapped hot dogs and a fat guy who died of a heart attack.  Nutrition disinformation.

If you ran a diet study with 3 intervention groups for 5 years, and by the end of the study everybody (in all 3 groups) was on more prescription medications, would you conclude any of the diets were “healthy?”  If so, then we should work on your definition of “healthy.”

Study details: big study, lasted roughly 5 years, and the diet intervention was pristine.  Mediterranean diet plus extra virgin olive oil (EVOO) vs. Mediterranean diet plus nuts vs. low fat control.  They even used biomarkers to confirm olive oil and nut intake (hydroxytyrosol and linoleate, respectively).  Compliance was good.

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Paleotard, meet potatotard, Op. 132

(credit to Dylan and Woo, respectively, for introducing me to those terms)

Empty calories – the potato

While it has a decent amino acid profile, with only 3 grams of protein it’d take a diabetic amount of potatoes to fulfill your daily protein.  By “diabetic,” I mean about a thousand grams of starch.  potatoes are just as glycemic as white bread.

potato

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Ketoadaptation

Athletes who drop carbs cold turkey suddenly suck.  It is known.  

But with a smidge of stick-to-it-iveness, performance completely recovers, in virtually every.  measurable.  aspect.  

This was shown years and years ago, in a seminal study by Drs Phinney, Bistrian, Evans, Gervino, and Blackburn.

The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation (1983)

Normally, fatty acids fuel low intensity exercise and carbs fuel high.  This is because high intensity exercise requires a high rate of ATP production, and glycogen to lactate generates ATP faster than a speeding bullet.  This is what makes power.  Getting ATP from fatty acids is like draining maple syrup from trees [at first].

mito pic

However, go low carb for long enough and the syrup begins to flow like water.  I lack the time to show what “long enough” entails, but  4 out of 5 studies on low carb diets and performance that only last a few days will show this.  Ketoadaptation takes time; ~3 weeks.

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diabulemia

This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.

Yes, I think sugar and empty calories, and the associated hyperinsulinemia are the bane of anyone with obesity or any sort of hyperplastic fat tissue disorder.  And yes, this is the worst type of evidence to support such a stance, but when you’ve got lemons, well…

Make no mistake, diabulemia may as well be spelled DIE-abulemia.  It’s not a laughing matter.  But yeah, well, lemonade, etc.  So here it goes

Diabulemia

Type I diabetics have low insulin and are lean; type II diabetics have high insulin and are not.  Insulin injections in either population promotes hyperplastic fat growth.  Sounds scary, right?  It is:

insulin

This poor soul unfortunately restricted his insulin injections to only two sites.  Make all the jokes you want, but the effect is obvious…  this is happening everywhere in hyperinsulinemic heavyweights (not just two specific sites).

CHO III Picture 279

 So what do Type I’s do when they want to lose some fat mass?  Stop jabbing themselves with insulin. Unfortunately, it’s really that simple.  Type II’s and anyone with excess or hyperplastic fat tissue can do the same with low carb or keto, although this would be a great benefit to their overall health.  But for Type I’s… not so much – they need insulin to prevent the horrific manifestations of ketoacidosis, which includes but is not limited to: death.

Type I’s are hyperglycemic because of low insulin; insulin therapy prevents diabetic ketoacidosis, a deadly condition.  But for those who simply choose to selectively reduce their insulin dosage, they: 1) don’t die; 2) lose fat; and 3) get hyperglycemic and incur all the damage that ensues (retinopathy, nephropathy, neuropathy).  Furthermore, they’re walking on thin ice – DKA is lurking.  It is just as stupid yet more dangerous than using tapeworms to lose weight.

tape-worms

Type II’s are hyperglycemic because of insulin resistance; a condition that is pathologically neutered via carbohydrate restriction.  Type I’s who reduce insulin injections to decrease fat mass are doing just as much damage as Type II’s who DON’T reduce carbohydrate intake.


Diabulemia is akin to an eating disorder.  Biologically, the lack of insulin allows fat to be released from adipose tissue with gravitas, and it prevents glucose from being stored in any meaningful capacity.  You’re literally pissing calories here, burning ’em like crazy there; all of which is a helluva lot easier than “eating less moving more” … which is why diabulemics do it (because they have the option [unlike the rest of us]).  Diabulemia is good from a fat loss perspective, but will most definitely contribute to severe and possibly deadly complications down the line.   Carbohydrate restriction, however, is a win-win-win… (for everyone except The Man, so perhaps it’s a win-win-win… fail)

This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.


Humans aren’t big rats, but here it is again, anyway:

Leptin deficiency causes insulin resistance induced by uncontrolled diabetes (German et al., 2010)

I’m ignoring the brunt of this paper and only focusing on the positive control groups.  [Positive controls… meaning they were included because they would definitely exhibit the expected response.]

Force rats into a state of diabulemia, and their insulin levels plummet, blood glucose soars, and they become ravenously hungry (open squares in the graphs below).German I

But lo and behold, fat mass atrophy ->German II

Eat less move more?  Well, they certainly didn’t “eat less…” (see above) … and:German III

nor were they “moving more.”  Low insulin seems to have a way to bypass that whole “eat less move more” thing (eg, Metabolic rate per se).

 

Throwing the baby out with the bathwater works if the baby is fat and the bathwater is insulin.  (no, not a fat baby.)

 

calories proper