Category Archives: Advanced nutrition

Research studies, hypotheses, data, etc.

Physiological Insulin Resistance in Circadia

If you haven’t read Petro Dobromylskyj’s posts about Physiological Insulin Resistance, then just go do it.  Highly recommended.
I’ve written about it as well, albeit in a slightly different context:
What is our proper “natural” diet?
40 years ago a group of researchers turned ketosis into poetry.

But now on to more pressing matters.  In the food deprived state, Physiological Insulin Resistance develops, in part, to spare muscle (yea yea yeah and glucose for the brain).  But how much of this is due to ‘food deprivation’ per se as opposed to something else… like circadian rhythms.

Exhibit A. Hat tip to Dr Kruse for writing about this TED talk.  In it, Jessa describes a crab that lives on the beach; scurries up the beach when the tide comes in and back down when it goes out.  Scientists captured a few, flew them halfway around the world and put them in little tilted cages.  The crabs still scurried up & down, in time with the tides.

Exhibit B. Evidence that the lunar cycle affects human sleep.  People tend to sleep a little less during the full moon.  Subjects were recruited to a windowless sleep lab and had no exposure to sun/moon/anything outside – they maintained this circadian rhythm for 3 days  (Cajochen et al., 2013).  Different from the crabs, but similar (in a way).

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Energy Balance > CICO

The regulation of energy balance is a long-term process, and it can’t be maintained by counting calories on a day-to-day basis.  Taubes once wrote that exercise doesn’t cause weight loss because it builds up an appetite, so you end up sucking down a Starbuck’s Jumbo Calorie Bomb on the way home from doing Yoga at the gym.  This is probably somewhat true, but this little gem from 1955 exposes some very interesting nuances.

Edholm(Edholm et al., 1955)

These researchers rigorously measured food intake and did a comprehensive assessment of energy expenditure during a wide variety of activities – lying down, standing, walking, gun cleaning, stair climbing, dressing, etc., etc.

Divide and conquer

The individual differences: big people expend more energy on life.  most of the time.

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Silent Leptin Resistance

Conventional leptin resistance has something do with obesity.  It is known.  Silent leptin resistance is … err … complicated. 

Divide and conquer

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding (Shapiro, Scarpace, et al., 2008 AJP)

A remarkable 60% fructose diet fed to rats for 6 months had absolutely no effect on energy balance.  Nil. QED.
Fig 1

Food intake and body weight were unaffected because the levels of and sensitivity to endogenous leptin were identical in both groups.

Enter the Dragon

Enter the Dragon

“Silent Leptin Resistance” – The fructose-fed rats are, however, profoundly resistant to the satiating effects of Metreleptin (a pharmaceutical grade injectable leptin analog):

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On calorie information posted in restaurants

“This is biology, not mathematics.”

It’s law in some places.  It’s a burden on restaurants.  And it will do nothing for the cause – like trying to put out a candle by pressing the off button on your remote control.  In other words, a waste.

Here’s some of the “science” behind it.

Exhibit A.
In a study by Dumanovsky, fast-food customers were surveyed prior to and after mandatory calorie labeling in New York.  25% of the people reported “seeing calorie information,” and 10% of them said it affected their buying decision (ie, 2.5% of all fast-food consumers surveyed thought they knew enough about “calories” to be scared of them).  After the law went into effect, 64% of people noticed the calorie information, and 20% of them were affected by it (=12.8% of all fast-food consumers thought they knew enough about “calories” to be scared of them).  Sooo, the proportion of people making misinformed decisions quintupled.  Calorie Labeling = Nutrition Disinformation.  It’s misleading, and usually wrong.

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Dopamine

“When we block the D2 receptor in humans, it is expected they will develop glucose intolerance, obesity, and sedentary behavior.” -Jane Plain, in her series on The physiology of body fat regulation.  It’s probably true.

Randomized pilot study of cabergoline, a dopamine receptor agonist: effects on body weight and glucose tolerance in obese adults (Gibson et al., 2012)

Cabergoline is primarily used to treat prolinactinoma, or prolactin-secreting tumors.  In women (& men apparently), prolactin stimulates milk production; in men, it is associated with the refractory period after orgasm.  In both genders, dopamine inhibits prolactin secretion.  Cabergoline targets the D2 receptor, but it’s a dirty drug.  It’s used off-label for gyno and to improve sexy times (Kruger et al., 2003 <– yes, that was actually tested).

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Eating in the Absence of Hunger

Hat tip to Jane Plain and her ongoing series on “The physiology of body fat regulation” for citing this study as it provides a rather interesting insight into the psychoendoneuropathophysiology of the obese condition.  Eating in the Absence of Hunger.  

Caloric compensation and eating in the absence of hunger in 5- to 12-y-old weight-discordant siblings (Kral et al., 2012)

They were all full or half, weight-discordant, same-sex siblings and each sibling pair had the same mother; same mitochondrial DNA, shared a womb, etc.

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Westside Barbell, Hormesis, and Antifragility

Some people think Westside makes some of the strongest athletes in the world because unlike most other training regimes, they are constantly lifting very heavy weight.  Other protocols restrict heavy lifting to certain times of the year, in-season / off-season, etc.  At Westside, you’re going heavy on an exercise that changes very frequently (every 1 – 3 weeks).  And it’s this latter point that provides the basis for why other people think Westside works.  By constantly changing which exercise is lifted at maximal intensity, the body never fully adapts, or gets into a rut – this is part of Westside’s ‘Conjugate Method.’

The principle is embraced by Crossfit, as per their random workouts-of-the-day, and also follows a tangent of the Hormesis theory: small doses of individual exercises, eg, conventional deadlifts one week, good mornings the next, sumo deads the next week, and so on and so forth – will improve your squats; the body never knows what’s coming (even though you might have planned it weeks in advance, or at least planned to check The WOD Shop).  Also discussed albeit briefly, in Taleb’s Antifragile, wherein being prepared for “random” shocks seem to benefit the system as a whole, or make it stronger.  Sedentary makes you fragile, weak, and soft; exercise makes you robust; Westside is Antifragile.

Antifragile

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Pocket Guide to Intermittent Fasting

Intermittent Fasting (IF) is all the rage these days, and there are a variety of different protocols out there, pioneered by people ranging from Ori Hofmekler (The Warrior Diet), Kate Harrison (The 5:2 Diet), Michael Mosley (The Fast Diet), Bert Herring (Fast-5), John Daugirdas (The QOD Diet), and Martin Berkhan (LeanGains), all the way to Jack Kruse (Epi-paleo Rx).  Chances are you’re probably unwittingly already doing one of them, at least intermittently.  The theoretical benefits are seemingly endless (albeit via few human trials), beyond the scope of my brain.

Tl;dr:

Non-IF: grazing; 6-8 meals per day.  Only significantly fasting duration occurs while asleep.
Normal-ish?: 3 squares.  Two 5-hour fasts, then fasting while asleep.
Eat Stop Eat or The 5/2 Bikini Diet: Eat only a small dinner 2 days/wk (600 kcal), eat normally other 5 days.
ADF: Alternate Day Fasting – 75% restriction on day 1; 25% surplus on day 2.
Leangains: Skip breakfast.
The Warrior Diet: Skip breakfast & lunch. (+1)
EOD: eat only Every Other Day.  36 hour fasts – from dinner on day 1 until breakfast on day 3.

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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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