Category Archives: TPMC

calories proper

The incredible camping experiment, circadian proper

Entrainment of the Human Circadian Clock to the Natural Light-Dark Cycle (Wright et al., 2013)

Abstract (edited): The electric light is one of the most important human inventions. Sleep and other daily rhythms in physiology and behavior, however, evolved in the natural light-dark cycle, and electrical lighting is thought to have disrupted these rhythms. Yet how much the age of electrical lighting has altered the human circadian clock is unknown. Here we show that electrical lighting and the constructed environment is associated with reduced exposure to sunlight during the day, increased light exposure after sunset, and a delayed timing of the circadian clock as compared to a summer natural 14 hr 40 min:9 hr 20 min light-dark cycle camping. Furthermore, we find that after exposure to only natural light, the internal circadian clock synchronizes to solar time such that the beginning of the internal biological night occurs at sunset and the end of the internal biological night occurs before wake time just after sunrise

In other words, they compared circadian events during 2 weeks of normal life to 2 weeks of 100% camping.  And camping won.

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Summer is fattening. Don’t do it in winter.

Seasonal eating proper

More on seasonal eating in what appears to be the primary model for its justification for use in humans – hibernating mammals.

How it goes, or so they say: in summer, hibernators massively overeat, including carb-rich foods, in order to generate muscle and liver insulin resistance, so as to promote body fat growth.  The long light cycle reduces evening melatonin, which pushes back the usual nighttime peak in prolactin, which causes an abnormal resistance to leptin, which induces hypothalamic NPY and subsequent carbohydrate craving.  Ergo, summer is fattening.  In today’s day, increased artificial lights guarantee year-round pseudo-summer; and we no longer experience the benefits of the short light cycle: longer sleep times (akin to hibernation) and fasting – either complete fasting as in hibernation, or pseudo-fasting, ie, a ketogenic diet.

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Nutrition Disinformation III

but they actually get it right this time.   Big HT to George Henderson for bringing this ms to my attention.

In Nutrition Disinformation, Part I, the Mediterranean diets employed by Estruch & colleagues were discussed.  The study subjects’ need for antidiabetic drugs, insulin, and anti-platelets all increased over the course of 5 years.  The media and even the authors themselves reported the opposite, touting the benefits of Mediterranean diets.  Thus begat the Nutrition Disinformation series.

Nutrition Disinformation 2.0 was a follow-up to an older post on the Look AHEAD study, when the results were finally published.  The intensive lifestyle intervention consisted of a pharmaceutical-grade low fat diet (ie, LFD + a little bit of Orlistat), and exercise.  By the end of 10 years, medication use was modestly lower in the intensive lifestyle group compared to controls, but it was markedly increased from baseline.  Therefore, I deemed it egregious to say their intervention was “healthy.”  In the context of Nutrition Disinformation, “healthy” means you’re getting better.  The need for insulin, statins, and anti-hypertensives should decline if you’re getting better.

In part 3 of the series, Yancy must’ve been following the Nutrition Disinformation series 🙂 and decided to conduct a subgroup analysis on the patients in his previous low carb vs. low fat + Orlistat study.  Weight loss was roughly similar, but all other biomarkers improved more on low carb.  In the new publication, Yancy analyzed data selectively from the diabetic patients in his original study to generate a “Medication Effect Score (MES).”  MES is based on what percentage of  the maximum dose was a patient given, and adjusted for the median decline in HbA1c experienced by patients on said drug.  A bit convoluted, but I’m on board (at least tentatively).

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Calories schmalories, alcohol, and chocolate

Some calories count, others don’t.  Some calories work in some people, but not others.  Does this sound like an irrefutable Law of Nature?  No, but it is a perfectly acceptable tenet of the Laws of Energy Balance (a construct of my design).

Do alcohol calories count?  Sometimes, but not this time:

The energy cost of the metabolism of drugs, including ethanol (Pirola & Lieber 1972)

This was a study on bona fide alcoholics who participated because they were promised treatment.  Metabolic ward.  FYI, one gram of alcohol burned in a calorimeter produces ~7.1 kilocalories; alcohol = 7.1 kcal/g.

Calories required to maintain body weight (ie, = total energy expenditure) was assessed the old-fashioned way: feeding them enough calories to maintain a stable body weight – they counted calories but relied on the bathroom scale to establish a baseline.  #TPMC.  After a week of weight stability, they ISOCALORICALLY exchanged carbohydrates for alcohol, and broke CICO.

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Sarcopenia has little to do with aging

It has to do with the duration of time spent being sedentary.

They say a picture is worth a thousand words, but luckily enough today you get both.

Sarcopenia: “poverty of flesh,” or the age-induced loss of skeletal muscle mass, strength, and function = reduced quality of life.  Sorry old-timers, but I hereby officially revise the definition from “aging-induced” to “sedentary-induced.”  Herein, I present evidence that sarcopenia is not a phenomenon of aging per se, but rather of disuse atrophy.  Dear Webster’s & Britannica, please revise accordingly.

Skeletal muscles: use ‘em or lose ‘em #TPMC

Thanks to Julianne Taylor & Skyler Tanner for directing me to these images.

divide and conquer

Exhibit A. Chronic exercise preserves lean muscle mass in masters athletes (Wroblewski et al., 2011)

This study evaluated “high-level recreational athletes.”  “Masters” just means they were over 40.  And “high-level” doesn’t mean “elite,” it just means they exercised 4-5 times per week.  These weren’t super-obsessed gym rats… it’s probably who I’ll be in 7 years [sigh].

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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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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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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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Brown adipose tissue

Once thought to be the holy grail of energy expenditure manipulators and a potential cure for obesity – fail.  I don’t have great evidence for this; it’s really just a hunch.

A new mouse study has provided some additional fodder for speculation, however.

The theory & background info: increased BAT activity can effortlessly burn away excess fat mass by using fuel to create heat instead of energy.  This model was most aptly summarized by the title of Dr. Efraim Racker’s 1963 ediorial: “Calories Don’t Count-If You Don’t Use Them.”  At best, I don’t think BAT is a panacea.  At worst, we might’ve learned our lesson long ago from DNP (circa 1938; also McFee et al., 2004; Miranda et al., 2006; Tewari et al., 2009; and Grundlingh et al., 2011).

drug banned

In a slurry of publications in 2009, researchers re-ignited the quest by showing cold-induced BAT activation in healthy humans (Virtanen et al., 2009):Virtanen BAT

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