Category Archives: diet

Biohacking holiday weight gain

What should you eat before the big feast?  (hint: eggs.)  And don’t try to compensate in advance by eating less, this will only make you hungrier.  Furthermore, foods in your regular diet are probably healthier than holiday fare, so you definitely don’t want to eat fewer healthy foods to make room for empty calories.

Tip 1. 

Variation in the effects of three different breakfast meals on subjective satiety and subsequent intake of energy at lunch and evening meal (Fallaize et al., 2012)

Participants were served only one of these for breakfast:

And given unlimited amounts of these for lunch and dinner:

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Philosophy of the faux-low carb mouse and others like it

The Laws of Energy Balance are always maintained.  Here are some insights into how this is accomplished from a mouse perspective.  A hormonal milieu which is unfriendly for fat storage will make you lean, but not by magic.  We’ve got: 1) reduced food intake; and/or 2) increased energy expenditure.

Recall the faux-low carb mouse (Ins1+/-; Ins2-/- aka InsKO; Mehran et al., 2012).  They can’t get fat because of an inability to develop hyperinsulinemia.  Food intake isn’t reduced, so energy expenditure goes up.  Since the fat isn’t stored, it needs an “out,” so it either inhibits food intake or ramps up energy expenditure; InsKO gives us the latter.

While not hormonally-mediated, PPARg+/- mice can’t get fat because of defective adipogenesis and they handle this problem both ways; by reducing food intake and increasing energy expenditure (Kubota et al., 1999).  Similar to InsKO, PPARg+/- have lower insulin, but the primary defect in these mice is defective adipogenesis.  They can’t store fat, so this unstored fat: 1) tells the brain there’s plenty of fuel around so stop eating; and 2) ramps up energy expenditure to burn itself off:

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The faux-low carb mouse and a diatribe

The faux-low carb mouse

Hyperinsulinemia drives diet-induced obesity blah blah blah (Mehran et al., 2012)

The researchers generated a mouse with half as much insulin as normal mice.  Physiological insulin levels remain intact, but hyperinsulinemia is genetically inhibited.  For the sake of simplicity, we’ll call them “InsKO.”

When fed a high fat diet, normal mice become markedly hyperinsulinemic (pink line) whereas InsKO mice maintain relatively normal insulin levels (red line).  Blue lines are chow-fed mice; similar trend but less interesting.

divide and conquer

InsKO mice don’t get fat,

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Sir Philip Randle and the effects of blocking fat oxidation

The Randle Cycle, put forth in 1963, dictates that increased fatty acid oxidation inhibits glucose uptake and increased glucose oxidation inhibits fatty acid oxidation – it just makes sense.  Insulin enhances glucose uptake and oxidation while suppressing lipolysis; growth hormone, cortisol, and adrenaline enhance lipolysis and fatty acid oxidation which suppresses glucose oxidation.  Low carbohydrate diets reduce insulin, and the reduced glucose oxidation is metabolically irrelevant because of reduced glucose intake (by definition).  This is critical information.  And as a student of basic intermediary metabolism, I prefer the Randle Cycle over any number of alphabet soup recipes to explain metabolic phenotypes (eg, fat and carbs as opposed to IRS, Akt, Jnk, ERK, etc., etc.).  Many valuable lessons can be learned from understanding permutations of the Randle Cycle.

For example,

Inhibition of carnitine palmitoyltransferase-1 activity alleviates insulin resistance in diet-induced obese mice (Keung et al., 2012)

divide and conquer

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NRT = nicotine replacement therapy

NRT improves quitting success rates and reduces cessation-induced weight gain.  It’s a fact; and there are a lot of anti-addictive pharmacological interventions that do too.

Dear obesity researchers, primary care physicians, and smokers,
Pay attention.
Sincerely,
Bill

Rimonabant is the anti-“munchies” drug that blocks the marijuana receptor CB1.  It causes weight loss.  But 20 mg daily also increases the odds of successfully quitting smoking by 50 – 60% (Cahill and Ussher, 2007).

Relevance?
Marijuana: not really addictive.
Obesity diets: delicious, but not really addictive.
Cigarettes: definitely addictive.
Rimonabant: anti-addictive.  It causes weight loss in overweight but not lean people, perhaps because lean people don’t eat obesity diets (?).

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The curious effects of calories in mice

What is the biological impact of a history of obesity and weight loss?  The metabolic trajectory of two calorically restricted skinny mice depends entirely upon whether or not they used to be fat.  The end of this story might be: ‘Tis better to have lost and re-gained than never to have lost at all; or it’s just an interesting new take on the body weight set point theory.

Caloric restriction chronically impairs metabolic programming in mice (Kirchner et al., 2012)

divide and conquer

Part 1.
Study 1. Calorie restricted lean mice: the effect of diet composition.

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Fish oil. Pills or directly from the source? Opus 118.

As a proponent of consuming fatty fish (sardines, salmon, etc.), I was interested to read the new fish oil study; as an opponent of meta-analyses, however, not so much.  A meta-analysis is a type of study whereby the researcher thinks of something they want to prove, then cherry picks studies that best support their point.  Or perhaps I’m just biased.  Nonetheless,

Association between fish consumption, long chain omega 3 fatty acids, and risk of cerebrovascular disease: systematic review and meta-analysis (Chowdhury et al., 2012)

In brief, regarding whole fish consumption, 3 servings per week reduced stroke risk by 6% and 5 servings by 12%.  Surprisingly, there was no effect of fish oil pills that contained ~1.8 grams of long chain omega 3 fatty acids.  What this study lacks is any information about the dose of EPA and DHA (the major bioactive fatty acids in fatty fish); and with 38 studies analyzed, I’m not about to try to figure it out (sorry team)…  a serving of fish can have anywhere from 0 to 1 gram of EPA and DHA; 1.8 grams of long chain omega 3 fatty acids can have anywhere from 0 to 1.8 grams of EPA and DHA.  Therefore, I’ll resort to reviewing two of my favorite fish studies of all time: DART and GISSI.  For a more detailed review of fish oils and these studies, check out The poor, misunderstood calorie (chapter 9).

divide and conquer

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Up in smoke

I’m not pro-big tobacco or cigarettes, but I am anti-scare tactics.  It is usually the news media or politicians, exaggerating and/or grossly misinterpreting some study findings in order to make a great headline or secure votes.  But in this case, it wasn’t. The predators who were preying on our fear were the scientists.  Smokers of the world, unite!

Myocardial infarction and sudden cardiac death in Olmsted County, Minnesota, before and after smoke-free workplace laws  (Hurt et al., 2012)

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Exenatide and tapeworms, Op. 116

The great Dr. Schoeller can polish a turd like no other.  Dale Schoeller’s claim to fame is his extensive work on one of the best ways to measure total energy expenditure in free-living individuals: doubly-labeled water.  In doubly-labeled water, subjects drink stable isotope-labeled water; instead of hydrogen + oxygen = H20, the stable isotope-labeled water is deuterium + oxygen-18 = D218O.  Deuterium is excreted just like hydrogen, in water as urine & sweat.  Oxygen-18 is excreted just like oxygen, in water and carbon dioxide.  So the subjects lose deuterium & oxygen-18 in water at equal rates, but only oxygen-18 in carbon dioxide; so this technique basically measures carbon dioxide production, which is proportional to energy expenditure.  Clever. 

Being that Schoeller practically invented the technique, his interpretation of these total energy expenditure data are not flawed, but that’s not where he went astray.

Alterations in energy balance following exenatide administration (Bradley et al., 2012)

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“An adult conversation” about the Look AHEAD study

Extra! Extra!    Read all about it!  (after you sign up for the new EMAIL NOTIFICATIONS on the right)

Moderate weight loss alone doesn’t lower heart disease risk in diabetics, study shows
Diabetes study ends early with a surprising result
NIH trial of lifestyle intervention for type 2 diabetes stopped for futility after 11 years

Notice none of the headlines read “Low fat diet is not heart-healthy for diabetics,” but that’s exactly what the latest epic fail demonstrated.  Reminiscent of the Women’s Health Initiative (circa 2006), the Look Ahead study tested a long-term low fat diet in diabetics.  If a protective effect had been shown, this study would’ve gone done in the history books as definitive proof that a low fat diet is superior.  But it wasn’t, and unfortunately that probably won’t count as anything for the opposition.  In brief, the planned 14 year study was stopped after 11.5 years because cardiovascular events weren’t lowered by the low fat diet (and might even have been increased; the manuscript hasn’t been published [yet?]).

The Women’s Health Initiative, which cost taxpayers something in the ballpark of $625,000,000 (six hundred twenty five million dollars > a half billion), showed that reducing dietary fat by 8 percentage points (from 37.8% to 28.8%; a 23.8% reduction) for 8 years had no effect on heart health and was even detrimental for people with CVD at baseline.  I repeat: CVD patients assigned to the low fat dietary intervention experienced more cardiovascular events than those in the control group (you heard it here first).  But for some reason, the Look AHEAD researchers thought they might get a different result if they tried this in diabetics?  A low fat high carb diet in patients with bona fide carbohydrate intolerance?  really?

REALLY?

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