Author Archives: Bill

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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Milo of Croton vs. concurrent training

Lesson 1.  Milo of Croton

Every day since a very young age, Milo would drape his calf over his shoulders and do his daily exercises.  As his calf grew, so did Milo’s strength.  Many years passed and by the time of the Olympic games, Milo’s calf had become a full-grown bull and Milo’s strength became unparalleled in all the land (or so the story goes).

This is how strength-training works.  Increasing the amount of weight you lift progressively, consistently, and frequently makes you stronger.

Lesson 2.  Concurrent training

Resistance training builds muscle and strength.  Endurance exercise is good for the heart, burns fat and muscle, but doesn’t make you stronger.  Endurance exercise hinders the gains reaped from resistance exercise, not vice versa.  Interpretation: runners should lift; lifters shouldn’t run (sprints don’t count).

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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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Coffee and cigars, the breakfast of champions

Or more specifically, caffeine and nicotine… or really just nicotine.  Today is about the lesser of two evils: nicotine, Mother Nature’s little helper (the other evil being cigarettes [not coffee]).  This curious little molecule is an anti-inflammatory memory boosting appetite suppressant.  If it didn’t screw with the reward mechanisms in your brain, it’d be a vitamin. Part 1.  Cigarettes, nicotine, and metabolic function Exhibit A: Activation of the cholinergic anti-inflammatory pathway ameliorates obesity-induced inflammation and insulin resistance  (Wang et al., 2011) translation: “nicotine is good for mice.” Continue reading

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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Another -cetrapib fail

don’t fuck with your cholesterol levels.

Dalcetrapib, a CETP inhibitor that raises HDL cholesterol, just failed for Roche:  Effects of dalcetrapib in patients with a recent acute coronary syndrome (Schwartz et al., 2012)

Not surprisingly, as Pfizer’s version also failed 5 years ago:  Effects of of torcetrapib in patients at high risk for coronary events (Barter et al., 2007)

must read –> …if it ain’t broke… 

 

 

calories proper

 

 

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

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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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Metabolic rate per se

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Admittedly, the effect of diet on metabolic rate is small (i.e. statistically non-significant in most cases), but its incredible consistency across space and time suggest it could be true.  And given the difficulty of maintaining a reduced body weight after dieting, it might even be important.  The following studies are examples of widely differing subject populations in various metabolic conditions; yet the effects of diet on metabolic rate exhibit a phenomenal degree of similarity.

disclaimer: I don’t know what’s more important – metabolic rate per se, the diet behind it, or the resulting hormonal adaptations.  All of the diets that are associated with a higher metabolic rate are also predicted to result in lower insulin levels and higher fat oxidation.  Thus, we are left with a triumvirate of diet, hormonal milieu, and energy expenditure… all of which are important for body composition and quality of life.

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