Monthly Archives: August 2011

Empty calories, part I

Posted on August 25, 2011 | Leave a comment

Empty calories, part I

 

Moderation- the avoidance of excess or extremes

Balanced- arranged in good proportions

What is a well-balanced diet?  Everything in moderation?

WRT nutrition, these phrases are meaningless.  There are healthy people around the world who consume a wide variety of diets.  A dietary staple in one culture may be completely absent or even shunned from another equally healthy culture.  And that same dietary staple could be the cause of disease in yet another culture.  Furthermore, “moderation” and a “well-balanced diet” are generally used reflectively, whereby the speaker is referring to their own diet as the healthy baseline, and any deviations can be included but only in “moderation,” as any deviations would certainly be less healthy, otherwise the speaker would be touting that diet instead.

Does it refer to whole foods, or the individual food components.  IOW, should we consume in moderation processed foods? How about the trans-fats found in hydrogenated soybean oil from said processed foods?

If a diet contains 100 grams of fat how much of that would be considered “moderate?”  Half?  Not if we are talking about industrial trans fats.  Certain foods should be minimized or avoided altogether…  neither in moderation nor as part of a well-balanced diet.

For a very basic example, carbohydrate’s provide ~62% of the calories for Indian city-dwellers, yet the rate of carbohydrate intolerance is 14%!

Dietary intake and rural-urban migration in India: a cross-sectional study (Bowen et al., 2011)

But the Kitavan’s get 69% of their calories from carbohydrates and there isn’t a diabetic on the entire island!

How can this be?  There are too many confounding variables to put an exact number on “moderation.”   The Indian urbanites from Bowen’s study consumed over 3,200 kcal per day, while the Kitavans are closer to 2,100…  But ¾ of the Kitavans smoke and they get little physical activity…?

Low serum insulin in traditional Pacific Islanders—the Kitava Study (Lindeberg et al., 1999 Metabolism)

The “well-balanced diet” does not exist.

The Mediterranean diet might be optimal for people living in Italy and Greece, but the long-term consequences of mismatching diet and the seemingly infinite lifestyle variables confounds the application of this to other cultures.  And even within a given culture, there will be pen pushers and manual laborers who would be optimally suited with vastly different macronutrients and calories.

And the reverse is also true.   Exercise and a high level of physical activity may keep one population lean and fit, but that doesn’t mean increasing exercise and physical activity will prevent a different population from becoming obese.

Physical activity energy expenditure has not declined since the 1980s and matches energy expenditure of wild animals (Westerterp and Speakman, 2008 International Journal of Obesity)

WRT nutrition, “moderation” is meaningless.

 

Calories proper

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an elusive rogue criminal mastermind

Posted on August 14, 2011 | Leave a comment

Hyperinsulinemia.  Whether it’s caused by insulin resistance, too many carbs, or industrial insulin secretagogues found in processed foods, high insulin levels are problematic.

Octreotide is a synthetic version of somatostatin and it inhibits the secretion of a variety of hormones, namely insulin.  A group of researchers set out to determine the effects on obesity of pharmacologically lowering insulin via octreotide.  In this setting, it doesn’t matter how insulin became elevated in the first place, only whether reducing it has any impact on obesity.

A multicenter, randomized, double-blind, placebo-controlled, dose-finding trial of a long-acting formulation of octreotide in promoting weight loss in obese adults with insulin hypersecretion (Lustig et al., 2006 International Journal of Obesity)

Octreotide dosing is surprisingly convenient, monthly injections, and there were no other dietary or behavioral interventions.  Lustig’s hypothesis was simply that high insulin levels were making things worse, like causing weight gain and hunger, preventing weight loss, etc.  The intervention was only octreotide; no dietary or behavioral interventions…. Another way of thinking about this hypothesis is: if dietary or behavioral factors were contributing to the obesity phenotype, then perhaps high insulin levels were in part causing those very same dietary or behavioral factors (?).  That seems backward, like an enigma wrapped in a riddle surrounded by a mystery, but this study addressed the possibility by also assessing a variety of psychological and dietary/behavioral factors (whether these could be caused by reduced insulin levels, per se, as opposed to some other effect of octreotide would be difficult to determine, but this study demonstrates the possibility).

This was a population of relatively young (~40-ish), fairly heavy (~240 lbs), but otherwise healthy subjects.  And most of them stayed in the study for the entire duration (which means, in part, that octreotide isn’t an unpleasant therapy).

To make a long story short, octreotide worked, but not very well…

 

In the table above, the “mean percent change from baseline” was less than 2%, which amounts to about 4 pounds (in 6 months).  As a graph (note the ordinate):

 

But the treatment was well-tolerated, and a variety of quality of life measurements were significantly improved, such as physical function, self-esteem, and sex life.  And interestingly, “carbohydrate cravings” were significantly reduced, which suggests the possibility that high insulin levels may in part be self-promoting.

Although a more selective drug would have been preferable to the pan-inhibitor octreotide, another interpretation of the modest weight loss results presents itself.  A recent study by Willett, which I previously blogged about showed that in general, people gain about a pound a year and some of the largest contributors to that weight gain are potatoes, potato chips, and French fries.  All three elicit a robust insulin response, and the latter two most likely contribute to other metabolic abnormalities which also lead to elevated insulin levels (insulin resistance, insulin hypersecretion, etc).  The current study demonstrated the possibility that high insulin levels, per se, might be an important cause of weight gain or the maintenance of an obese state.  AND carbohydrate craving was reduced by octreotide.  Willet’s study showed that foods like potatoes, which cause high insulin levels, are associated with weight gain.  Lustig’s study showed octreotide reduces insulin levels, which reduces carbohydrate cravings and leads to weight loss.  Abandon carbs?  Monthly octreotide injections?  Going on the Atkins diet would cause a much more rapid weight loss than octreotide, but octreotide therapy would cause literally zero lifestyle disruption… and the speed of weight loss would be closer to the how fast the weight came on in the first place.

On a more philosophical note, there is a subtle continuity between the magnitude of weight change and the foods implicated in Lustig’s and Willet’s studies.  On one hand, the most influential foods associated with age-dependent weight gain were starchy carbs (which induce insulin secretion); on the other hand, lowering insulin via octreotide reduced carbohydrate cravings and caused weight loss.  It’s difficult to clearly connect these observations with eloquence, but they seem to suggest a strong correlation.  The rate of weight gain associated with ‘potatoes, et al.’ was slow, similar to the rate of weight loss with octreotide…

So if you likened the cause of obesity to an elusive rogue criminal mastermind, and the cure to a cunning stealth superhero, then you’d be unimpressed with “potatoes” and “a few pounds gained or lost.”  …  obesity doesn’t happen overnight.

 

Calories proper

 

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Posted in Advanced nutrition

the boob tube

Posted on August 3, 2011 | Leave a comment

it’ll kill you!  (too much, i.e.)

OK, FTR I don’t think any amount of TV watching will kill you, and I think that any study showing otherwise is under the control of some major food company , big pharma, or downright statistical sorcery.

Playing in traffic? Perhaps.  Watching TV? No.

Without further ado, some recent studies showing I’m wrong.

Television viewing and risk of type 2 diabetes, cardiovascular disease, and all-cause mortality (Grontved and Hu, 2011 JAMA)

First, a meta-analysis.  Not good.  The first paragraph in the intro starts out with [sic]: “40% of daily free time is occupied by TV viewing within several European countries.”  At first, 40% seems like a lot; how much “free time” do we really have?  Sleep 8 hours, work 8 hours, commuting to and from work, chores, eating, showering, etc… so maybe 3 hours of free time?  40% of 3 hours = 1.2 hours.  But the authors cite “4 hours” of TV viewing which means these people have almost 7 hours of free time per day… which means commuting to and from work, chores, cooking & eating, showering, etc. only takes about 1 hour (unless they either don’t work or don’t sleep.  IOW 7 hours seems like a horrendous overestimate.  There are a few other inconsistencies in the intro, but rather than spend more time nit-picking, on to the data:

To make a long story short, every additional 2 hours of TV viewing per day increased the risk for:

Type II diabetes by 0.0176%

Fatal CVD by 0.0038%

All-cause mortality by 0.0104%

And just to be clear: yes, those are very very small numbers.

The authors searched relevant databases for every study on the topic, excluded the ones that didn’t support their hypothesis (jk… kind of*), and then independently analyzed the resulting studies.  Any disagreements were “resolved by consensus,”  which I’m not exactly clear how is accomplished when there are only 2 authors (rock, paper, scissors?).  In their favor, whenever possible the data were analyzed with and without diet and body weight in their multivariable-adjusted models.

*out of 1,655 relevant studies, 8 (agreed with their hypothesis [jk… kind of]) were included.

Divide and conquer

As seen above, increasing hours of TV viewing is associated with increasing risks for diabetes, CVD, and all-cause mortality.  Yikes!

The risk for diabetes was linearly related with TV viewing, but the risk was modestly attenuated by controlling for diet, and greatly reduced by controlling for body weight… IOW a poor diet is bad but excess body weight is worse (lean people can watch more TV than obese people).

Risk for all-cause mortality was less than CVD and diabetes and wasn’t affected by diet or body weight.  The inflection was around 3 hours…  which means that the risk dying isn’t appreciably increased by TV viewing if you watch less than 3 hours per day.  Phew!  (the applies to adults only).  In sum, 3 hours seems to be a safe amount of TV for lean healthy people; less if obese or pre-disposed to diabetes.

Something similar was found in an EPIC study.

Television viewing time independently predicts all-cause and cardiovascular mortality: the EPIC Norfolk Study (Wijndaele et al., 2011 International Journal of Epidemiology)

 

Although the overall risk for all-cause mortality associated with increased TV was about a third less than in Hu’s meta-analysis, it was 1) statistically significant, and 2) unaffected by diet or body weight (similar to Hu’s findings).

 

The relationship between TV viewing and all-cause mortality was attenuated after controlling for a variety of confounding factors (HR Model A = 1.08, p<0.001; HR Model B = 1.05, p=0.01), which means that someone who watches a lot of TV also has other risk factors which contribute to their risk of dying that have nothing to do with TV (like smoking, for example… unless they smoke because of the show their watching [?]).

Interestingly, the relationship was unaffected by controlling for physical activity (compare HR in Model B to Model C), which seems to imply that sitting too much (watching TV) is not necessarily equal to exercising too little… and in this population, ‘exercising too little’ was statistically unhealthier than ‘sitting too much.’

one from down under:

Television viewing time and mortality.  The Australian diabetes, obesity and lifestyle study (AusDiab) (Dunstan et al., 2010 Circulation)

In AusDiab, TV increased the risk for all-cause mortality slightly moreso than EPIC-Norfolk, but was similarly attenuated by controlling for other risk factors:

 

Oddly, there is a blip at 4 hours in both AusDiab and EPIC-Norfolk.  I have no idea what this means, but it is very interesting that in both England and Australia, people who watch 4 hours of TV per day have a higher risk for all-cause mortality than those who watch for 3 or 5 hours… if you find that you’ve spent 4 hours watching TV one day, throw on a pot of coffee and watch another hour.  Food for thought.

WRT health outcomes, excessive daily TV viewing seems to be a marker for other risk factors such as obesity, smoking, etc (may even be an indirect marker for ‘family history of CVD, diabetes, etc.).  TV watching per se is not the problem, nor is I suspect the TV.  Eat less, move more?

calories proper

 

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Posted in Advanced nutrition, Exercise