Tag Archives: mortality

Mediterranean Diet Fail – Nutrition Disinformation, Part I.

Do not get your hopes up, do not pass GO!  do not collect $200.  The Mediterranean Diet.  Fail.

Primary Prevention of Cardiovascular Disease with a Mediterranean Diet (Estruch et al., 2013)

This is one of the biggest diet studies we’ve seen in a while, and no doubt it was a very good one.  It very effectively put the Mediterranean Diet to the test.

I felt compelled to write about this study out of fear for the nutrition disinformation that it would likely inspire.  The Mediterranean Diet is associated with all good things, happiness, red wine and olive oil; whereas the Atkins Diet is associated with artery clogging bacon-wrapped hot dogs and a fat guy who died of a heart attack.  Nutrition disinformation.

If you ran a diet study with 3 intervention groups for 5 years, and by the end of the study everybody (in all 3 groups) was on more prescription medications, would you conclude any of the diets were “healthy?”  If so, then we should work on your definition of “healthy.”

Study details: big study, lasted roughly 5 years, and the diet intervention was pristine.  Mediterranean diet plus extra virgin olive oil (EVOO) vs. Mediterranean diet plus nuts vs. low fat control.  They even used biomarkers to confirm olive oil and nut intake (hydroxytyrosol and linoleate, respectively).  Compliance was good.

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Paleotard, meet potatotard, Op. 132

(credit to Dylan and Woo, respectively, for introducing me to those terms)

Empty calories – the potato

While it has a decent amino acid profile, with only 3 grams of protein it’d take a diabetic amount of potatoes to fulfill your daily protein.  By “diabetic,” I mean about a thousand grams of starch.  potatoes are just as glycemic as white bread.

potato

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Inflammatory, trans, or linoleate?

As much as I’d like to say this is the nail-in-the-coffin, omega-6 causes irreversible fatality, I have a confession.

I believe it’s the empty calories, not the inflammatory omega-6 devil linoleate.  Biscuits, cookies, processed foods of all shapes and sizes are simply the delivery vehicles for industrially modified and probably “trans” fats that started out innocent enough as soybean oil or omega-6 vegetable oils.

linoleate is the quintessential omega-6 fatty acid and is found at high levels in vegetable oils.  just like the omega-3 linolenate found in soybean oil, processing of the oils usually damages them – turns them into trans fats and/or oxidizes them (by “oxidizes” I don’t mean fat burning, see pictorial below)

So despite the impeccable statistical anvil thrown at these data, which seem to clearly implicate linoleate, I don’t think it’s the linoleate.  H E double hockey sticks, we probably don’t get enough normal unmodified linoleate.  Unless you’re cracking shells, even “raw” almonds are Pasteurized.  

unshelled nuts

don’t sanitize your food.  your meat needn’t be burned, nor your nuts Pasteurized.

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diabulemia

This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.

Yes, I think sugar and empty calories, and the associated hyperinsulinemia are the bane of anyone with obesity or any sort of hyperplastic fat tissue disorder.  And yes, this is the worst type of evidence to support such a stance, but when you’ve got lemons, well…

Make no mistake, diabulemia may as well be spelled DIE-abulemia.  It’s not a laughing matter.  But yeah, well, lemonade, etc.  So here it goes

Diabulemia

Type I diabetics have low insulin and are lean; type II diabetics have high insulin and are not.  Insulin injections in either population promotes hyperplastic fat growth.  Sounds scary, right?  It is:

insulin

This poor soul unfortunately restricted his insulin injections to only two sites.  Make all the jokes you want, but the effect is obvious…  this is happening everywhere in hyperinsulinemic heavyweights (not just two specific sites).

CHO III Picture 279

 So what do Type I’s do when they want to lose some fat mass?  Stop jabbing themselves with insulin. Unfortunately, it’s really that simple.  Type II’s and anyone with excess or hyperplastic fat tissue can do the same with low carb or keto, although this would be a great benefit to their overall health.  But for Type I’s… not so much – they need insulin to prevent the horrific manifestations of ketoacidosis, which includes but is not limited to: death.

Type I’s are hyperglycemic because of low insulin; insulin therapy prevents diabetic ketoacidosis, a deadly condition.  But for those who simply choose to selectively reduce their insulin dosage, they: 1) don’t die; 2) lose fat; and 3) get hyperglycemic and incur all the damage that ensues (retinopathy, nephropathy, neuropathy).  Furthermore, they’re walking on thin ice – DKA is lurking.  It is just as stupid yet more dangerous than using tapeworms to lose weight.

tape-worms

Type II’s are hyperglycemic because of insulin resistance; a condition that is pathologically neutered via carbohydrate restriction.  Type I’s who reduce insulin injections to decrease fat mass are doing just as much damage as Type II’s who DON’T reduce carbohydrate intake.


Diabulemia is akin to an eating disorder.  Biologically, the lack of insulin allows fat to be released from adipose tissue with gravitas, and it prevents glucose from being stored in any meaningful capacity.  You’re literally pissing calories here, burning ’em like crazy there; all of which is a helluva lot easier than “eating less moving more” … which is why diabulemics do it (because they have the option [unlike the rest of us]).  Diabulemia is good from a fat loss perspective, but will most definitely contribute to severe and possibly deadly complications down the line.   Carbohydrate restriction, however, is a win-win-win… (for everyone except The Man, so perhaps it’s a win-win-win… fail)

This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.


Humans aren’t big rats, but here it is again, anyway:

Leptin deficiency causes insulin resistance induced by uncontrolled diabetes (German et al., 2010)

I’m ignoring the brunt of this paper and only focusing on the positive control groups.  [Positive controls… meaning they were included because they would definitely exhibit the expected response.]

Force rats into a state of diabulemia, and their insulin levels plummet, blood glucose soars, and they become ravenously hungry (open squares in the graphs below).German I

But lo and behold, fat mass atrophy ->German II

Eat less move more?  Well, they certainly didn’t “eat less…” (see above) … and:German III

nor were they “moving more.”  Low insulin seems to have a way to bypass that whole “eat less move more” thing (eg, Metabolic rate per se).

 

Throwing the baby out with the bathwater works if the baby is fat and the bathwater is insulin.  (no, not a fat baby.)

 

calories proper

 

 

Non-sequiter nutrition IV. in vino veritas

The French Paradox is neither a paradox nor French, really.  Red wine isn’t saving the French from a saturated-fat induced heart attack epidemic….  Not to take anything away from red wine, however, as the metabolic effects of red wine (and alcohol in general) are rather interesting.

Background info: alcohol (ethanol) metabolism produces NADH (stick with me here, this article doesn’t get all technical on you I promise).

NADH inhibits gluconeogenesis (Krebs et al., 1969); as such, alcohol lowers blood glucose, regardless of whether if it’s pinot, cabernet, or straight moonshine (Harold  R. Murdock, 1971).

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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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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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skinny is the new fat, Op. 95

I’ve been known to rave about the phenomenon of metabolically obese normal weight (MONW), or fat skinny people.  In brief, this population exhibits insulin resistance, metabolic syndrome, hypertension… all things usually associated with obesity… but they’re lean.   In fat skinny people, I wrote about two epidemiological studies on markedly different populations (Americans and Koreans); these two peoples have virtually nothing in common (culture, foods, genetics, etc.).  Despite these differences, there was a strong similarity in the macronutrients associated with metabolic dysregulation in otherwise lean individuals (aka fat skinny people): in the first study, high carb and low protein diets were the major culprits, with a smaller contribution of low fat.  In the second study, high carb and low fat were at fault (protein intake wasn’t analyzed).

A new study that is about to hit the presses didn’t intend to say anything about fat skinny people, but they weren’t counting on ME.

Body mass index, diabetes, hypertension, and short-term mortality: a population-based observational study, 2000-2006 (Jerant and Franks, 2012)

This study included over 50,000 people aged 18-90.  Between the years 2000 and 2005 about 3% died, which was statistically just enough to ask “why?”  In brief, they compared body weight, blood pressure, smoking, and diabetes with mortality risk.  

In each BMI category, the square is higher than the circle.  DM = diabetes (the squares).  Diabetes increases mortality risk independent of BMI.  Now just focusing on the squares; as you move from left to right, body weight is increasing but mortality risk in diabetics is decreasing.  A 150 pound diabetic has a higher mortality risk than a 200 pound diabetic, who has a higher mortality risk than a 250 pound diabetic.  Huh?

Perhaps the lean diabetics are fat skinny people, the elusive MONW?  If so, according to the research discussed HERE, their diet might have made them that way.  The lean diabetics (aka fat skinny people aka MONW aka NOD [non-obese diabetics]) eat less protein, more carbs, and less fat.  This might be a reach, but collectively (1 + 2 + 3) these data imply a poor diet might be worse than obesity for diabetics.

disclaimer: this is not true in most circumstances, i.e., skinny people can usually whatever they want.  There are skinny diabetics, but they are significantly rarer than obese diabetics.  In other words, most type II diabetics are obese, the lean ones just eat a crappier diet. You might be wondering: “how are they skinny if they eat so poorly?”  My guess is that they just haven’t eaten enough of it [yet]; it’s rare to stay lean on a “crappier diet.”

So is skinny the new fat?  Being lean with type II diabetes is an indicator of EMPTY CALORIES; it could be riskier for all-cause mortality than obesity in diabetics.

“Attention endocrinologists, diabetologists, and general practitioners: don’t assume diet is not a problem in your skinny diabetics because they are skinny.  Indeed, diet might be THE problem.”

And no, if you’re a skinny diabetic, this DOESN’T mean gaining weight will make you live longer.  it just doesn’t.

 

it just doesn’t.

calories proper