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Resveratrol, energy balance, and another reason to distrust health journalism, Op. 79


The great red wine compound “resveratrol,” at it again.  Disclaimer: 150 mg of resveratrol per day is too low and 30 days is too short to detect anything close to what was seen in the infamous resveratrol mouse study (Baur et al., 2006 Nature), which showed resveratrol to be the best drug ever on the planet.

This study, on the other hand, utilized the highest quality study design and was published in a great journal, but was a flop.   And the media got it wrong too:  “Resveratrol holds key to reducing obesity and associated risks.”  No, it doesn’t.

Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans (Timmers et al., 2011 Cell Metabolism)

The study design was pristine.  Kudos.

Sample size too small (n=11) and study duration too short (30 days), but it was a randomized, double-blind, placebo-controlled, crossover study.  And although this type of drug study does not require such a thorough assessment of compliance (a pill count would’ve sufficed), the authors tested blood levels of resveratrol and its metabolites… cool.

On the docket: resVida, DSM Nutritional Products, Ltd.

Divide and conquer

The table above shows baseline characteristics in placebo and treatment groups, but this is peculiar because although the study was randomized (which is confirmed by the high degree of similarity between the two groups), it was also a crossover.

Brief review of my Prelude to a Crossover series (I  & II):

phase 1) half the subjects get drug and half gets placebo

phase 2) both groups get nothing for a washout period

phase 3) everybody switches and gets the other treatment

There are technically two baseline periods (before phase 1 and before phase 2), and all the subjects are in both.  As such, there is only one set of baseline values, so I’m not sure what the data in the above chart actually reflect.  Is this a mistake? or are these data only representative of one of the treatment sessions (which would be an egregious insult to the prestigious crossover design).

In any case, the subjects were all clinically obese, ~100 kg (220 pounds), BMI > 30, body fat > 25%, but otherwise metabolically healthy (fasting glucose levels of < 100 mg/dL).

But here’s where it starts going from technically flawed to weird:

Insulin levels may have been statistically significantly lower after resveratrol compared to placebo, but not after considering baseline insulin was ~15-16 mU in both groups.

insulin proper

The authors noted that after treatment, insulin levels were 14% lower in resveratrol compared to placebo (green circle).  BUT whatever was in that placebo pill was almost twice as good!  The placebo reduced insulin levels by 27% (red circle)!  (take THAT!)  I’m glad the authors reported these data instead of burying them, but they illustrate yet another flaw.

150 mg resveratrol (10-15 bottles of red wine) for a 220 pound person = 1.5 mg/kg; 200x less than what Baur gave his mice (300 mg/kg). Interestingly, however, this produced plasma levels of resveratrol almost 3x higher (180 vs. 65 ng/mL). I have no idea how this happened, but the benefits and lack of toxicity [at such a low dose] bode well for recreational resveratrol supplementation.

As mentioned above, resveratrol was totally safe, but how to interpret this is unclear.  Our options are: 1) good; 2) meaningless; or 3) simply not bad (which I suppose is kind-of-like #2).  It could be interpreted as meaningless because resveratrol, the anti-aging drug, is meant to be taken for a very VERY long time (i.e., forever).  This study proved that resveratrol was safe when taken for 30 days which is considerably shorter than forever.

Furthermore, the dose was phenomenally low, ~150 mg/d, so anything other than “totally safe” would be a huge red flag.

Does resveratrol in fact mimic calorie restriction, as stated in the title?  During calorie restriction, food intake declines (by definition), metabolic rate and insulin levels also decline, but free fatty acids and fat oxidation increases.  In the resveratrol group metabolic rate and insulin declined (recall however that the placebo was pretty impressive also in this regard), but free fatty acids and fat oxidation decreased.  Although proper calorie restriction trials in humans haven’t happened yet, some of these  effects don’t jive.  A decline in metabolic rate will reduce the amount of fat burned.  But relative fat oxidation also declined, leading to what could be a profound reduction in fat burning… coupled with no change in food intake (noted by the authors) this will result in increased fat mass.  Energy Balance 101- no ifs, ands, or buts.  This study was far too short-term to detect a meaningful increase in fat mass, but if these preliminary findings are true (and my interpretation of the data are correct), then this drug might just make you fat.

Oddly enough, they did detect an increase in fat accumulation in skeletal muscle:

(perhaps instead of calling it a calorie restriction-mimetic, the authors should’ve gone with exercise-mimetic, citing the athlete’s paradox (e.g., van Loon and Goodpaster, 2006)

In contrast to the popular antidiabetic drug rosiglitazone, which shifts fat storage from liver (where it causes a host of health maladies), to adipose, where it can be stored safely indefinitely, resveratrol shifted fat storage from liver to skeletal muscle.  This is interesting because while the fat storage capacity of adipose is seemingly unlimited, I doubt the same is true for skeletal muscle, which needs to do a lot of stuff, like flex.

If these findings are true, which I seriously question, then it would be interesting to see what happens to skeletal muscle fat stores after a few months, considering they doubled in only 30 days (this is unbelievable, literally).

The authors try to make the case that the increased muscle fat came from adipose, but until they report body composition data, this is a tough sell.  The elevated fasting free fatty acids support their claim, but the accompaniment of unchanged meal-induced FFA suppression with lower adipose glycerol release don’t; perhaps the missing glycerol is being re-esterified to nascent adipose-derived free fatty acids?  Increased adipose tissue glucose uptake would be supported by the lower glucose levels, but that is already more-than-accounted for by the increased RQ (indicative of increased skeletal muscle glucose oxidation).

There are some mysteries in these findings, and the improper handling of crossover data do not help.  If this paper is true and my interpretation of the energy balance data are correct, resveratrol might just make you fat :/

Unless of course you’re a mouse, in which case it’ll make you better in every quantifiable measure.

calories proper

p.s. I don’t think resveratrol will really make you fat, I think this study elucidates nothing.

taking the fun out of FODMAPs

bring a gun to a knife fight, part II: why “oligosaccharides” are the odd-man out.

The “O” in FODMAPs refers to “oligosaccharides” and includes a very important group of gut-friendly nutrients: prebiotics.  While some specific oligosaccharides are problematic, others are highly beneficial.

The good guys: isomalto-oligosaccharides (MOS), inulin and FOS, and galactooligosaccharides (GOS).  These nutrients stimulate the growth of healthy gut bacteria (bifidobacteria), alleviate gastrointestinal distress, and promote overall well-being.  These are all oligosaccharides, which are unfortunately excluded from the low FODMAPs diet.

support for the above claims:

MOS: Yen et al., (2011)

FOS: Costabile et al., (2012)

GOS: Walton et al., (2012)

Yen showed that at doses of 11 – 22 grams of MOS increased both bifidobacteria and lactobacilli, and improved gut symptoms in a dose-dependent manner.  Similar symptomatic improvements were seen by Chen et al. (2001) with 10 grams MOS per day.  MOS are rarely found in the diet but are present in physiologically relevant doses in Quest Protein Bars.

Inulin is a more complex version of FOS and the form found in the diet (garlic, onions, endive, etc.).  In 1995, Gibson and colleagues showed that both inulin and FOS were roughly equivalent in efficacy: 15 grams of either one increased bifidobacteria and lactobacilli.  Later, Menne et al. (2000) showed that as little as 8 grams of inulin per day increased both bifidobacteria and lactobacilli (moreso than 22 grams of MOS) with a greater effect on the former.  And Kleeson (1997) showed that up to 40 grams was even more effective and was relatively well-tolerated (confirming my suspicion that not all oligosaccharides are created equal…).  Both NOW Foods and Jarrow make high quality inulin/FOS supplements.

Overall, GOS is the most promising.  Depeint and colleagues (2008) showed that 3-7 grams of GOS per day for a week caused a huge and selective increase in bifidobacteria in healthy adults.  Silk (2009) showed even greater benefits in IBS patients.  IBS patients usually exhibit some degree of dysbiosis; indeed, while it isn’t a perfect comparison, Depeint’s healthy subjects had 10 times more bifidobacteria at baseline compared to Silk’s IBS patients.  Unfortunately, however, GOS is yet to go mainstream.  It can be found in Bimuno, which isn’t cost-limiting  until you factor in shipping charges (only sold from the U.K.).  GOS are also present in a variety of infant formulas, which, given their relative scarcity, is a pretty good indicator.

Why is this article sub-titled “bring a gun to a knife fight”?  Because supplementing the bifidobacteria or lactobacilli directly have little impact on the gut microflora.  Even at doses in the billions, almost none of them even survive (see Larsen et al., [2006]; and Tuohy et al., [2006]).  But when combined with some of these oligosaccharides, their effect is markedly improved (Bartosch et al., [2005]).  Probiotics are far more expensive than these prebiotic oligosaccharides, so unless someone had severe GI symptoms, inulin/FOS is the way to go.  On the other hand, if you have IBS, are experiencing gastrointestinal distress, or have recently undergone a course of antibiotics, then a combination of a blend of bifidobacteria combined with inulin/FOS is probably the best treatment.

Be good to your gut.

“Death sits in the bowels; a bad digestion is the root of all evil” – Hippocrates, circa 400 BC

 

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calories proper

 

 

the opposite of food, Op. 76

Processed non-junk food

or

as close to “non-junk” as processed food can be

Notice the inverse relationship between fat content and the number of ingredients in these three commercially available sour cream products.  This is processed food.

Regular:
Cultured pasteurized grade A cream and milk, enzymes.

Low-Fat:
Cultured Milk, Cream, Nonfat Dry Milk, Whey, Modified Corn Starch, Sodium Phosphate, Guar Gum, Carrageenan, Calcium Sulfate, Locust Bean Gum, Gelatin, Vitamin A Palmitate.

Fat Free:
Cultured Low-fat Milk, Modified Corn Starch, Whey Protein Concentrate, Propylene Glycol Monoester, Artificial Color, Gelatin, Sodium Phosphate, Agar Gum, Xanthan Gum, Sodium Citrate, Locust Bean Gum, Vitamin A Palmitate.

 

 

Fat-Free Half & Half

not cream

In general, “Half & Half” refers to a 50:50 blend of whole milk and cream.  People think it’s better than cream because it has less fat.  Whole milk is about 3% fat by weight, while cream is about 30%.  Mix ‘em together and you end up with Half & Half, which is somewhere in between (12-14%).  Fat has a profound effect on flavor and texture… so how exactly does “Fat-Free Half & Half” taste and feel just like regular Half & Half?!?  Muah ha ha ha haaaa!

divide and conquer

From what I can gather, the fat is replaced with corn syrup and pharmaceutical grade thickeners, emulsifiers, etc., scientifically engineered to mimic the precise flavor and texture of Half & Half.  There are even artificial colors added to make it look like cream.  There are artificial colors added to make it look like cream?  AYFKM?  For some reason, I find this oddly offensive.  It is to these artificial colors which I object.  I want this concoction (that is advertised as better than cream) to look like whatever “corn syrup, carrageenan, sodium citrate, dipotassium phosphate, mono and diglycerides, and vitamin A palmitate” looks like.  And it should release a pale green mist upon contact with coffee.

The sugar in Fat-Free Half & Half comes from corn syrup, while that in real dairy is lactose.  Glucose is sweeter than lactose, and there’s 2-3x more sugar in Fat-Free Half & Half.  Does this mean people use less of it?  I doubt it, because the additional sweetness is probably necessary to compensate for the lack of fat.

And what about all the other additives in Fat-Free Half & Half?  This is reminiscent of the introduction of trans fats into our diet by way of replacing butter and lard with margarine and shortening…

Carrageenan is partially responsible for improving the mouthfeel and texture of Fat-Free Half & Half.

carrageenan. Looks scary, right?

At high doses, it’s an inflammatory gut irritant.  Given coffee’s not-so-gut-friendly reputation, do you really want to push it with carrageenan?

On another note, carrageenan is used to design some of the most beautifully artistic desserts.

In this context, I’m reminded of the phrase: “the dose makes the poison.”  In other words, those dishes are a dietary rarity, reserved for the most special of occasions.  At that level of exposure, it could be a blend of carrageenan, trans fat, sucrose, and Red #40, you could eat 5 of them at a time, and you’d never experience any malevolent effects.  But what about a few tablespoons in your coffee every morning for 30 years???  (alternatively, perhaps I’m underestimating carrageenan exposure a bit) (other, more sordid uses of carrageenan)

Avoid processed foods, especially when they’re no more convenient or healthy their conventional counterparts.

 

calories proper

 

P.S.  Perhaps I was a little too hard on Fat-Free Half & Half.  It’s not as bad as microwave popcorn, or this classic:

One 43 gram Twinkie contains 5 grams of fat, 25 grams of sugars, 1 gram of protein, no fibre, 150 kcal, and over 35 ingredients:

  • Enriched Wheat Flour – enriched with ferrous sulphate, B vitamins (niacin, thiamine mononitrate, ribofavin and folic acid).
  • Sugar
  • Corn syrup
  • Water
  • High fructose corn syrup
  • Vegetable shortening – containing one or more of partially hydrogenated soybean, cottonseed or canola oil, and beef fat.  [trans fat]
  • Dextrose
  • Whole eggs
  • Modified corn starch
  • Cellulose gum
  • Whey
  • Leavenings (sodium acid pyrophosphate, baking soda, monocalcium phosphate)
  • Salt
  • Cornstarch
  • Corn flour
  • Corn syrup solids
  • Mono and diglycerides
  • Soy lecithin
  • Polysorbate 60
  • Dextrin
  • Calcium caseinate
  • Sodium stearol lactylate
  • Wheat gluten
  • Calcium sulphate
  • Natural and artificial flavours
  • Caramel colour
  • Sorbic acid (to retain freshness)
  • Colour added (yellow 5, red 40)

 

 

a novel gut health diet paradox, Op. 75

The low FODMAPs diet

FODMAPS  – Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols.  Basically, FODMAPs are a bunch of sugars that are poorly digested in some people and cause a fantastic variety of health problems ranging from bloating and abdominal pain all the way to chronic fatigue and anxiety.  AND a low FODMAPs diet seems to provide some relief (Ong et al., 2010; Staudacher et al., 2011).

Just like it’s weird name, it’s difficult to simplify the rules of the low FODMAPs diet, so here it is graphically:

FODMAPs vs. GFCF

Grains are excluded from GFCF due to gluten and from FODMAPs due to oligosaccharides.  Dairy is excluded from GFCF due to casein and from FODMAPs due to lactose (not sure where FODMAPs stands on fermented dairy like kefir or FAGE).  Thus, both GFCF and FODMAPs exclude grains and dairy.  However, GFCF doesn’t restrict fructose, which is excluded in FODMAPs (monosaccharide).  And last but not least, GFCF but not FODMAPs allows polyols, but as I’ll explain later, I don’t think polyols belong on this list (perhaps “FODMAPs” was just more pleasant-sounding than “FODMAs”).

“polyols”

FODMAPs vs. low carb

A low carb diet is low in both FODMAPs and gluten.  But perhaps similar to polyols, some leniency should also be applied to casein, as standard low carb diets don’t restrict casein but still improve a variety gastrointestinal symptoms (and quality of life in IBS patients; Austin et al., 2009).  Alternatively, a dairy-free low carb diet would cover all your bases.

or you could bring a gun to a knife fight, part I.

Alterations in gut bacteria are frequently associated with gastrointestinal problems, and two classes of nutritional supplements aimed at modifying the gut flora seem to help.  “Probiotics” contain the buggers themselves, while “prebiotics” contain their fuel.

divide and conquer

Bifidobacteria

With regard to the former, “bifidobacteria” seem to be the major player.  Bifidobacteria are the highest in the gut of breast fed babies and lowest in elderly folk.  They are lacking in IBS sufferers (Kerckhoffs et al., 2009; Parkes et al., 2012), and supplementation with bifidobacteria-containing probiotics improve a variety gastrointestinal symptoms (B. infantis 35624 [Whorwell et al., 2006]; B. animalis DN-173 010 [Guyonnet et al., 2007]; B. bifidum MIMBb75 [Guglielmetti et al., 2011])

B. infantis 35624 is found in Align.

B. animalis DN-173 010 is found in Dannon’s Activia yogurt.  But as with most yogurt products, it comes unnecessary added sugars.

Personally, I’d recommend a blend like that found in Jarrow Bifidus Balance (which comes preloaded with its own stock of prebiotics, to be discussed later).

Back to the paradox (or a shameless teaser for next week’s episode): the low FODMAPs, GFCF, and low carb diets all have beneficial effects on gut health but reduce bifidobacteria.  Bifidobacteria supplements and bifidogenic prebiotics are also good for the gut.

a far more enigmatic paradox than the French one, IMO, to be continued…

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calories proper

 

 

Candy in disguise, Op. 73

on the chopping block:To recharge between hunting, gathering, and avoiding predation, our Paleolithic predecessors snacked on gluten-free energy bars comprised of a variety of fruits nuts, and vegetable oils all stuck together with Mother Nature’s sweet sticky honey and dates.  <end sarcasm>

For the record, I’m not a card-carrying member of the Paleo community; just looking out for a respectable nutrition movement.

NoGii No Gluten Paleo Bars” should not be confused with anything healthy.

INGREDIENTS: Dates, Honey, Organic Cashews, Almonds, Apple Juice Sweetened Cranberries (Cranberries, Apple Juice Concentrate, Sunflower Oil), Sesame Seeds, Dried Unsweetened Tart Cherries, Sunflower Seeds, Unsulphured Dried Apples, Freeze-dried Strawberries, Strawberry Juice Concentrate, Organic Sunflower Oil. ALLERGENS: Contains Tree Nuts (Almonds and Cashews).

Full disclosure:

Case closed.

On a more positive note, NoGii No Gluten Paleo Bars have no added sugars.  Indeed, those were saved for their “NoGii Kids Bar.” 

INGREDIENTS: Soy Protein Crisps (Soy Protein Isolate, Tapioca Starch), Marshmallow Creme (Sugar, Brown Rice Syrup, Crystalline Fructose, Invert Sugar, Water, Egg Albumen, Agar, Gum Arabic, Natural Flavor), Brown Rice Syrup, Organic Brown Rice Crisps (Organic Brown Rice, Organic Brown Rice Syrup, Sea Salt), Rice Syrup Solids, Maize Dextrin (Dietary Fiber), Organic Canola Oil, Organic Agave Syrup, Whey Protein Isolate, Organic Palm Oil, Vanilla Yogurt Drizzle (Sugar, Fractionated Palm Kernel Oil, Whey Powder, Nonfat Dry Milk Powder, Cultured Whey, Soy Lecithin [emulsifier], Vanilla), Vegetable Glycerine, Natural Flavors, Sea Salt, Soy Lecithin, Mixed Tocopherols (Natural Vitamin E), Purified Stevia Extract, Lo Han Extract.

NoGii proudly advertises “NO HIGH FRUCTOSE CORN SYRUP” and “ALL NATURAL,” but this is despicable, ESPECIALLY because these are targeted at children.

Divide and conquer

  1. Agave syrup has MORE fructose than high fructose corn syrup (it’s like higher fructose corn syrup).  Why brag about “no high fructose corn syrup” if you’re only going to include a higher fructose substitute?
  2. Crystalline fructose.  (yes, that would be 100% fructose).
  3. Invert sugar is chemically virtually identical to high fructose corn syrup.  This is deceitful… it wouldn’t be so bad if they didn’t advertise (in all capital letters) “NO HIGH FRUCTOSE CORN SYRUP” directly on the website.
  4. Lastly, there’s nothing “Brown Rice” about “Brown Rice Syrup.”  It’s just plain syrup.  It may not have fructose, but it’s still just a blend of simple sugars.

NoGii is pulling no punches, so neither am I: they are trying to trick parents into feeding their kids something that they may not have had they known what was really in it.

NoGii.  Worst company of the week.  No, of the month, because they are targeting children.

A superior alternative:

Quest Low Carb Gluten Free Protein Bars

calories proper

Taxes, saturated fat, and HDL, Op. 71

Since red meat won’t kill you (it will make you stronger), why is taxing saturated fat still up for discussion?  The Danish proposal will add a $1.32 per pound to foods with >2.3% saturated fat; the cost of butter will increase by 30% more and olive oil by 7.1%.  I know, right?  WTF?

Again, I don’t think taxation is the solution, but for the sake of comparison: Arizona’s proposed “fat fee” would cost an extra $50 annually for childless obese patients; Rhode Island’s $0.01/oz of soda; or France’s 3.5% tax on all sugar-sweetened beverages.

Nutritionally speaking, saturated fat should be off the political chopping block; any intervention designed to reduce its consumption will do more harm than good.  In brief, here’s one example of what might happen if it worked, i.e., if dietary saturated fat consumption was reduced:

The effect of replacing dietary saturated fat with polyunsaturated or monounsaturated fat on plasma lipids in free-living young adults (Hodson et al., 2001 EJCN)

Subjects were given a high saturated fat diet and then switched to either a high polyunsaturated fat diet (trial I) or high monounsaturated fat diet (trial II).  In both cases, as seen in the table below, HDL decreased.

 




 

Alternatively, here’s what might happen if dietary saturated fat consumption was increased (in brief):

Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia (Krauss et al., 2006 AJCN)

The bottom two groups in the chart above ate similar diets except monounsaturated fats were replaced by saturated fats in the last group.

As seen in the table below, saturated fat significantly increased HDL.

 

 

So did weight loss, but I’d choose a steak over a stairmaster any day…  (daydream thought bubble: “indeed, ‘adherence’ and ‘compliance’ would be things of the past”)

 

If you believe HDL is important, taxing saturated fat might be a bad idea.  unless you have stock in statins.

 

calories proper

 

 

 

Paleo schmaleo, Op. 69

Brief refresher:

Paleo: lean meat, fish, fruits, vegetables, potatoes, eggs, and nuts; NO grains or dairy

Paleo carbs: fruits, veggies, nuts, and beans… NO starches, cereals, whole grains, added sugars, etc.

Paleo is GFCF-friendly

Atkins is similar to Paleo but allows fewer carbs

Mediterranean diet (from last week): whole grains, low-fat dairy, vegetables, fruits, fish, oils, and margarines (the Paleo diet improved insulin sensitivity WAY more than the Mediterranean diet in patients with CHD).

Diabetic diet (this week; see below): vegetables, root vegetables, dietary fibre, whole-grain bread and other whole-grain cereal products, fruits and berries, and decreased intake of total fat with more unsaturated fat.

Paleo vs. the “diabetic diet” in type II diabetics (Jonsson et al., 2009 Cardiovascular Diabetology).  Lindeberg designed this particular Paleo diet with a much lower carb content (32% vs. 40%) than in the previous study with CHD patients.  A cynic, who might think that some of Paleo’s benefits are due to its low carb content, might think that since traditional Paleo and the comparison “diabetic diet” have a similar carb content (42% and 40%, respectively), Lindeberg intentionally modified Paleo for this study to make sure carbs were significantly lower than in the “diabetic diet” (stacking the deck in Paleo’s favor, according to the cynic).  I can’t find any reason to disagree with the cynic, but it didn’t work out so well for Lindeberg et al.

As detailed in a series of posts about crossover studies (part I and part II), this one was botched due to: 1) what appears to be improper randomization (baseline glucose values were 7.1 and 8.6 mM); and 2) a washout period that was too short to allow one of the primary endpoint variables (HbA1C) to return to baseline.  As such, data presentation was convoluted, which said cynic might think was intentional.  But if we take it at face value, Paleo still fails.  For example, according to this figure (which is NOT crossover data), although Paleo has a lower final HbA1C, the HbA1C reduction is much greater on the diabetic diet.Paleo: 0

Diabetic diet: 1

AND weight loss was similar despite Paleo dieters consuming significantly less food (1581 vs. 1878 kcal/d):So yes, in accord with the Jonsson study (above), Paleo may have been more satiating (i.e., spontaneously lower food intake), but no, this didn’t translate to greater weight loss.  Someone needs to measure energy expenditure in Paleo dieters because it looks like this pattern of food intake either lowers basal metabolic rate or simply makes people tired (though this conclusion would be vehemently denied by Paleo loyalists).  The reduced leptin levels (Jonsson study) may have caused lower energy expenditure, but this would not entirely align with my lower-leptin-equals-higher-leptin-sensitivity hypothesis and thus cannot POSSIBLY be true :/   Alternatively, perhaps the Paleo diet really does lower energy expenditure; this would’ve been irrelevant and possibly even beneficial in Paleolithic times because: 1) they would’ve conserved more energy for “hunting” (hunter-gathers) or fleeing; and 2) weight loss was much less a concern compared to starving or being predated.

The Paleo diet is interesting in that it eludes low-carb status by selectively excluding grains, and I’m pleased that high quality studies (randomized crossover) are at least being attempted, but data thus far suggest we haven’t found anything magical about Paleo (yet)… just need better studies, especially those controlling for total carb content.

Paleo:

+1 for excluding grains, but not much else

 

calories proper

Yogurt black belt test, Op. 65

Proper yogurt can serve as a delicious and healthy addition to any meal of the day.  It contains probiotics, whose role in promoting a healthy gut flora and overall well-being is widely appreciated.  As such, yogurt can be considered an acceptable source of a little bit of sugar in your diet.  (I don’t say that very often… actually, that was probably the first time.)

BUT (you had to know there was a “but”) there are a lot of caveats.  First and foremost is selecting the best yogurt product, since not many people are down with DIY fermentation (which is unfortunate given its tremendous ease).  The yogurt with the most gravitas on the market: FAGE.  It’s supposedly Greek, but I’d say given it’s macronutrient composition, it’s more Spartan.  There are considerable differences between the plain and fruity varieties worth considering.  For example, one serving of plain contains 190 kcal, 10g fat, 8g sugar, and 19g protein, whereas one serving of the blueberry-flavored variety contains 170 kcal, 6g fat, 16g sugar, and 11g protein.  twice the sugar! This is unacceptable, primarily because while I’m not really clear what’s in the “blueberry fruit preparation” that’s listed in the ingredients, I’m sure it’s not real blueberries.  Since real blueberries have negligible protein, we can assume the total protein content of the final product is entirely from the yogurt; therefore, their ambiguously named “blueberry fruit preparation” contributes about 27 grams to the entire 150 gram serving.  This adds 12 grams of sugar, whereas 27 grams of real blueberries would provide only 3 grams of sugar (and some fiber and phytonutrients).

And pass on the 0% fat version; one serving contains all of the sugar but none of  the healthy fats that slow down sugar absorption and contribute to satiation.

On to more pressing, or ‘popular,’ matters.  Dannon is the most widely purchased yogurt on the market.  One serving of plain Dannon yogurt contains 160 kcal, 8g fat, 12g sugar, and 9 grams of protein (less protein and healthy fats, and more sugar than its Spartan counterpart).  Their vanilla-flavored variety has a whopping 25 grams of sugar (and it’s certainly not natural dairy sugar…).  One serving of blueberry-flavored Fruit-on-the-Bottom contains 140 kcal, 1.5g fat, 26g sugar, and 6g protein.  If you added real blueberries to the plain variety this would only yield 15 grams of sugar (still more than FAGE, FTR).  Again, this additional sugar is not coming from real blueberries; unlike FAGE, who disguises their mystery flavor as “blueberry fruit preparation,” Dannon doesn’t even try to hide it.  Right in the ingredients list you’ll find strike 1: sugar, strike 2: fructose syrup, and strike 3: high fructose corn syrup (I honestly don’t know why that’s listed as three separate ingredients.  It’s like they’re trying to boast about it).  I feel pre-diabetic just reading it.  Yoplait is just as bad (high sugar and low protein); come on, Trix -flavored yogurt?  Really?

With regard to promoting a healthy gut flora:  Dannon contains only 1 probiotic strain: L. acidophilus; Yoplait has 2: L. bulgaricus and S. thermophiles; FAGE has 5, L. acidophilus, L. bulgaricus, S. thermophiles, Bifidus, and L. casei.

FAGE: winner.

 

calories proper

Diet, diabetes, and death (oh my)

Fatty acid face off: saturation vs. chain length
or
an homage to pioneers of nutrition research

While both fats contain a lot of 8-12 carbon fatty acids (C8-C12), coconut oil contains more of the 12-carbon fatty acid “lauric acid” whereas medium-chain triacylglycerols (MCT) have more of the 10-carbon fatty acid “capric acid.”  Both exhibit remarkably protective effects against diabetes and this has been known for quite a while.  Coconut and MCT oils are also phenomenally ketogenic, which contributes to their healthful effects (although this eluded early researchers).

Experimental diabetes and diet (Houssay and Martinez 1947 Science)

This study used alloxan to deplete insulin-producing beta-cells rendering these rats essentially type I diabetic.  In the first experiment, they injected alloxan and counted how many rats were still alive after one week.  This study is cruel by today’s standards, but things were different in 1947.  It does, however, provide valuable information as the rats were also being fed one of 16 (16!) different diets.  The major finding was that all the rats fed lard died (d, e, and i in the table below), while all those fed coconut oil survived (o in the table).  And additional coconut oil, methionine, or thiouracil, but not protein, sulfanilamide, or choline reduced the deadliness of lard.  Both lard and coconut oil contain saturated fat, but lard has longer chain fatty acids and more unsaturated fat than coconut oil suggesting fatty acid chain length and/or degree of unsaturation may be important.

In the follow-up experiment, rats were rendered diabetic by surgical removal of 95% of their pancreas and fed high carb, high protein, or high lard diets (a, b, and d from the table above).  In agreement with the first experiment, lard is bad news.  On the other hand, whereas a high protein diet wasn’t helpful for alloxan diabetes, it was remarkably protective in pancreatic diabetes. 

Influence of diet on incidence of alloxan diabetes (Rodriguez and Krehl 1952)

These researchers measured mortality and diabetes incidence in alloxan-treated rats and found that: 1) coconut oil is protective against mortality and diabetes; 2) lard is not; and 3) high protein is modestly protective.  IOW, these data confirm Houssay’s from 5 years earlier.These authors added some information to the picture by measuring body weight and showing that the protective effect of coconut oil is not due to reduced body weight, because these coconut oil-fed rats weighed as much as those fed a low protein diet, and low protein diet-fed rats fared rather poorly.

To add yet more information to the picture (kudos!), they fed rats diets containing the most abundant fatty acids found in coconut oil (caprylic acid) or lard (palmitic acid) and showed that coconut oil’s benefits may be due to caprylic acid because this fatty acid alone was similarly protective against mortality and diabetes.  They also showed lard’s malevolence is not due to palmitic acid because these rats were almost just as protected as those fed caprylic acid.  This somewhat excludes a role of fatty acid length as caprylic acid has 8 carbons while palmitic acid has 16, but both are fully saturated (suggesting a possible detrimental role for unsaturated fatty acids [?]).

So why is coconut oil so good?

One possible reason:  saturated fatty acids are protective, which is supported by the beneficial effect of coconut oil, caprylic acid, and palmitic acid.  Similarly, lard and Swift’ning have a lot of unsaturated fats and both were detrimental.

Unsaturated fatty acids and alloxan diabetes (Rodriguez et al., 1953 Journal of Nutrition)

Rats fed saturated fats of varying chain length were remarkably more protected than those fed unsaturated fats.  Lard has a lot of oleic acid, and rats fed oleic acid didn’t do so well; corn oil is predominantly unsaturated fat and rats fed corn oil were phenomenally unhealthy.  They also showed that rats fed stearic acid (18-carbons, fully saturated) were much healthier than those fed oleic acid (18-carbons, monounsaturated). While none of these studies explored the ketogenic effects of C8-12 fatty acids, they clearly demonstrated that saturated fatty acids of any chain length are good for diabetics, while unsaturated fatty acids are bad.  Good sources for C8-10 fatty acids are MCT oil and goat’s milk, and a good source for C12 fatty acids is coconut oil.

As to the role of ketones, which I think is quite important… to be continued

calories proper

 

 

 

 

Gluc-a-gone wild, Op. 60

optional pre-reading

Q. What happens to a type I diabetic when you 1) withhold insulin, 2) provide insulin, or 3) withhold insulin and suppress glucagon?  (Charlton and Nair, 1998 Diabetes)…

A. You learn glucagon is the bad guy.

Divide and conquer

Zero insulin makes you hyperglucagonemic, hyperglycemic, and ketoacidotic (see first column).  Insulin cures all of these things (second column), but they aren’t caused by insulin deficiency, per se… they’re caused by high glucagon, which itself is cured by insulin (second column) and SRIH (somatostatin, third column).  Cure the hyperglycemia by inhibiting glucagon and pathological diabetic ketoacidosis suddenly becomes physiological ketosis.

Uncontrolled diabetes also wastes muscle:Zero insulin makes you hypermetabolic and increases amino acid oxidation.  Insulin cures this, but again, it appears to be driven by hyperglucagonemia, not insulin deficiency.

Glucagon directly correlates with energy expenditure, and this isn’t the good metabolic rate boost sought by dieters, it’s the type that indiscriminately burns everything including muscle.  High protein diets also increase energy expenditure, but in pathological hyperglucagonemia, the amino acids come from muscle, not food.

The above mentioned study is most relevant to type I diabetes.  The following study is about glucagon and the far more common type II diabetes (Petersen and Sullivan, 2001 Diabetologia).

The effects of hyperglucagonemia can be blunted by glucagon receptor antagonists (GRAs).  In the figure below, a GRA (Bay-27-9955), was administered immediately prior to a glucagon infusion.  The GRA significantly reduced blood glucose levels, an effect largely attributed to the reduction in endogenous glucose production:One of the ways GRA’s accomplish this is by keeping glucose tied up in hepatic glycogen instead of flooding into the plasma (Qureshi et al., 2004 Diabetes; “CPD” is the GRA used in this study).  The figure on the left is primary human hepatocytes; on the left is in mice.Another way of looking at this is in mice chronically treated with glucagon or glucagon plus a GRA.  Glucose tolerance is obviously deteriorated by glucagon treatment, but is completely restored by a GRA (Li et al., 2008 Clinical Science):

One of the most severe side effects of diabetic hyperglycemia is nephropathy, which is similarly cured by GRA treatment:

The physiological role of glucagon is to prevent hypOglycemia; but hypERglycemia is the problem most of the time.  Don’t get me wrong, hypOglycemia can be deadly, but 1) it’s not nearly as prevalent as hypERglycemia, and 2) inhibiting glucagon doesn’t cause hypoglycemia, there are a battery of counterregulatory hormones that prevent hypoglycemia.

Furthermore, reducing glucagon action isn’t limited to glucagon receptor antagonists (GRAs), leptin and amylin can do it too!

And while gastric bypass surgery is easily more extreme than GRA’s and leptin or amylin therapy, it’s magical effect on diabetes remission might also be partly attributed to glucagon suppression (Umeda et al., 2011 Obesity Surgery):

Convinced yet?

 

calories proper