Tag Archives: protein

Insulin resistance is a spectrum

The history of low fat diets is riddled with crappy low fat food-like products.

Food quality matters.

Free full article on Patreon! <- link

Take a group of obese people and assess insulin sensitivity however you like: some researchers demand nothing less than a hyperinsulinemic-euglycemic clamp (Gold Standard), others are OK with insulin levels during an oral glucose tolerance test.

Next, divide the people up based on this — there are a few ways you can do it.  You can: take the top half vs. the bottom half (a method which includes everyone); take the top third vs. bottom third (excluding the middle third); take the top quarter vs. bottom quarter (excluding the middle 50%), etc.

THIS MATTERS because in referencing this topic, many people claim most obese are insulin resistant.  They may be more insulin resistant than lean people, but even within obese people, there’s a spectrum, and the spectrum matters in this #context.

 

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Rodent keto studies

Next time someone says VLC/keto is harmful or at least not helpful for fat loss because of a new rodent study, they’ll probably be wrong.

BOOKMARK THIS ONE GUYS.

Rodent studies on ketogenic diets or exogenous ketones are valuable and interesting in a variety of #contexts, although I’d argue that regulation of fat mass isn’t really one of ’em.

For starters, rodents aren’t particularly ketogenic – it’s rare to see ketones >1 after an overnight fast even in long-term ketoadapted mice.  Also, many rodents gain weight until they die, whereas humans plateau and stay relatively weight-stable for their entire lives (at least historically, and I’m not talking about yo-yo dieting).

Skeletal muscle, on the other hand, seems more similarly regulated: keto isn’t muscle-sparing in either specie… most people, perhaps unwittingly, increase protein intake on keto, and THIS spares muscle (N.B. this is simply to spare muscle, whereas in non-keto dieters, it’s not uncommon to see increased muscle in the #context of high protein).  That’s because carbs are more anabolic than fat.  QED.

There’s just a fundamental difference in the way fat mass and appetite is regulated between the species.  There are many similarities, which is why these studies are still valuable, but fat mass isn’t one of ‘em.

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Chris Gardner strikes again!

Weight loss on low-fat vs. low-carbohydrate diets by insulin resistance status among overweight and obese adults: a randomized pilot trial (Gardner et al., 2015)

 

diet compositions

 

Low carb diet: participants went from 230 grams/d to less than 50 for the first 3 months, then creeped up to ~80 over the next 3 months.

Will the critics say “the carbz weren’t low enough!”?  REALLY?

 

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AMYLIN

Brief background reading: amylin (according to Wikipedia)

 

In a study by Hollander on type II diabetics, the synthetic amylin analog pramlintide was tested (Hollander et al., 2003).  In this year-long RCT, over 600 patients were treated with placebo or up to 120 ug pramlintide BID (twice per day).  On average, these subjects were obese (BMI 34), diabetic for ~12 years, and had an HbA1c of 9.1%.  After one year, HbA1c declined 0.62% and they lost about 1.4 kg… not very impressive.

 

But it’s not all bad news; after viewing those relatively negative results (3 lb weight loss over the course of 1 year), another group of researchers led by Louis Aronne and Christian Weyer believed amylin had yet to be tested proper.  So they designed a better study; it was shorter, used higher doses of pramlintide, and they enrolled obese yet non-diabetic patients (Aronne et al., 2007).  They opted for higher doses of pramlintide (240 ug TID [three times per day]) because in dose-escalation studies, the incidence and severity of adverse drug reactions was consistently low at all doses tested.

 

They chose to study obese-er subjects (BMI 38, compared to 34 in the Hollander study) because obese subjects lose fat more readily than lean people, so if the study is designed to measure fat loss, then it is better to select a population of subjects where more fat loss is predicted.  They selected non-diabetic subjects for a similar reason; diabetics must regularly inject insulin which promotes the accumulation of fat mass — this could counteract any fat reducing effects of pramlintide.
In other words, it was a more powerful and better designed study.

 

After 16 weeks, pramlintide-treated subjects lost an average of 3.6 kg (~8 lbs), or about half a pound per week.  30% of patients lost over 15 pounds (1 lb/wk)!  Importantly, the weight loss didn’t appear to have reached a plateau by week 16, so it would have most likely continued along a similar trajectory had the study been longer.  There were no side effects, and a battery of psychological evaluations showed that the patients receiving pramlintide felt it was easier to control their appetite and BW, they didn’t mind the daily injections, and overall well-being increased.  At the very least, these evaluations meant the subjects weren’t losing weight because of nausea or malaise.  In fact, it was quite the opposite.

 

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Ketone supps

1st Generation: ketone salts.  Only problem is the huge dose of salt limits how much you can take without adverse effects… but these are the ones on the market.

 

2nd Generation: ketone esters.

Advantage: no salt, and probably “slow-release.”

Disadvantage: gonna be WAY more expensive than the salts (which are still pretty expensive).

 

 

~40 grams of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate (a ketone ester) (from Clarke et al., 2013):

 

ketone ester

 

They did this thrice daily, so some people were getting up to 170 grams.

ONE HUNDRED SEVENTY GRAMS

 

[keep that number in mind]

 

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Muscle growth sans carbs

1.  net muscle growth = synthesis – breakdown

2.  need =/= optimization

3.  #context

 

muscle sans carbs

 

I’m totally cool with keto, honestly!  but still don’t really like seeing stuff like the above graphic and people interpreting it to mean “KETO IS MUSCLE-SPARING.”

 

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New low carb protein bars

Warning: this post isn’t #Paleo Certified.   It’s more about convenience, choosing the lesser evil.

Quest Nutrition led the charge in low carb, high protein, fibre-rich bars.  “Fibre-rich” is really the key in allowing a bona fide “low carb” bar with shelf-stability and decent texture.  Sugar alcohols have also been used in some, but due to the high incidence of maltitol-induced GI discomfort, ymmv.  But in general, you need one or the other to provide bulk and keep it together (except Epic Bars, which use black magic).

For the most part, the new bars have basically copied Quest’s formula with some new flavors.

 

Disclaimer #1: I’m a whole foods guy.  Not really #Paleo, but when it comes to people’s actual lifestyles, I recognize convenience is a huge factor… and selecting the lesser evil is frequently the best option — eg, you can store a couple LC protein bars in your office, car, etc.; not so much with hard-boiled eggs or other protein-rich foods… and these options are WAY better than many other snacks or “fast-foods” out there.

Disclaimer #2: yeah, I keep a few of these bars in my office, just in case…

Quest recently switched from isomaltosaccharides to soluble corn fibre (SCF), which will likely impact GI effects.  YMMV!  Isomaltosaccharides are cool, but I’m not prepared to say they’re superior to SCF for everyone, in every #context (personally, for the ‘biome, I prefer brassicas, alliums, the gristly bits, galactooligosaccharides, et al.).
[it’d awesome if Bi2Muno would collaborate with one of these companies]

 

In these n00bs to the protein bar market, some of the biggest differentiating factors are cost, net carbs, ratio of fibre to sugar alcohols, flavor profiles, etc.

 

With no further ado, here are the newcomers:

[or just skip to the chart at the bottom]

 

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Personalized Nutrition II

More on Zeevi et al. (2015) (this is a follow-up to part 1)

I like this study a lot, or at least the fundamentals… or new tools that it might bring to the table.  Like, we know sleep and physical activity are important, and we know all calories aren’t created equal.  This study is the next level, showing there are even big differences in specific carb-rich foods depending on who’s eating them.

And more interestingly, if I’m interpreting the results of the intervention study correctly (which may not be the case), gut microbial responses to specific foods were very individualized… and predictable!

But first, the main part of the study — standardized meals (after overnight fast): 50g carbs from glucose, white bread, bread and butter, bread and dark chocolate, and fructose.  All repeated at least once (except fructose).  Everyone responded pretty similarly to fructose (little to no blood glucose spike), but a wide range of responses to glucose.

PPGR = PostPrandial Glucose Response

 

glucose and fructose

 

Bread:

 

bread

 

The range of PPGR to bread was ~15 to 79!

Again, here are some of the findings I found most interesting (besides the huge range in glycemic response to bread):

 

 

banana and cookie

 

Participant #468 has a consistently higher response to glucose than to white bread.  Participant #663 is the opposite.  And participant #445 is still winning.

I truly wonder if there’s a gut microbe (or something) that’s involved here…

 

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Personalized Nutrition by Prediction of Glycemic Responses

“please stop asking gurus how many carbs you need to optimize health”

 

bananas cookies

An interesting paper came out recently by Zeevi et al. (2015), showing, in part, that we’re all unique snowflakes (in some contexts).

 

#context

#context

 

Mini-rant: this study is in line with a lot of my beliefs about individuality in human biology.  We don’t know all the mechanisms, but we do know that some people respond better to some interventions than others.  We learn a lot from studies on diet, light, sleep, physical activity, etc., but the findings rarely/never apply equally to everyone (and some people experience completely opposite effects; eg, see studies where individual data are reported).  LIGHT exposure can improve sleep quality in some but cause agitation in others.  Low carb diets can help weight loss in some people but low fat is better for others.  Dairy, wheat, protein, the ‘biome, and fibre/resistant starch all fall into this category.  Sleep ‘requirements’ vary by person, season, geography, etc., etc…  there’s no QED answers in many of these contexts.

anecdote: some people say they’ve never had better blood glucose than when they were having a few servings of beans/legumes per week; others just report bloating & farts (no bueno).

End rant.

Background reading:

  1. The Atlantic ran a decent piece on this study (certainly more colorful than my take)
  2. Reddit AMA with some of the people involved in the study

 

In this particular study (video summary below): they continuously monitored the blood glucose responses in 800 people to all of their meals for a week, including a variety of test meals.  Main result: many different responses, even to the same foods!  An oversimplified example: some people had smaller relative postprandial glucose excursions after 50g carbohydrate from rice compared to 50g carb from potatoes, and other people responded oppositely.  And friggin’ tomatoes?!

Translation: need to move beyond recommending #IIFYM.

Some foods were universally well-tolerated [in this population] in the context of mixed meals, like quinoa and salmon; other foods did the opposite, like chocolate chip cookies and sushi.  And lastly, some foods like cottage cheese and hummus were good for some people but others.

 

bananas cookies[participant 445 is winning]

 

*In general, I don’t believe in labeling foods as categorically good or bad, which is pretty much confirmed by this study, but some patterns emerged wrt postprandial glucose excursions in this population…

#context

 

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HANGRY!

So the theory goes: high carb meal -> blood glucose spike -> insulin spikes a little too hard -> hypoglycemia -> hunger, so you eat to replenish blood glucose.

In the original theory of hangry, hypoglycemia was a core component, although as Jane Plain pointed out, it could be the relative, not absolute levels of blood glucose that count (&/or free fatty acids, but that’s a story for another day).  This could be true, in part because:
1) symptoms of hypoglycemia rarely correlate with actual hypoglycemia;
2) many episodes of actual hypoglycemia are asymptomatic; and
3) hunger isn’t even one of the main symptoms of hypoglycemia.

 

Tl;dr: hangry might be a real phenomenon, but there are little/no data to support it, and much to the contrary.

 

The low carb brigade says “LCHF = no hangry.”
Turns out, the same can be said by the high carb brigade (in some contexts), so does it really matter? (see below)

 

What we know: obese insulin resistant patients undergo a spontaneous reduction in appetite upon initiating a carbohydrate-restricted diet.  FACT (P<0.05).  Low carb, high protein meals also induce more satiety than high carb meals in acute scenarios…

Imho, hunger and satiety are complicated biological phenomena that can’t be so easily simplified into cute concepts like “hangry.”

 

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