Category Archives: insulin

Allu-lujah: the new Quest Hero bars

On that sweetener in the new Quest Hero bars: allulose (formerly known as D-Psicose).

1. I’m sure they were quick to adopt the alternate nomenclature because it’s hard not so say Piss-cose lol

2. Nutrition-wise, Hero bars are basically Quest Lite. A bit less fibre. But I really think they’re getting much better at texture.

3. On to allulose. It’s not really like sugar – even though the FDA says it must be labeled as such – because it carries virtually no calories and actually blunts the blood glucose spike from a meal.

 

Exhibit A. n=20 healthy peole: 7.5 g D-psicose alone, 75 g maltodextrin alone, 75 g maltodextrin + 2.5, 5, or 7.5 g D-psicose (Iida et al., 2008)

amazeballs

 

 

 

 

 

Exhibit B. n=26, zero or 5g psicose with a standardized meal (Hayashi et al., 2010). Note: there are ~12 grams of allulose in a Hero bar.

It works better in diabetics.

 

 

They did a 12-week study where psicose was dosed 3 times a day, 5 grams each time, and showed it was perfectly healthy. Some markers even improved.

 

Exhibit C. Psicose metabolism (Iida et al., 2010)

In doses ranging from 5 to 30 grams, up to 70% is excreted intact and the rest does not go to farts.

It’s virtually calorie-free:

 

 

and is barely fermentable (compared to FOS):

 

 

compare to other low carb protein bars here, get the new Quest bars here, or just buy some straight allulose and experiment with it!

Mechanisms? 1) it’s not sugar, but it still enhances glucose disposal; and 2) some animal studies show it enhances liver glucose uptake. Idk.

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FOOD PROFILE

Hey Fam, announcement: I’m moving to Patreon soon — will still post about 4-5 articles per month with at least 1 open to the public. The rest will be for Patrons. I’m still trying to figure it out and I’m open to suggestions!

 

I loved this – when describing the two study diets, which differed markedly in carb content (10% vs. 53%), the authors said they were similar in energy, protein, and “FOOD PROFILE,” meaning low-processed, lower-glycemic foods.

Non-industrial foods.

Hunger-free Diet(s).

BOOM!

Visceral adiposity and metabolic syndrome after very high-fat and low-fat isocaloric diets: a randomized controlled trial (Veum et al., 2016)

 

What happens when you give up industrial foods and start following a Hunger-free Diet (regardless of carbz)?

 

 

EVERYBODY LOSES WEIGHT

 

 

And le saturated fat? Industrial foods are the problem, not saturated fat. One group went from 48 to 31 grams per day (LFHC), the other group went from 42 to 81 (VLCHF): all metabolic parameters improved in both groups.

 




 

Even their livers shrank:

 

 

My only qualm: everyone lost a bit of muscle. NOT SURPRISING when you cut calories & protein and don’t exercise. Protein dropped by about ~25 grams in both groups. When you cut calories, you need to up protein or start lifting heavy shit otherwise you’ll lose muscle. The ketonez won’t help.

 

 

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The alkaline diet is bullshit. Proof: vinegar is the bomb

1. Whether it’s Balsamic, sherry, red wine, apple cider, or even plain distilled white, vinegar is a great condiment (P<0.05). Try cutting your favorite with a more concentrated one for more fun (be careful, it can burn you; I’d start with 1:20 or 5%).

2. It reduces the glucose and insulin response to a meal.

World’s coolest fatty acid?

[Patreon link] (open access)

Exhibit A: 20 g apple cider vinegar, 40 g water, and 1 tsp saccharine two minutes prior to “a white bagel, butter, and orange juice (87 g total carbohydrates)” (Johnston et al., 2004)

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Hormesis of the AGEs

Some semi-random thoughts (ie, I might’ve had too much coffee haha)

-I’ve never really been a fan of the concept of “hormesis,” because you can basically say it of just about anything.  Kinda like “vestigial,” because, like, you technically don’t need your legs…

-We’ve seen actual human trials on AGEs, I even wrote a relatively mature blog post about ’em (this isn’t gonna be like that). Tl;dr: they really do some bad things in experimental settings. No, not bad like playing in traffic; bad like inflammation, oxidative stress, etc.

-Some say the ability to cook was a major evolutionary factor. Improved digestibility, nutrient bioavailability, energy extraction, reduced toxins, etc. I don’t know, maybe it was just seafood/DHA. Whatevs, I don’t really buy this line of reasoning anyway.  Maybe AGEs are not hormetic and are outright harmful; but cooking was better for our species because we died from other things long before the AGEs got us… or maybe this is a good reason to eat more baked mushrooms (as per Roncero-Ramos et al., 2016) haha.

-I follow the BTD (Blow Torch Diet™)* so seared meat and to a lesser extent plants can’t be unhealthy, right?

*seriously, I use this and these all the time.

 

 

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High protein magic

Remission of pre-diabetes to normal glucose tolerance in obese adults with high protein versus high carbohydrate diet: randomized control trial (Stentz et al., 2016)

n=12/group

Duration = 6 months

Diet: all food provided.  Mucho gusto!

 

Critique #1: if my calculations are correct, we’re comparing low protein (0.675 g/kg) to adequate (1.35 g/kg) (not “high”).

The diets were decent:

 

 

Results:

 

 

Author’s conclusion was that this was due to high protein alone, but I’d say it was at least partially due to weight loss.  BOTH groups lost weight and improved insulin sensitivity.  Statistically significant in both groups.

 




 

Glucose (A) and insulin (B) in response to a 75g OGTT (red is high protein, blue high carb):

 

 

I still say weight loss was the primary driver, but must concede, however, that protein did have a little magical effect: high carb group actually lost slightly more weight, but insulin sensitivity improved more in the high protein group.  The high protein magic: reduced insulin secretion yet still greater reduction in glycemia.

 




 

Well, maybe not magic…

 

 

Despite having more insulin, high carbers lost slightly more fat mass but way more muscle.  THAT’s high protein magic lol

 

However, the meal tolerance tests show a slightly different trend:

 

 

We expect glucose and insulin excursions to be greater in HC (blue), because they had a high carb meal whereas the HP group had a high protein meal.  From this perspective, if we graphed the results as “change from time zero,” I think the reduction in glycemia from baseline to 6 months would be similar in both groups suggesting weight loss as bigger factor.  We’d still give some props to high protein because it lowered glucose just as much despite having less insulin.  High protein magic.

 

Note to self: gotta stop saying this was “high protein.”  1.35 g/kg is not “high,” seriously.  But still, High protein magic haha

 

Oh and one other thing, high protein usually induces greater weight loss:

Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity (Skov et al., 1999)

High protein vs high carbohydrate hypoenergetic diet for the treatment of obese hyperinsulinemic subjects (Baba et al., 1999) (not ad lib)

Comparison of high-fat and high-proein diets with a high-carbohydrate diet in insulin-resistant obese women (McAuley et al., 2005)

The effect of a low-fat, high-protein or high-carbohydrate ad libitum diiet on weight loss maintenance and metabolic risk factors (Claessens et al., 2009)

 

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Conserved lean body mass? O_o

Alternative title: keto isn’t muscle-sparing if you compare it to any remotely sensible control group.

Exhibit A. Resistance training in overweight women on a ketogenic diet conserved lean body mass while reducing body fat (Jabekk et al., 2010)

The exercise intervention was resistance and progressive.  The diet was ketogenic, confirmed by urinary ketones… of note, presence of urinary ketones is a better indicator of ketosis than any information about diet (although they were advised to start at <20g carb/d).

 

 

As per usual, the LC diet was higher in protein… but that wasn’t enough to induce skeletal muscle growth, even when combined with resistance exercise… worded another way, resistance exercise and more protein prevented ketogenic diet-induced muscle loss:

 

 

Neither group was instructed to restrict energy intake, but from the above graph it’s relatively safe to assume the LC diet counteracted exercise-induced hunger.

Confirmed:

 

 

However, exercise-induced hunger isn’t conducive to fattening because the cause is exercise.  I think.

Ketones may spare muscle during starvation, but not in the context of regular people eating a ketogenic diet.  Otherwise, muscle mass would’ve increased in that study relative to the control group.  Confounded by negative energy balance?  Perhaps, but from where I’m standing, the LC diet did almost exactly what we expected: reduced food intake and induced a selective loss of fat mass.  And exercise also performed as expected: increased muscle mass.  In other words, if you want to gain muscle, you need calories, protein, and exercise.  Keto provides no advantages in this context.

 




 

Exhibit B. The effect of weight loss by ketogenic diet on the body composition, performance-related physical fitness factors, and cytokines of Taekwondo athletes (Rhyu and Cho, 2014)

Keto dieters got 33% more protein (40% vs. 30%), and still managed to lose almost twice as much lean mass as non-ketogenic dieters.

 

(figure from Suppversity)

 

The participants were physically active, and thus likely fairly insulin sensitive, so this may be why those assigned to a ketogenic diet lost less body fat…

 




 

Exhibit C. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women (Volek et al., 2004)

And in this study on sedentary insulin resistant folk, keto still wasted muscle (NS) despite more protein and calories:

 

 

If you’ve been paying attention, this wasn’t unexpected.

Sedentary and overweight: more fat loss on keto.

Keto and sedentary: muscle loss.

Sleep well, get your circadian rhythms entrained proper — otherwise these efforts will give you a mere fraction of the benefits.

 




 

Other~

Protein + exercise works: Interactive effects of an isocaloric high-protein diet and resistance exercise on body composition, ghrelin, and metabolic and hormonal parameters in untrained young men: A randomized clinical trial (Kim et al., 2014)

Simply replacing carbs with fat, or resisting food for as long as possible after waking up and staring at your smart phone all night: doesn’t work.

#context

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Cyclical ketogenic diet and carb refeeds

Potential conclusion (pending full texts): “if you’re gonna keto, no need to carb”

I think these three abstracts are all referring to the same studies.  I haven’t seen the full texts.  My takes are in italics, after each abstract.

Exhibit A. The Effects of an Eight Week Ketogenic Diet vs. a Cyclical Ketogenic Diet on Performance and Testosterone in a Resistance Training Program (Lane, Lowery, Volek, D’Agostino, Wilson, et al., 2015)

Introduction: Our lab recently examined the effects of the ketogenic diet (KD) compared to a western diet regarding strength related performance; additionally, free and total testosterone was evaluated. Individuals on the KD saw similar adaptations in strength and similar changes testosterone. Comparisons of the KD against a cyclic (CKD) in strength, endurance, and testosterone have not been previously demonstrated in literature.

Purpose: Therefore the purpose of this study was to investigate the effects of the KD versus a CKD on performance and testosterone in resistance-trained males.

Methods: Sixteen resistance trained males participated in the study (age: 23.5 ± 3.3; weight: 187.6 ± 32.6). Participants on the KD consumed 5% carbohydrate, 25% protein, and 70% fat for 8 weeks. The CKD group applied the same macronutrient ratio to their diet Monday through Friday, while altering the ratio on weekends (50% carbohydrate, 25% protein, 25% fat). A periodized resistance training program was strictly followed 3 days per week throughout the duration of the study with high intensity interval training implemented on intermittent days 2 times per week by all participants. Participants were placed on a 500 kcal deficit derived from basal metabolic rate determined by the Mifflin St. Jeor equation. One repetition maximum (1RM) strength was assessed on deadlift, bench press, and leg press at baseline with a repeat assessment performed Week 8. Strength endurance was assessed on the leg press at baseline and re-assessed at Week 8. Free and total testosterone was evaluated at baseline and at Week 8. An ANOVA with repeated-measures was used to scrutinize the effects of KD and CKD on dependent variables assuming group (KD and CKD) and time (pre and post) as fixed factors. The significance level was set at p ? 0.05.

Results: There were no differences between groups in the performance tests or testosterone levels detected at baseline (p > 0.05). A time effect was observed for bench press and deadlift 1RM (p < 0.01). There was a trend towards a group by time interaction (p = 0.07) which favored an increase in the leg press 1RM in the KD group. There were no significant differences for leg press strength endurance in both groups. For free testosterone, there were no group or group × time interactions (p > 0.05). For total testosterone, there was a group × time interaction following the diet treatment (p < 0.02). The pairwise comparisons revealed that only the cyclic group decreased in total testosterone (10.3%, p < 0.02).

Conclusions: In regards to performance, a strict KD seems to augment positive strength related adaptations when compared to a CKD. These responses may be explained by sustained total testosterone levels seen in the KD group compared to reductions in total testosterone as a result of the fluctuations in macronutrient intake.

Practical Applications: Individuals attempting to optimize adaptations in strength performance while maintaining testosterone levels should perform a KD compared to a CKD.

My take: no difference between KD & CKD, despite testosterone declining in CKD.  This isn’t surprising because small fluctuations within the physiological range are not expected to affect these outcomes.

When protein and calories are controlled, and the #context is a 500 kcal deficit, not really sure what they were expecting.  Because of the constant deficit, insulin will be low even on the carb-up days, and those carbs are more likely to be burned off than replenish glycogen.

 

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The DietFits Study

Preliminary results from Chris Gardner’s follow-up to this study suggest insulin resistance may not be as big an influence on the success of LC/LF diets as prior studies have shown.  Maybe I was wrong.

We aren’t given many details in the abstract or interviews, and there are still some good studies showing otherwise (eg, those by Cornier, Pittas, Ebbeling, and Gardner himself), although this one is bigger (n = 609) and longer (1 year).  However, the range of weight change was huge, something like +20 lbs to -80 lbs, so the devil might be in the details… time will tell.  Might be subtle yet important changes in body comp or other metabolic indicators.

If it turns out to be true, my best guess: they were all following Hunger-Free Diet(s)… which work regardless of whether low fat or low carb.

 

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Whole grains aren’t all they’re cracked up to be

WUUUT *rimshot*

A new study on whole grains demonstrates how nuanced & complicated nutritional science can be.

Substituting whole grains for refined grains in a 6-wk randomized trial favorably affects energy-balance metrics in healthy men and postmenopausal women (Karl et al., 2017)

Sounds simple enough…

Study design: adequate to address the questions being asked.  Isocaloric, weight-maintenance diets.  Biggest differences between the two diets were whole grains (0 vs. 200 g/d) and insoluble fibre (15 vs. 30 g/d).

Disclaimer: I’m not a huge fan of cereal fibre, but that’s irrelevant for the point of this post.

 

 

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GLP-101

Insulin secretion happens pretty quickly after a meal, in part, due to nutrients and gut-derived incretins like GLP-1.  GLP-1 secretion only happens with a meal, so the insulinemic response to oral glucose is greater than that to i.v. glucose:

 

 

Part 2. The liver sees WAY more insulin than peripheral tissues when this happens.  And it’s probably that way for a reason; ie, perhaps you need more insulin to shut down hepatic glucose output than to stimulate muscle glucose uptake and shut down lipolysis, etc.

 

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