Category Archives: diabetes

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?

 

 

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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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)

 

calories proper

 

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The BROAD Study or Meat

Is eating meat necessary?  Optimal?

THE ANSWER MAY SURPRISE YOU

Hint: it’s more important to not eat processed refined junk foods.

 

Exhibit A. The BROAD study: a randomized controlled trial using a whole food plant-based diet in the community for obesity, ischaemic heart disease, or diabetes (Wright et al., 2017)

Tl;dr: it worked.

 

 

The longer version: it was a low-fat vegan diet supplemented with 50 ug B12 (methylcobalamin) daily.

 

Participants were advised to eat until satiation.

We placed no restriction on total energy intake.

Participants were asked to not count calories.”

 

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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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The Hunger-Free Diet(s)

It started out as “lose weight without hunger on LCHF” and went all the way to “effortless fasting on keto.”  Works for some and it might be true, but the same can be said for low fat diets!  The key, I think, in both contexts, is simple: fewer processed & refined foods… something the Paleo movement got right, imo (although I still think many low-calorie sweeteners are way less unhealthy than HFCS & sugar).

The logic:

1) add “good calories” like almonds to your diet and appetite spontaneously compensates by eating less other stuff: energy neutral

2) you don’t compensate for added “bad calories” like sugar-sweetened beverages: positive energy balance

3) remove bad calories from your diet and you don’t compensate by eating more other stuff: negative energy balance

 

Book: Good Calories, Bad Calories

 

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Keto myths & facts

:::begin rant:::

Trigger warning?  Maybe.

Disclaimer: I’m pro-LC (P<0.05), but not anti-LF because LF works better than LC for some people.  And with the exception of things like keto for neurological issues, I think macros take a back seat to many other factors.

Myths: carbs cause insulin resistance (IR), diabetes, and metabolic syndrome.  Carbs are intrinsically pathogenic.  If a healthy person eats carbs, eventually they’ll get sick.

And the only prescription is more keto.

 

cowbell

 

And of course all of this could’ve been prevented if they keto’d from the get-go.

Proponents of these myths are referring to regular food carbs, not limited to things like Oreo Coolattas (which would be more acceptable, imo).  Taubes, Lustig, Attia, and many others have backed away from their anti-carb positions, yet the new brigade proceeds and has even upped the ante to include starvation.  Because “LC = effortless fasting?”

Does this sound sane?

“No carbs ever,
no food often…
otherwise diabetes.”

 

 

oreo-coolatta

 

no one in their right mind would say lentils & beans cause diabetes

 

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Circadian arrhythmia in different types of obesity

This study was pretty interesting.

Three groups of women:

1) normal weight

2) gynoid obesity (stores more fat in hips & butt), defined by WC/HC < 0.85

3) android obesity (stores more fat in belly, which is rare in women), defined by WC/HC > 0.85

 

First, we get confirmation that insulin sensitivity (IS) is better in morning than evening.  But then we get these interesting glucose tolerance curves:

 

circadian-glucose-tolerance

 

Fat stored in your hips & butt is thought to be healthier than that stored in your belly region.  This is confirmed here.  Gynoid obesity, while exhibiting an attenuated AM/PM difference, was able to restore euglycemia by the end of the experiment at both time points.  Ie, gynoid obesity selectively improved IS in the evening.

 




 

Android obesity, which is more nefarious than gynoid (also confirmed here), had a similar though not as robust effect in the evening but deteriorated IS in the morning.

One potential interpretation: it’s better to have a little extra fat stored in your hips and butt than to be lean or have belly fat.  However, I have a qualm with that interpretation.  Healthy people show a robust circadian difference in glucose tolerance.  Just as insulin resistance (IR) is an accepted physiological phenomenon observed in some ketogenic dieters, I view this circadian difference, also, as physiological.

 

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Circadian timing with REV-ERB and PERIOD

The circadian proteins Bmal and casein kinase (CK) enhance and degrade Period (PER), respectively, by completely different mechanisms.  Both are necessary, but at different times of day… #context

Gross oversimplification: the Bmal party is kicked off in the morning by LIGHT, and acts to increase PER by night (among many, many other things).  As the day progresses, REV-ERB the Repressor slowly shuts down Bmal, so that peak PER occurs in the evening and doesn’t carry over until the next morning.  GSK3b activates REV-ERB the Repressor.  Lithium puts the system in fast forward, leading to phase advance* and ZZZ’s when timed right, at night… I think

 

Lithium GSK3b image

 

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Insulin resistance and obesity

Some people believe insulin resistance (IR) causes obesity, and they are not pleased when I say this is actually a controversial topic in the field…

“Bill isn’t toeing the company line.  Again.”

So I asked a simple question: if IR causes obesity, how?

 

 

The Common Response: 1) IR -> 2) hyperinsulinemia -> 3) more insulin = more fat mass.

However, this is flawed.

Easiest rebuttal (somewhat of a strawman, but whatevs): Barbara Corkey and her group has done a lot of work showing that insulin hypersecretion (caused by dietary additives, preservatives, weird chemicals, etc.) may actually precede & causes IR… not enough insulin hypersecretion to induce hypoglycemia, just enough to induce IR.

So that basically breaks the 1st step in the Common Response, but doesn’t really disprove the possibility that IR still causes obesity (or can cause obesity).

In any case, check out Corkey’s 2011 Banting Lecture.  Highly recommended, a lot of food for thought.

 

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the insulin-obesity hypothesis is under attack

…but it isn’t dead, imo, because that would be really hard to do.  Like, seriously.

 

 

side note: please consider the modern views of Taubes, Lustig, Gardner, Attia, and others on Carbs™.  They’re less “Carbs-cause-obesity, keto-for-all, etc.,” and more thinking it might not be Carbs™ per se, but rather processed and refined foods.  And #context…  And I tend to agree at the moment (nuances and caveats are subject to change, as more evidence accumulates).

 

disclaimer: I haven’t seen the full text of Hall’s recent study, but that’s not really relevant to what I want to discuss.  In other words, I don’t think the full text will provide any additional details on this particular point.

 




 

Tl;dr: this study was not designed to prove or disprove metabolic advantage or the insulin-obesity hypothesis.

It’s in the study design:  four weeks of low fat followed by four weeks of low carb.  We KNOW that weight loss slows over time (especially if calories are controlled, as they were in this study).  It has to do with the order of treatments.

Weight loss-slowing over time in the Minnesota Experiment:

 

 

Minn-Starvation-weight

 

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