Category Archives: TPMC

calories proper

Insulin resistance and obesity

Posted on June 25, 2016 | 32 comments

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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Posted in Advanced nutrition, angiotensin, Bromocriptine, Cabergoline, chronopharmacology, circadian, diabetes, diet, Dietary fat, Dopamine, insulin, Leptin, Protein, TPMC

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Hey CICO, I’m playing by your rules.

Posted on June 15, 2016 | 6 comments

Brief background: the notorious Ebbeling study of 2012 showed an apparent metabolic advantage of a ketogenic diet.  After losing some weight, participants were assigned to low fat (LF), low GI, or ketogenic diets.  As expected, energy expenditure (EE) declined in all groups after weight loss.

 

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Posted in Advanced nutrition, diet, Dietary fat, empty calories, Energy balance, fat, fiber, insulin, Ketosis, microbe, microbiome, microbiota, muscle, TPMC

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Dopamine and breakfast

Posted on June 5, 2016 | 39 comments

T.S. Wiley wrote a lot about the protein-rich breakfast; here’s my understanding of her take on it.

N.B. I highly recommend her book, Lights out: sleep, sugar, and survival.

Quotes are mainly taken from the text. I’ve tracked down some of the cites; the rest are in the back of the book, albeit somewhat unorganized :/

Part 1. We naturally have a cortisol spike first thing in the morning, known as the Cortisol Awakening Response (CAR).  This peak, which can be screwed up by artificial light at night or a big evening dinner, helps support morning light-induced dopamine.

CAR

Dopamine is great, but may induce impulsivity if it’s unfettered.

Enter: the protein-rich breakfast. It provides tryptophan and a bit of insulin to promote serotonin synthesis (eg, Manjarrez-Gutierrez et al., 1999).

Not enough serotonin to make you crazy, just enough to balance the dopamine = impulse control.

~ circadian balance achieved ~

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Posted in Advanced nutrition, angiotensin, Bromocriptine, Cabergoline, chronopharmacology, circadian, diet, Dopamine, fat, Fish, insulin, Leptin, melatonin, Protein, sex, sleep, Sun, TPMC, Vitamin D

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the insulin-obesity hypothesis is under attack

Posted on May 15, 2016 | 25 comments

…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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25 Comments

Posted in Advanced nutrition, diabetes, diet, Dietary fat, empty calories, Grains, insulin, Ketosis, Leptin, Protein, sleep, Sun, TPMC

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Melatonin sensitizes the system

Posted on April 15, 2016 | 12 comments

Bear with me here… this could be very important (or just all in my imagination haha)

Fact: melatonin secretion happens at night (or at least that’s when it’s supposed to happen):

circadian melatonin

And it’s important to adopt healthy circadian behaviors early on to prevent or minimize the age-related decline in melatonin secretion:

melatonin in aging

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Posted in Advanced nutrition, chronopharmacology, circadian, Dopamine, Leptin, melatonin, muscle, sleep, TPMC

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Rodent keto studies

Posted on April 5, 2016 | 9 comments

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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9 Comments

Posted in Advanced nutrition, diet, Dietary fat, Energy balance, fat, insulin, Ketosis, muscle, pair-feeding, Protein, TPMC

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Chris Gardner strikes again!

Posted on March 25, 2016 | 154 comments

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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154 Comments

Posted in diet, Dietary fat, Energy balance, fat, insulin, Protein, TPMC

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AMYLIN

Posted on March 15, 2016 | 33 comments

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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Posted in Advanced nutrition, diet, Dietary fat, Energy balance, fat, insulin, Ketosis, Leptin, liver, microbiome, muscle, pair-feeding, Protein, TPMC

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Ketone supps

Posted on March 5, 2016 | 16 comments

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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Posted in Advanced nutrition, circadian, coconut, diet, Dietary fat, Energy balance, fiber, insulin, Ketosis, Leptin, microbiota, muscle, TPMC

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Tissue-specific fatty acid oxidation

Posted on February 19, 2016 | 17 comments

Does it matter where fatty acids are oxidized, liver or skeletal muscle?  Of course, they’re oxidized in both tissues (quantitatively much more in the latter), but relative increases in one or the other show interesting effects on appetite and the regulation of fat mass [in rodents].

Warning: a lot of speculation in this post.

A LOT.

It’s known that LC diets induce a spontaneous decline in appetite in obese insulin resistant patients.  Precisely HOW this happens isn’t exactly known:  the Taubes model?  improved leptin signaling?  probably a little bit of both, other mechanisms, and possibly this one:

 

Exhibit A. Oxfenicine

 

oxfenicine

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Posted in coconut, diet, Dietary fat, Energy balance, insulin, Ketosis, Leptin, liver, muscle, TPMC

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