Tag Archives: leptin

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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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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Dopamine and breakfast

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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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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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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Ketosis is a hack: here’s why

There are multiple distinct flavors of diabetes/obesity, as evidenced by the fact that some people have: 1) impaired glucose tolerance (but normal fasting glucose); 2) others have impaired fasting glucose (but normal glucose tolerance); and 3) others have both.  This means there isn’t a linear relationship between these phenomena*.  There are also: 4) obese patients with normal glucose metabolism; and 5) lean patients with type 2 diabetes.

*I think the great Dr. Kraft may have missed some of the nuances here.

There is not 100% overlap among these, suggesting [confirming] distinct diabetes/obesity phenotypes (and probably causes & best treatments).

 

 

midnightsun

 

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Summer is fattening. Don’t do it in winter.

Seasonal eating proper

More from T.S. Wiley and Dr. Kruse on seasonal eating in what appears to be the primary model for its justification for use in humans – hibernating mammals.

How it goes, or so they say: in summer, hibernators massively overeat, including carb-rich foods, in order to generate muscle and liver insulin resistance, so as to promote body fat growth.  The long light cycle reduces evening melatonin, which pushes back the usual nighttime peak in prolactin, which causes an abnormal resistance to leptin, which induces hypothalamic NPY and subsequent carbohydrate craving.  Ergo, summer is fattening.  In today’s day, increased artificial lights guarantee year-round pseudo-summer; and we no longer experience the benefits of the short light cycle: longer sleep times (akin to hibernation) and fasting – either complete fasting as in hibernation, or pseudo-fasting, ie, a ketogenic diet.

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Silent Leptin Resistance

Conventional leptin resistance has something do with obesity.  It is known.  Silent leptin resistance is … err … complicated. 

Divide and conquer

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding (Shapiro, Scarpace, et al., 2008 AJP)

A remarkable 60% fructose diet fed to rats for 6 months had absolutely no effect on energy balance.  Nil. QED.
Fig 1

Food intake and body weight were unaffected because the levels of and sensitivity to endogenous leptin were identical in both groups.

Enter the Dragon

Enter the Dragon

“Silent Leptin Resistance” – The fructose-fed rats are, however, profoundly resistant to the satiating effects of Metreleptin (a pharmaceutical grade injectable leptin analog):

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Dopamine

“When we block the D2 receptor in humans, it is expected they will develop glucose intolerance, obesity, and sedentary behavior.” -Jane Plain, in her series on The physiology of body fat regulation.  It’s probably true.

Randomized pilot study of cabergoline, a dopamine receptor agonist: effects on body weight and glucose tolerance in obese adults (Gibson et al., 2012)

Cabergoline is primarily used to treat prolinactinoma, or prolactin-secreting tumors.  In women (& men apparently), prolactin stimulates milk production; in men, it is associated with the refractory period after orgasm.  In both genders, dopamine inhibits prolactin secretion.  Cabergoline targets the D2 receptor, but it’s a dirty drug.  It’s used off-label for gyno and to improve sexy times (Kruger et al., 2003 <– yes, that was actually tested).

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Obesity is not permanent

Take a group of obese people (> 250 lbs) and put them on a massive calorie restricted diet.  They lose weight and metabolic rate plummets.  Weight loss fail?  In most cases, yes.  But a recent study showed that the decrepit post-weight loss metabolic rate gradually improves in parallel with an increase in dietary fat ingestion to such a degree that even after two long years: totally food intake was almost back to normal, energy expenditure improved, and all this happened despite continual weight loss.  In other words, obesity is not permanent. 

creme brulee

Decreased energy density and changes in food selection following Roux-en-Y gastric bypass (Laurenius et al., 2013)

Statistically speaking, no diet on Earth comes close to RYGB in terms of weight loss success.  Long term.  Seemingly permanent.  It’s the closest thing to a cure we’ve got.

Laurenius

Body weight is down by 30%, and energy expenditure is rising faster than a speeding bullet.  because food intake is increasing while body weight is dropping – they’re probably more active too ** weight loss than more exercise –

But there’s a more mystical aspect to RYGB that warrants attention.  (it could be the increasing fat intake, but for now let’s just say it’s RYGB per se).  According to this pearl, weight loss of only 10% via diet alone causes energy expenditure crash by 394-500 kcal/d, and physiological replacement of leptin via subcutaneous injection can increase this by 234-454 kcal/d (Rosenbaum, Murphy, Heymsfield, Matthews, and Leibel, 2002).

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