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Endogenous circadian system and circadian misalignment impact glucose tolerance via separate mechanisms in humans (Morris et al., 2015)

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“Glucose tolerance is lower in the evening and at night than in the morning.”

THE FIRST FRIGGIN’ LINE! Come on fam, please stop arguing against this fact. A basic tenet of circadian biology is our preparedness for food intake in the morning. “Skipping breakfast” is not hormetic. It’s CICO and not in a good way. Metabolism is gimped at night, so you end up having to eat less so you’re double-restricted (no breakfast and less food at night).

The point of this study was two-fold, in my estimation: 1) determine the normal circadian influences on glucose tolerance; and 2) influence of circadian misalignment.

When comparing the glycemic response to identical meals ingested after an identical period of fasting, either at 8 AM (subjective morning or “breakfast”) or 8 PM (subjective evening or “dinner”): postprandial glucose was 17% higher (ie, lower glucose tolerance) in the biological evening (8:00 PM) than morning (8:00 AM; ie, a circadian phase effect).

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It started here: Effect of intermittent versus continuous energy restriction on weight loss, maintenance and cardiometabolic risk: A randomized 1-year trial (Sundfor et al., 2018)

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I’ll just leave this here https://t.co/WeMdfeU9ss

— Bill Lagakos (@CaloriesProper) July 29, 2018

If intermittent fasting (IF) works for you, awesome. If not, don’t worry, you’re not missing out on much. The above study was a year long and showed no difference between IF and plain old just cutting out some junk food. IF group lost 8 kg, regular dieters lost 9 kg.

“Intermittent and continuous energy restriction resulted in similar weight loss after one year in men and women with obesity.”

In this study, the IF protocol they employed was most similar to 5:2 wherein you eat normally for five days a week and consume minimal food on two non-consecutive days.

“Feeling of hunger may limit long-term adherence to intermittent energy restriction.” [this seems somewhat unwarranted because, well, they made it a whole year which is pretty “long-term,” imo] [although they consistently reported higher feelings of hunger which may be unpleasant]

Backlash to the above tweet was savage lol and a lot of people cited a 2016 study with which I was familiar… that doesn’t really make their case…

HEADLINE vs. STUDY, people

disclaimer: if you’re hell bent on IF, I’m still a little biased toward #eTRF

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LOOK AT THE DATA, PEOPLE.

I get asked about this a lot. Gluconeogenesis. The brain uses the equivalent of 120 g glucose/d. During starvation, brain still uses glucose, but less (because ketosis) and a bit differently (less oxidation, more lactate release).

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The brain and the obligatory glycolytic tissues always use at least some glucose.  During starvation, this glucose comes from gluconeogenesis.

The substrates for gluconeogenesis are primarily lactate, pyruvate & alanine, glycerol, propionate, and some amino acids (not leucine or lysine). The relative proportions change depending on #context, eg, the duration since your last meal, diet composition (keto, LF, etc.), etc.

Recommended textbook: Stipanuk or Gropper.

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calories proper

For more on renal gluconeogenesis, see HERE.

PRELIMINARY FINDINGS. PRELIMINARY.

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“It is clear that centrally mediated circadian rhythms play an important role in human health and our results provide initial information about how appropriate sunlight exposure to subcutaneous white adipose tissue (scWAT) might act as a peripheral circadian sensor that contributes to metabolic health. In contrast, a lack of sufficient bodily exposure to sunlight may contribute to long-term scWAT dysfunction and the current epidemics of obesity, diabetes and cardiovascular disease.”

WUUUUUT

Melanopsin is the blue light photon receptor in our eyes responsible for relaying sunlight to the SCN to entrain the central pacemaker. Well, a group of scientists accidentally discovered it fat cells:

Subcutaneous white adipose tissue express a light sensitive signaling pathway mediated via a melanopsin/TRPC channel axis (Ondrusova et al., 2017)

Figure “C” takes the cake. Electrophysiology studies show this receptor is highly sensitive to 465 nm blue/green, meaning it’s probably definitely melanopsin.

and guess what it does?

LIPOLYSIS — see Figure “E” above. Activation of melanopsin reduces the size of lipid droplets and lowers leptin. Interestingly, it also reduces adiponectin.

They also discovered this in mice, who are covered with fur and most of their melanopsin-containing scWAT is on their bellies which would never be exposed to the sun anyway. So….

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20% off some delish stocks and broths from Kettle and Fire HERE. 

If you want the benefits of  ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS. I recommend Lion’s Mane for the brain and Reishi for everything else. 

calories proper

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HAMMER TIME

Breakfast

Sunlight

The power of a good walk

Circadian rhythms: blocking the blues. AND THE GREENS

Symptoms: fatigue, cold-intolerance, hair loss, decreased libido, constipation… sound familiar?

Hypothyroid-like symptoms occur relatively frequently during times of rapid fat loss, and this may be at least partially dependent on diet quality.  Another component is the fact of being in an energy deficit, but this is difficult to evade on a weight loss diet.

Tl;dr: large energy deficit = hypothyroid-like symptoms.

Food choices and diet quality is important, too.

The negative impact of low calorie diet-induced weight loss on thyroid biology and energy metabolism is well established, but this figure from Agnihothri and colleagues sums it up rather nicely (2014):

Rapid fat loss causes a decline in TSH and T3.

And in this study on long-term calorie restriction (3-15 years), a similar phenomenon occurred (Fontana et al., 2006).  However, TSH was normal (unlike in Agnihothri’s study), possibly because they were not actively losing weight:

Note: calorie restricted diet had adequate protein…  low T3 because they’re weight-reduced and hypoleptinemic, and normal TSH because they’re not actively losing weight.

But then there’s this study, which shows active weight loss does not necessarily cause reduced TSH levels, if the diet is ketogenic (Yancy et al., 2005):

Also, this study showed reduced T3 after 11 days on a ketogenic diet, but it didn’t impact TSH or resting energy expenditure , suggesting no hypothyroid-like symptoms (Bisschop et al., 2001):

And lastly, from the [notorious] Ebbeling study:

Low TSH and low T3, but highest energy expenditure in weight-reduced patients on very low-carbohydrate diet.

Summary

Agnihothri: Low calorie diet-induced active weight loss: low T3 and low TSH; probably low energy expenditure and hypothyroid-like symptoms.

Yancy: Ketogenic diet, active weight loss: normal TSH.

Fontana: Weight-reduced, weight-stable (CR): low T3, normal TSH.

Bisschop: Ketogenic diet, weight-stable (11 days): low T3, normal TSH, and normal energy expenditure (indicative of no hypothyroid-like symptoms)

Ebbeling: Very low-carbohydrate diet, weight-stable (4 weeks): low T3, low TSH, normal energy expenditure (indicative of no hypothyroid-like symptoms).

In all of the above studies, leptin mirrored body fat.  And all of the old Rosenbaum & Leibel studies showed the reduction in thyroid function after low calorie diet-induced weight loss could be repaired with leptin treatment.  Their 2002 paper had it all (Rosenbaum et al., 2002)… replacing leptin levels to pre-weight loss levels, which required roughly 3 mg/d, completely restored thyroid levels and energy expenditure:

Carbohydrate restriction appears to throw a wrench in the gears.

We also know from rodent studies that excess carbohydrates, particularly fructose, can induce leptin resistance.  Perhaps by improving leptin sensitivity, carbohydrate restriction attenuates some of the hypothyroid-like symptoms associated with an energy deficit.  This would explain the findings of Bisschop’s and Ebbeling’s studies, and would be in line with the known impact of carbohydrate restriction on lowering plasma triacylglycerols, and the theorized (and somewhat controversial) association between high triacylglycerols and low leptin sensitivity.

If you’re on a weight loss diet and are experiencing cold intolerance, fatigue, low libido, or any other hypothyroid-like symptoms, consider either upping the calories or lowering the carbs (or this?).

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UPDATED Affiliate links: still looking for a pair of hot blue blockers? Carbonshade  is offering 15% off with the coupon code LAGAKOS and Spectra479 is offering 15% off HERE.

If you have no idea what I’m talking about, read this then this.

20% off some delish stocks and broths from Kettle and Fire HERE.

If you want the benefits of  ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS. I recommend Lion’s Mane for the brain and Reishi for everything else.

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Part I.  Ketones are made from fat in the liver.  But dietary fat has a lot of places to go and people to see, so it rarely gets to the liver en masse to a degree great enough to stimulate ketosis.  Not so much for medium chain triglycerides (MCTs).  Upon entry (ingestion), MCTs go to the liver and are metabolized to ketones without passing GO or collecting $200… but is this sufficient to reap the benefits of a ketogenic diet?

MCTs (C8-10) comprise ~14 of the fat in coconut oil, and 9.2% in dairy.  As such, average MCT intake is low – ~2% of total fat intake [because we eat a lot of vegetable oil and not a lot of coconuts].

Exhibit A.  Weight-loss diet that includes consumption of medium-chain triacylglycerol oil leads to a greater rate of weight and fat mass loss than does olive oil (St-Onge and Bosarge, 2008)

Healthy people assigned to either ~21grams of either MCTs or olive oil (~12% of total calories on a hypocaloric 1650 kcal/d weight loss diet) for 16 weeks:

This.

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