Saturday, May 12, 2018

Nighttime Eaters have an elevated RQ on a given macro ratio diet. They're getting fat

I picked up this paper via Face-ache so cannot recall to whom I should credit for the find. Sorry. The post is also highly speculative.

Higher 24-h Respiratory Quotient and Higher Spontaneous Physical Activity in Nighttime Eaters

It's worth noting that the difference is small but probably biologically significant. Statistically p is less than 0.05. Before we think about it we need some background. That comes from the same group in an earlier paper:

Nighttime eating: commonly observed and related to weight gain in an inpatient food intake study

They looked at accurately measured food intake for Nighttime Eaters (NEs) under in-patient conditions at near identical macros to non-NEs:

and at weight gain over the subsequent 3.4 years, while the subjects were free living. Weight gain is, not surprisingly, higher in the NEs:

To me, NEs wake up in the night and go to the fridge and eat some food because they are hungry. Control subjects do not get up at night and do not go to the fridge and do not eat food, because they are not hungry. Note that hunger is a slippery term and these researchers have a psychiatry based view of obesity*. In Table 2 there is no significant difference in "cognitive hunger" between NEs and non-NEs. However in the methods the term used is "perceived hunger" and this is described thus:

"... perceived hunger (ie, the susceptibility of eating in response to subjective feelings of hunger)"

So NEs may not eat any more than non-NEs when they are "subjectively" hungry. My argument is that they are simply hungry more frequently, including right through the night in fact.

*Aside: But they are learning! Quote of the century from the paper: "These differences in substrate oxidation and SPA indicate that the night eating behavior phenotype may have physiologic underpinnings"

OMG gluttony may just be physiology!!!!!!!!!!!!!! End aside.


Why might NE people be hungry more often than non-NEs? From the adipocentric view of obesity, when dietary fat falls in to their adipocytes and stays there, NE subjects "lose" this fat. In the absence of a decent supply of metabolisable fat there is nothing left to oxidise except carbohydrate, with its high associated RQ (pax protein). Once the bulk of the ingested carbohydrate is metabolised and the fat is in the adipocytes for the duration, there is nothing for it but to get some more carbohydrate to eat and metabolise. The signal for this need to eat is called hunger. The fat loss phenomenon is not huge, the RQ for NEs is 0.85 and for non-NEs is 0.83. But I think that is enough.

Eating another mixed meal or mixed macro snack supplies necessary glucose for oxidation but the fat is again "lost" in to adipocytes. This keeps happening.

So. Are these folks going to get heavier? Of course they are. That is intrinsic to the elevated RQ compared to non-NEs while eating a similar macro ratio diet. It can only occur during fat accumulation. People with high RQs gain weight over the years. The high RQ is a direct result of the loss of dietary fat in to adipocytes. From the respiratory chamber study it would be about ten grams of fat per day "lost" in to adipocytes. In the background paper the NEs weight gain over 3.4 years was actually roughly five grams per day rather than ten grams per day, but people are more active when outside a respiratory chamber! Obviously fat "lost" in to adipocytes is fat gained on the scales.

Are NEs insulin sensitive or insulin resistant?

That's easy. Their RQ is high, they are losing fat in to storage. The fat is staying in storage within the adipocytes. They must be insulin sensitive. Think of the Laron dwarf humans, genetically GH-receptor deficient with subsequent exquisite insulin sensitivity. Short of stature and seriously obese at the same time as maintaining that exquisite insulin sensitivity...

To look for data to confirm my biases we have to move along to

Circadian rhythm profiles in women with night eating syndrome

This is by a different group. They are less psychiatric in outlook but fail to perceive that obesity might be a significantly adipocyte related problem. They mention stomach and liver and circadian rhythms, but not adipocytes. Their data are a little shaky but certain features come through as plausible. They measured a ton of (mostly) hormones but the only two parameters which grab my attention are insulin and glucose.

Now, the x axis is as clear as mud (like much of the rest of the paper). It really is "time of day", sort of. The first sample was taken at 8am, this is the start of each of the graphs, eight is interpolated between six and ten. Twenty four hours later, 8am next day is at 32 on the x axis and we get an extra data point taken at 9am on the second morning, ie 25 hours in to the study, it's at 33 on the x axis. Simple huh? Sorry if I've insulted the clarity of mud.

Three meals were served during daytime and snacks were available and consumed ad-lib, including through the night if so needed. Solid lines are controls, dashed lines are NEs. Macros of intakes were not controlled.

Control group (non-NEs) eat through the day. Glucose and insulin peak at around 5pm, probably around evening meal time, and both trough at around 4am because these folks would like to sleep through the night (they were blood sampled once an hour so...) and don't eat while asleep or wanting to be asleep.

The insulin peak is lower for the NEs as (I am assuming) they are insulin sensitive so they easily distend their adipocytes. Insulin sensitive adipocytes need less insulin to squirrel away diet derived fat. The insulin peak is delayed because these people are NEs, nighttime eaters, by definition. Eating later gives a later insulin peak. The NE insulin curve also never shows that drop in the early hours because NEs continue to eat at night. Because they're hungry at night. That's why they are called... You get the gist.

The glucose curve is equally explicable in terms of pathological insulin sensitivity. Just a little insulin lowers the blood glucose and facilitates its oxidation (daytime dip in glucose) and facilitates uptake in to adipocytes to generate glycerol for triglyceride sequestration. Gradually falling insulin due to lower (but not zero) food intake in the early hours of the morning allows some recovery of blood glucose levels, probably assisted by the surge of growth hormone in the early hours of the morning with its mild glucose raising, insulin resistance effect.

Night Eaters are pathologically insulin sensitive. Like the Laron dwarf humans and Laron mice, extreme insulin sensitivity causes obesity, given ad lib food. Unlike the Laron individuals with their genetic oddity of long term preserved insulin sensitivity, NE people will eventually distend their adipocytes to the level of leaking free fatty acids.

But until their adipocytes become dysfunctional NE people are insulin sensitive, hungry, and lose the fat component of their diet in to their adipocytes. Of course, once their adipocytes become distended and start to leak FFAs they will stop getting fatter and start to access the spilled fat. Oxidising this will drop their RQ but they will at this time become IGT/diabetic due to unregulated and inappropriate FFA release.

If I had to suggest an explanation for NE patho-physiology it would be PUFA, mostly linoleic acid... I'd expect NEs to be people who avoid saturated fat and prefer corn oil, over the long haul. More victims of the cardiologists.



Matthew said...

Dr. Jason Fung (promotes intermittent and extended fasting for type 2 diabetes) says you release 30% less insulin for the same meal eaten in the morning vs eaten at night.

Peter said...

Hi Matthew,

Yes, Dr Fung has many ideas, some better than others. He's not trying to explain why NEs have their peak insulin at 7pm which is so much lower than the non-NEs insulin peak at 5pm... I would class both of these times as "evening".

Interestingly the AUC for insulin over the full 25 hours for NEs and non-NEs is remarkably similar in the last study discussed above. I do wonder how easy it would be to detect a difference in daily insulin exposure responsible for the 5-10g/d of fat storage mis-match...... Once you start on calorie restricted studies all bets are off, but we know how well calorie restriction works in the long term, so one has to question the usefulness of such chronic semi-starvation studies relative to free living ad-lib studies.


Eric said...

Hi Peter,

the non-NE were eating 4000 kcal a day and only gained about 1 kg? what kind of exercise were they getting?

And it's no surprise that the NE were gaining weight if they were having on the order of 4700 kcal. Do you think that genetics and PUFA are needed to get into this pattern?


Peter said...

Yes Eric, quite a lot of calories. These folks had spent three days eating what an american dietitian had calculated as a weight maintenance diet (LOL!) followed by 24h at 80% of this in the respiratory chamber. Then they were given three days at an "eat all you like, it's free, buffet" for three days. This might not be the same a a guilt ladened trip to eat tomorrows ice-cream from the fridge at midnight while at home. The 2008 study also involved 3 days of what the subjects might have considered near starvation before the ad-lib section of the study too. Obviously the study design is by obesity researchers so you have to select what aspects they cannot "tweak" away from reality. I doubt they faked or forced the RQ data (or the long term weight changes) to fit any sort of agenda. But who can be sure?


James said...

Hi Peter,

Do you have any human studies showing n-6 PUFAs causing IR? I've followed your previous posts on "varnish" and the like, but they are all rat studies.

I've tried finding some myself, but cannot find any that replicate the IR issues.


This one is hypercaloric, but the PUFA group gained less fat than the SFA group -

This was hypocaloric, but again, the PUFA group lost more weight than the MUFA -

This one at least shows that n-3 is beneficial but n-6 is neutral -

That's pretty much my summary from human studies:

n-6 = "meh" (but not harmful)
n-3 = good

I had hoped to "prove" n-6 = bad, but cannot.

Eric said...

Is 4000 kcal/d a normal intake anywhere, with elite athletes and folks doing hard work such as digging tunnels by hand excepted?

Peter said...


I don't think PUFA cause insulin resistance per se. They cause a failure of insulin-induced insulin resistance in the post prandial period. That leads to extended insulin sensitivity, extended fat storage and obesity. Only once obesity is established do adipocytes leak FFAs in the face of elevated insulin and this then triggers whole body insulin resistance. Very secondary to the direct effects of PUFA and only occurs once obesity is well established.

You have to realise that hypo caloric diets tell us nothing about the real world. If hypo caloric diets were sustainable no one would be obese. Paying people to survive a study tells you nothing about what causes 5g/d accidental weight gain over 30 years.

For Risperus see Hypercaloric studies are problematic. Would the palm oil group have continued to eat to weight gain if they were not being paid to do so? If their adipocytes were saying "no" (i.e. they weren't hungry) to more fat storage (due to palmitate) where would the paid-for fat ingestion end up other than liver and visceral fat? Would the PUFA people have said "yes please" to an extra two muffins per day? The study tells us nothing about the real world.

What you need is the weight changes in the suppressed Sydney Diet Heart Study (can't find ref at the moment) or the Minnesota Study which I can't see in the modern retrieved-data papers.


Peter said...

Eric, they wouldn't eat like this outside of the 3 days in the study!


karl said...


First - insulin resistance in adipose tissue is not a bad thing - one can't lose weight with out it. Second, we shouldn't really talk about insulin resistance without defining the tissue. And I recommend not talking in the negative - but about insulin sensitivity.

I think that is is pretty clear that PUFAs induce inappropriate adipose insulin sensitivity - resulting in weight gain.

My personal observations seem to fit with this - wide spread obesity did not occur in the USA until the marketing of vegetable oils starting about 1960.


A second observation is when I was in the Philippines in the late 80's and again in the '90s I did not observe obesity like I saw in the USA - and in the market - they were selling buckets of lard to cook in (and when I returned to the US - seeing the public - so large - was clearly notable) . But now - high PUFA veg oil is for sale and folks in the Philippines are getting fat.

Someone could do a epidemiological study following the introduction of cheap Veg-oil into different countries - at different times - and look for the predicted change in average BMI that should follow - again at different times. Would they get a Noble prize - or just never get another research grant?

ctviggen said...

What I'd like to see: a crossover study with french fries fried in (1) beef tallow or (2) high omega 6 oil. Then see how many calories people eat.

I'm about to buy a fryer to use with beef tallow, mainly for low carb meals (fried cheese, chicken wings, maybe fried chicken). (I'll need to find some substitute for wheat, will have to experiment.) I will make my kids some fries with beef tallow, but I'm not sure I could subject them to oil.

Peter said...

Oil would be emotionally difficult!


Shaza said...

Speaking of nocturnal eating, I am taking my cat off processed food. WHAT do I feed him then! I have been reading labels and they all have horrid ingredients for animals.... Thank anyone who can get me started! AN article a study?? Thanks all

Shaza said...

ctvigggen, remember when Julia Child said MacDonald's fries were the best thing in the world until they stopped cooking them in tallow! I cook with tallow a lot..

cavenewt said...

Shaza... I took my cat off dry food a couple of years ago. Dry food is pure poison. So now I give her only canned food, not the cheapest. I also share my dinner meat with her occasionally. She does do a lot of hunting, especially in the summer. At six years old, she's svelte and energetic.


The author cites Gary Taubes quite a bit.

altavista said...

Peter, I want to get some blood tests done (lipids, glucose, insulin) and I was thinking about the timing. I eat only one meal/day around 2pm. Do you think the results will be accurate/useful if I take the test next morning say 10am? Or should I take them closer to the meal time say 5pm the same day?
I'm thinking after 20hours there wont be much insulin etc. left in the system so the results wont tell me anything useful?

Peter said...

Hi altavista,

They tell you different things. Fasting perhaps gives you a benchmark to compare yourself with others but you are looking at yourself as a LCer and comparing yourself to the general SAD population. I doubt that has been done in bulk before. Post prandial tells you more about what your choices mean when calorie income is supra-maximal. That might be more useful but when to sample and what to compare this to would still be a challenge.

I still recall thinking about which fat might be the best for LCHF eating. Even now PUFA under low insulin conditions appear different to PUFA under SAD conditions. I stll don't think that is settled as the hepatopathy in F3666 fed mice can be largely ameliorated by choline addition. Some hepatopathy might be PUFA related, but far from all of it.

If push came to shove I'd be interested in 1-2h post normal meal. But what would you compare it to?


altavista said...

True, I can't even compare it to mine since this is the first time I take the tests. But I can compare it to yours and woo's :)

Denise said...

Shaza, I feed my cat raw hamburger. The vet wanted to pull all her teeth, she was having such issues with her mouth, and in fact I started feeding her raw hamburger because the dry food she had been eating hurt her and she was wasting away. She loves it, and has regained weight, and seems to be doing well on it. She's a rescue, so no telling what happened to her, but she loves her raw hamburger. And it doesn't cost any more than the fancy canned food, which I decided to avoid because a friend who has done cat rescues for many years warned me that the BPA in the lining of the cans can cause hyperthyroid. She has 7 rescues that are all older, and all have to take medication because they are hyperthyroid.

altavista said...

Peter, I got the test results today (LDL is out of whack, a1c 4.8%) but I can't find yours here to do a n=2 sample.

The search function on your blog is terrible. How do I find the post you looked at your lipids?

altavista said...

Couldn't find them, but the 100% carnivore guy might be onto something as my GP was making fun of my testosterone too. I wasnt exclusively on meat (cream, eggs) but up until 1 month ago I ate 3-400g steak almost daily.

altavista said...

Peter, do you happen to have your ALT test result?

At 48 U/L, mine is a bit too high for comfort and it's also double Woo's who snacks on PUFA and skips the eggs.

I wonder if we're not poisoning ourselves with too much vitamin A from the egg yolks?