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.
*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.