What is the Dawn Phenomenon (DP)? A nice simple definition is available from here:
"The dawn phenomenon is a term used to describe hyperglycemia or an increase in the amount of insulin needed to maintain normoglycemia, occurring in the absence of antecedent hypoglycemia or waning insulin levels, during the early morning hours. To be clinically relevant, the magnitude of the dawn increase in blood glucose level should be more than 10 mg/dL or the increase in insulin requirement should be at least 20% from the overnight nadir. Controversy exists regarding the frequency, reproducibility, and pathogenesis of the dawn phenomenon. Approximately 54% of patients with type 1 diabetes and 55% of patients with type 2 diabetes experience the dawn phenomenon when the foregoing quantitative definition is used"
OK, I lied about the simplicity.
If you go back to 1988 this group seemed to think that the Dawn Phenomenon was pretty straight forward and amenable to pharmacological management. In the early hours of the morning humans have a growth hormone (GH) surge. GH causes lipolysis, lipolysis releases free fatty acids. No muscle wants glucose when it has access to free fatty acids. Muscle thus becomes insulin resistant and blood glucose rises. They studied type one diabetics as doing this eliminates all of those messy insulin responses to glucose that normal people produce.
Give an anticholinergic, block the GH surge and you block the DP. All nice and simple.
Then this group, in 1992, went out to check if this was true and gave a bolus of GH, again to some type one diabetics. Any old time of day as far as I can tell.
As expected GH caused a rise in FFAs but no insulin resistance in this paper! Quite how they managed this is a bit beyond me. FFAs should produce insulin resistance. Both papers report comparable peaks in GH but neither gives an AUC for GH. It's difficult to compare FFA changes between papers.
Then, when you get down to the nitty gritty, you find that the second paper was quite careful to produce only a SHORT physiological burst of GH, shorter than occurs at night in humans. They were ONLY looking for the effect of GH on insulin resistance, so they had to keep FFA changes to a minimum. This looks to be a very carefully crafted sentence to me, it's the "summing up" in the abstract (the section of the paper which actually gets read):
"Since no significant effect on glucose metabolism was recorded, we do not presently find evidence to support a primary role for small surges of GH in the pathogenesis of the dawn phenomenon"
A translation might read:
"A bolus of GH which is significantly lower than that needed to produce the lipolysis necessary for the Dawn Phenomenon does not produce the Dawn Phenomenon"
People don't work like this! The nightly GH surge in humans does crank up FFAs. Eliminating this effect from your study won't help elucidate what's happening in the DP, except to say it's not GH per se, but it's still the down stream effects of GH that matter. The 1988 paper looks far more convincing to me.
Current thinking seems to have forgotten about FFAs but does come up with the concept that there is no drop in insulin levels involved. This is interesting in so far as Dr Bernstein suggests that rapid hepatic breakdown of insulin is the cause of the problem. I've yet to see any evidence of this mechanism, unusual for a Dr B idea.
The other main support for FFA involvement is the roll of eating in terminating the DP. This has been discussed many times on the Bernstein forum. Many type two diabetics develop a vicious DP on LC eating and, if they continue to fast through the morning, their blood glucose will just keep going up and up. Eating CARBS stops this, presumably the carbs get insulin high enough to get ahead of the effects of FFAs on muscle, while the extra insulin can shut down hormone sensitive lipase and so drop FFA production... This is physiological insulin resistance taken to pathological extremes.
It's interesting to speculate whether it is the facility to indulge in lipolysis to excess, possibly related to the absolute fat mass available or insulin resistance in those adipocytes, or failure of the cross talk between alpha and beta cells in the pancreas or failure of hepatic vagal nerve supply which makes the DP such a big problem in some diabetics but not in others. I don't know.
Also the how and why of bed time alcohol blocking the DP effect is another big unknown, but it seems to work for many diabetics. Whether this is an hepatic effect, a GH effect or a lipolysis effect seems wide open. Wine lovers with DP just seem grateful when it works for them. Evening alcohol incidentally also drops my morning glucose in to the 4 point something range.
So it looks to me as if the DP is an insulin resistance phenomenon by which GH induced lipolysis bumps up morning glucose. I think this is physiological. When lipolysis is one step ahead of the extra insulin production needed to keep blood glucose in an "acceptable" range you can easily end up with an elevation of FFAs, insulin and glucose all at the same time. In fact, broken insulin sensitivity might well do this, and so you end up with type two diabetes markedly worsened by a GH surge, every night...