While I was writing the Essential Carbohydrate post, I got to thinking about another canard often bantied about in low carb circles. That being that our circulating blood glucose amounts to only about a teaspoon of sugar. Here's how that calculation goes:
Another way of looking at this is that for a normal person, a "glucose spike" to 125 mg/dL amounts to an increase in dissolved circulating glucose of perhaps 2g (85 mg/dL - 125 mg/dL) and a glucose intolerant person might see 10g dissolved glucose in circulation (200 mg/dL) following a meal. This small amount compared to the "large amounts" of carbohydrate in even a small serving of pasta or rice is often seized on by low carb advocates to foster carbophobia.
Now, nobody would argue against the fact that glucose is a signalling molecule in human metabolism. But there are other circulating signalling molecules such as amino acids, but I'll not be dealing with them in this post. The third class of nutrient signalling molecules are the free fatty acids, aka non-esterified fatty acids, NEFA.
So let's do that calculation for NEFA. The calculation is a little more complicated as usually NEFA are reported in molar concentrations and NEFA are a mixture of different fatty acids, but we can get a rough idea here using palmitic acid as our fatty acid. Typical fasting levels are 400 µmol/L and palmitic acid has a molar mass of 256 g/mol (I'm going to use 250 to make my math a bit nicer). Here's the math:
I can hear the clamoring in the audience ... but CS, CS!! ... NEFA is not from dietary fat, you know that! And indeed I do. However, you have only a half a gram of non-esterified fatty acids flowing in your blood in the fasted state. This is the level that contributes to the stimulation of basal insulin secretion. It is conceivable for dietary fatty acids that escape the esterification process to directly add to the circulating NEFA concentration.
Behold the PB&C shake from Cold Stone Creamery: And I'm going to use the "Like It" smallest size that weighs in at only 1322 cals* (the largest size tops 2000!!). This shake contains 82g of fat and 119g carb (104g sugar) ... oh, and a whopping 27g protein! FWIW, this works out to 56% fat, 36% carb, 8% protein. (* site claims 1280 cal but using macro grams and the 9/4/4 common values I get 1322)
So you get one of these concoctions. What happens in a normal person? Well, you're certainly covering those carbs with enough fat ;-) . One can presume that the 15 "non-sugar" carbs are actually a sugar after all, lactose, but even if we count those and 1/2 the sugar grams, you've ingested 67g glucose carb, and your Lustigometer registers just into the fructox zone at 52g. The whopping fat load gets packed up into chylo and hopefully whisked out of plasma in relatively short order thanks to both insulin and ASP. The insulin also suppresses NEFA release from adipocytes. BG stays normal, NEFA stays normal. In this study on normal post-menopausal women (I note the rather higher fasting NEFA) we see what happens to insulin, glucose and NEFA following a large breakfast (78g carb, 41g fat, 17g protein, about 750 cal), and a cheeze pizza lunch five hours later (68g carb, 6g fat, 21g protein , just over 400 cal). Of note, it is quite possible that the relatively low carb high fat PB&C might not elicit the appropriate trapping as seen in this case. (Note: the various curves are for different test oils 40g consumed in morning meal).
Note how the NEFA is shut down appropriately here despite the morning meal containing 41g fat.
But how about the metabolically damaged person consuming the PB&C? For an obese person with insulin resistance, insulin pours out of the pancreas and depending on the degree of compensation and IR, glucose gets cleared from the blood. The fat and fructose will elicit a transient IR that exacerbates that already existing. But the 52g fructose is not likely to overtax the liver, but perhaps it makes a couple of grams of additional fat from it. What of all that fat? This person's plasma is bound to be cloudier than Carly Simon's coffee and surely the adipocytes would love to get their grubby hands on those fatty acids. The scenario at right (from Frayn) is set in motion -- just as it would be for the metabolically normal person -- but impaired "trapping" in insulin resistant adipocytes leads to more NEFA "escapees" into circulation via the path on lower right of the diagram. Further, the insulin resistant fat cells do not answer the suppression call insulin is making on HSL. This results in inappropriate NEFA release from the fat cells. Thus, such a person would be starting out with slightly elevated glucose levels and NEFA levels, and it is likely that the NEFA are elevated to a greater extent than the glucose. Now add to that the inappropriate amounts of NEFA released from the fat and you're "starting out" even higher in terms of the level of signaling molecules before we consider the added NEFA from the esterification escapees.
In other words, if this same person had chosen a slim smoothie instead of this caloric abomination, they would likely still have the elevated postprandial NEFA, but with less sugar, perhaps avoid any pp hyperglycemia. But assaulting their body with the PB&C -- if even 1% of the fatty acids from the 82g ingested escape, that's 0.8g NEFA. Now ... yes, this doesn't all happen in an instant, but glucose spikes and is cleared rather rapidly whereas dietary fats last much longer. Indeed what doesn't get taken up the first time around (chylo remnants) is repacked by the liver and sent back out (VLDL). The levels remain elevated longer, including perturbations in NEFA.
As Frayn stated in this study, blogged on here, the obese experienced a slightly muted NEFA suppression after the first meal. But the real problem was that:
adipose tissue fat storage after meals was substantially depressed in the obese men. This was especially so for chylomicron-derived fatty acids,It's also been demonstrated that low carbohydrate meals exacerbate this problem.
So ... You have a deranged carbohydrate metabolism. Even Taubesians attribute this, ultimately, to a deranged fat metabolism and dysfunctional fat cells. So you go on a low carb diet and get the blood glucose levels under control. But at what "signalling" and metabolic expense? If you're obese and IR, you already don't properly suppress NEFA release from fat cells after a meal, and you've got a problem with chylomicron clearance! But it's worse from a signaling POV. With glucose the clearance of the signal is slowed. With fats, the impaired clearance is akin to converting chylo to signalling molecules (NEFA) --> metabolic mahem. Whatever the problem for the obese/IR, it can only be made worse, IMO, on a VLC diet if caloric reduction and weight loss does not result.
The teaspoon of sugar in the blood thing is interesting, but unless one becomes a diabetic, their BG isn't likely to be influenced in a chronic fashion that much from consuming many times that amount. But normal dietary fat consumption will certainly impact NEFA (and likely BG) considerably well before a diabetic state develops if it ever does. When fixing/treading lightly on one metabolic signalling molecule, it's worth remembering not to do so by making the other worse.