Far from trivia, this is the heart of the matter. I’m impressed that you want an explanation: the idea was meant to be provocative although we probably didn’t develop it well. We thought our article was a break-through but it is rarely cited.

Anyway, the idea is that there is confusion about metabolic syndrome. So the article is not alone in thinking there is no value to defining a syndrome and quotes “Attempts to define criteria that simultaneously predict risk for both cardiovascular disease and diabetes are unhelpful.” The argument is that lumping things together does not change how you would clinically treat each individually.

Well, let’s go with that. There are numerous ways of treating obesity, one of which is carbohydrate restriction. Of the ways to treat obesity, which of these is good for reducing triglycerides? Well, the ability of carbohydrate restriction to improve triglycerides has been known since the fifties and this is certainly the most robust response to any dietary intervention and is generally better than most drugs. To raise HDL, you can use high levels of niacin but this frequently has side effects that are characterized as unpleasant or intolerable (seems to depend on whether you are prescribing it or taking it). For small, dense LDL the so-called pattern B, this is linearly improved by reducing carbohydrate. There are many drugs for improved glycemic response and insulin but, of dietary interventions, if you go with low-fat you generally have to be sure to lose weight. but carbohydrate reduction will be effective even if you don’t. And so on. In other words, there are, many treatments for the individual markers characterized as metabolic syndrome but carbohydrate restriction will improve all.

What you want from the designation of a syndrome is some common biological feature, the major candidate here is currently insulin resistance. The close connection between dietary carbohydrate and insulin makes the above treatments meaningful in a physiological way.

The bottom line is that each demonstration of the broad number of factors that are improved by carbohydrate restriction provides evidence that they are, in fact, tied together, as you say, by “the collective symptom-group itself.” The evidence however is in the “response to treatment.” Conversely, though, if it is truly a syndrome, each feature may appear at a different time or in response to different environmental stimuli, but your best bet will be to treat one marker with the methodology that has the potential to treat all. There are many causes of most of the feature included in the syndrome and, as you say, there is no guarantee that they are not isolated disease states but, until we know how to identify those, carbohydrate restriction may be the “default” approach.

Does this make sense?

We will try to send an article to Lancet in response to the cited article but we anticipate some resistance because “it threatens the entire establishment of opinion,” rather than the “phenomenal income$ numbers” which we see as a minor player here.