OK, I sort of suggested the discipline – though I notice others use the descriptor now – so here is a very good use of it. What are the physiological interactions in the gut and in the bloodstream of these three. Obviously this has to include other inputs which provide the components – so, for example, the rapid boost in glucose after eating wheat carbohydrate – and rates of use of and/or disposal of all three.
Start to examine published works, blog investigations and even text book references and it becomes an exemplar of, well, the Tale of Six Blind men and the Elephant once more. “I can clearly see” they all write and go on to describe another non-integrated impression of the mechanisms working and of the outcomes of such. There is certainly an outpouring of certainties in the face of the interactions of biological subtleties. There is, it seems, to find definite answers to complex interactions.
“Fructose is a poison” is one such extreme. “No it’s not” might well be another! Better would be “What set of physiological circumstances can drive fructose consumption to yield toxic outcomes?”. It is a simple sugar, of the same formula but different structure to glucose and still occurs in two isomeric forms. Whereas glucose is used directly in the glycolysis and other energy generation processes, fructose has to be converted by enzymic action first. It does not trigger the all important insulin release into the blood stream and is also less readily absorbed from the intestine. Our most common dietary source of sugar, sucrose, is simply one glucose bonded to one fructose molecule. This bond is broken prior to intestinal absorption whereupon the glucose is very readily absorbed whilst the fructose is only slowly taken in, often in fact resulting in the excretion of a good percentage of this sugar.
The great rise in sucrose consumption in the post world war two, 1950s onwards era and the profound and hasty switch to “High fructose corn syrup” from the 1980s have raised obvious concerns about their driving obesity and diabetes, as well as a range of other associated conditions. As I have also chronicled, the much more recent contribution of Dr William Davis in bringing forward the role of the wheat grains in this pattern illustrates the source of rapid elevations in blood glucose levels. Palaeolithic diets, also widely promoted today, reach the same conclusions, albeit by a rather different route. Both describe the imbalances resultant in modern nutritional intake and both suggest that many, if not all, of us are consuming a constant essentially toxifying diet, whereby the sugars in our blood are constantly pushing against their homeostatic constraints and are chronically pushing emergency release metabolic pathways, such as glucose excretion in urine (diabetes) or fat deposition.
As William Davis points out, too great a concentration of glucose in the blood raises its osmotic pressure too high – water would be drained from cells in the tissues above such a level, causing drastic organ failures. Fructose obviously has the same impact. However, as fructose does not lead to insulin release, its blood level is far less well controlled, save by the speed of absorption from the gut, perhaps, or its utilisation in the liver, where it is metabolised. If modern far higher levels of dietary fructose, both in sucrose and in the corn syrup, lead to greater levels of fructose reaching the blood then the hepatic processing will be the limiting factor, fructose could “back up” and osmotic pressure increase independent of the glucose levels.
The ramifications are many and varied and the impacts often extreme. Nobody can argue that we eat a diet even close to that of our ancestors and so our evolutionarily established mechanisms cannot be being utilised optimally. Surely we can and do naturally digest fruits all of which have a high fructose content. Glucose, if anything, we would formerly have consumed far less of. Why there is no “fructose-insulin” is an interesting question which I do not hear asked elsewhere.
This topic seems to have overlaps, as I have previously described, into the central arena of these investigations. However I suppose I use it here as a reminder of the interconnectivity of physiological systems – as the global warmonger Donald Rumsfeldt noted in a probably unique moment of vision “There are things we know, there are things we know that we don’t know AND there are things we don’t know that we don’t know”. Such are these collateral damages, imbalances and knock-on effects.