The proposed deleterious effects of fructose and, therefore, sucrose (which is broken down in the gut to produce glucose and fructose) in the human diet has hit the headlines in London again this week. The notion that fructose is deleterious over and above any effect of excess energy intake leading to obesity has been around for a number of years now and is vigorously championed by Robert Lustig.
The argument that fructose is special in promoting the onset of type II diabetes and the rest of the ‘metabolic syndrome’ is equally vigorously opposed by a very large group of human nutritionists. Getting meaningful evidence in human nutrition is extremely difficult and every statement has political implications. Those who propose a deleterious rôle of any dietary component are attacked as anti-food industry while those who present evidence in opposition are dismissed by the former as corrupt food, or sugar, or fat industry lobbyists.
Stepping aside from the human nutritional aspects of fructose ingestion is not only a relief but also scientifically illuminating.
A number of commentators have pointed out that hummingbirds live on nectar (mainly sucrose, glucose and fructose) and a few insects. They ingest enormous quantities of sugar every day. Frugivorous birds and mammals also metabolise vast quantities of fructose.
There has been a fair amount of research on the digestion and uptake of sugars from the gut of nectarivores but very little on the metabolism of fructose per se. It would also seem that, at least in frugivorous bats and nectarivorous birds, fructose, like glucose, is used very quickly to provide energy. As I understand it, the story of fructose metabolism goes like this: if liver glycogen stores are low, fructose forms glycogen until the stores are replete (if the biochemical pathways are the same in nectarivorous birds, glycogen must be being formed and broken down very rapidly for fructose to provide an energy source) but If liver glycogen stores are replete, excess fructose is converted to triglyceride in the form of very low density lipoproteins. (At this point I am usually told off by young biochemists for not using the term triacyglycerol instead of triglyceride. I make a short reply.). It is these triglycerides that are blamed for causing insulin resistance (type II diabetes).
So, here is a chance for comparative studies and I do not mean just comparing rat and man. We need to see what happens to fructose in nectarivores and frugivores as well as in animals in which fructose is normally only a small part of the diet. Do nectarivorous and frugivorous birds and mammals ever get to the point at which glycogen stores are replete and there is excess fructose? If so, are triglycerides formed, and what effect do they have?
In a similar vein, does adaptation to high fructose intakes occur? All the experimental evidence I have seen involves suddenly subjecting rats or human volunteers to high intakes of fructose or sucrose. What happens later with continual or continuous ingestion, as in rats and mice living in cane or sugar beet fields or sugar refineries and warehouses?
To return to human nutrition, the question still remains of why some people continue to eat and drink vast quantities of food and/or energy-rich liquids, far in excess of energy expenditure? But again the comparative questions creep in: why do some animals also eat to excess when food is available ad libitum while others do not? For ‘animals’ in the last sentence you can write ‘individuals’ or ‘species’ and try to think of examples of each as an interesting exercise on what is and what is not known.
Does the ‘fructose is bad’ story help or hinder the research effort on these questions?
