In a recent issue of “Food Science and Technology”, Professor Judith Buttriss, who is Director General of the BNF, discusses the role of sugars in diet and health (1). Based on draft reports from the World Health Organisation (WHO) and the UK Scientific Advisory Committee on Nutrition (SACN) she concludes that the calories in sugar are no more responsible for obesity than other calories consumed in excess of expenditure. She goes on to suggest that the mechanism for weight gain is likely to be the excess energy intake rather than any physiological or metabolic effect of sugars per se. This is a remarkable position, which demonstrates an apparent ignorance of current scientific knowledge.

In reality we now have very convincing evidence that obesity is not caused by consuming more calories than are being used. There is overwhelming evidence that simply reducing the intake of calories just does not work.  This is all explained by in the excellent book “The Obesity Epidemic” by Zoe Harcombe (2).What is absolutely crucial is the content of the diet NOT the amount of food consumed. It is time the nutrition world woke up to the fact that the body does not utilise food in the same way as a bomb calorimeter. All calories are not equal because the metabolic processes which deal with fat, protein and carbohydrates are all quite different.

Sugar is broken down to glucose and fructose, which is now recognised as a disastrous combination with respect to health.

Raised levels of glucose in the blood will eventually cause Type 2 Diabetes (T2D). Obviously this is the result of excessive consumption of sugar and other foods containing starch which is broken down to produce glucose. In response the pancreas is stimulated to secrete insulin. One of the functions of the insulin is to reduce the level of blood glucose which it does by directing it to the liver where it is converted into fat, which is then stored. Hence body weight is gained and if the same type of diet is maintained over a period, the inevitable result is obesity. It also means that the body is effectively overloaded with fat. One consequence of this is that the level of triglycerides in the blood, a reliable risk factor for heart disease is raised. Another is that some of the fat accumulates in the liver, which results in the “fatty liver” condition.

Because the fat is stored, satiation is not achieved, which explains why a person consuming a diet high in carbohydrates is continually hungry and therefore consumes excessive quantities of food. Conversely a person consuming a diet low in carbohydrates and high in fat will find that hunger is satisfied quite easily.

It is also important to appreciate that the continual exposure of the body to high levels of insulin causes the condition of insulin resistance (IR). There is now convincing evidence that hyperinsulinaemia and insulin resistance are all related to heart disease, stroke, hypertension and obesity or what has become known as “metabolic syndrome”.

However the picture gets even worse when we factor in the role of fructose. This is because the metabolism of glucose and fructose are different.  First of all the presence of fructose in the blood does not stimulate the secretion of insulin by the pancreas. Consequently it has been promoted as a “healthy sweetener”. On the other hand it can only be metabolised in the liver whereas glucose can be utilised throughout the body. This places a huge demand on the capacity of the liver, which means that it limits the ability to cope with other carbohydrates. One of the by-products of the fructose metabolism is uric acid which causes gout and increases blood pressure.

The fructose also causes insulin resistance in the liver so that extra insulin has to be produced, which increases the demand on the pancreas that eventually leads to the failure of the organ resulting in T2D. The extra insulin forces fat into the cells giving rise to weight gain and obesity. Over the years the increased consumption of sugar and High Fructose Corn Syrup (HFCS) which is a mixture of glucose and fructose has been closely followed by increased incidence of obesity. Confirmation of the damaging effects of fructose are shown by the following investigations:

  • The level of triglycerides in the blood was raised when young men were given a diet which was supplemented with 200 g sucrose/day but when the sucrose was replaced with starch, which breaks down to glucose only there was no change(3)
  • A comparison was done over 8 weeks in which healthy men and women consumed 25% of their energy either as fructose or glucose. Although both groups gained the same amount of weight, those consuming fructose synthesised more fat in the liver and had a greater amount of subcutaneous fat. This is consistent with the fact that virtually all the fructose has to be utilised by the liver which primarily converts it into fat that is stored. The fructose group also had more oxidised LDL Cholesterol and a higher concentration of small dense particles of LDL Cholesterol, both of which are risk factors for heart disease. Insulin sensitivity was reduced in the fructose group but not in those consuming glucose (4).


Excess sugars in the body react with proteins to form Advanced Glycation Endproducts (AGEs), which means that the normal functioning of the proteins is impaired. In particular they contribute to premature aging, the development of atherosclerosis and complications in long-term T2D. The affinity of fructose for proteins is about 8 times greater than that of glucose (5).

Even further confirmation is provided by the research which demonstrates that those who reduce their sugar and other carbohydrates can successfully cure T2D (6,7). On top of this they invariably lose weight and improve the risk factors for heart disease by reducing the level of triglycerides in the blood and raising the HDL Cholesterol. In spite of the fact that mainstream medicine regards T2D as incurable, hundreds if not thousands of individuals have successfully overcome the disease by reducing the amount of sugar and other carbohydrates in their diet.

Finally it is essential to explain what has happened over the past 30 years during which time obesity, T2D and kidney disease have all increased to unprecedented levels, despite the fact that the official recommendation to reduce the intake of saturated fat (SFA) by 25 % was achieved by about 2000. Although there are no detailed statistics on how the intake of sugar has altered, there can be no doubt that it has increased very substantially over this period. Between 1975 and 2000 the consumption of soft drinks increased 4-fold. There has also been a huge increase in the sales of “low fat” products. Many of these, such as yoghurts, are often devised by replacing the fat with sugar. The latest UK survey shows that for children aged 4 to 10, the average intake of sugar is 14.7% of energy for those aged 11 to 18 years it is 15.6% (8). It is clear that sugar has to implicated in the deterioration of public health.


We now have overwhelming evidence from a range of different sources and disciplines which have established beyond reasonable doubt that excessive consumption of sugar is damaging to health. It has been a major contributor to the increased incidence of obesity and T2D that has occurred in so many countries over the past 40 years. From a public health perspective there are very sound reasons that every effort should be made to reduce the consumption very substantially.

The conclusion of Professor Buttriss that:

“…evidence to support sugar as a primary cause (of obesity) is incomplete at best…”

Is somewhat disingenuous and is obviously based on the discredited concept that obesity is simply caused by consuming more energy than is expended. We now know that obesity is a disorder of the metabolism, which is primarily caused by excessive insulin production. The solution is obvious: reduce the amount of carbohydrates, especially the sugar!


  1. J Buttriss (2015) Food Science and Technology 29 (1) pp14-15
  3. P A Akinynju et al (1968) Nature 218 (5145) pp 975-977
  4. K Stanhope et al (2009) Journal of Clinical Investigation 119 (5) pp 1322-1334
  5. C G. Schalkwijk et al (2004) Diabetes/Metabolism Research and Reviews 20 (5) pp 369-382
  6. J V Nielsen et al (2005) Upsala Journal of Medical Science 1 (10) pp 69-74
  7. RD Feinman et al (2015) Nutrition 31 (1) pp 1-13