Special Report: The diabesity epidemic: Whose fault is it?

Clore Laboratory University of Buckingham

Clore Laboratory University of Buckingham

At a recent conference it was claimed that adult obesity and overweight rates, in both males and females, are projected to increase in almost all countries in Europe by 2030. Using a statistical modelling protocol, the authors concluded that obesity levels (defined as BMI > 30kg/m2) are projected at 15% in the Netherlands and Belgium to 47% in Ireland. In females the highest projected obesity rate was 47% in Ireland and the lowest 10% in Romania. When considering both overweight (BMI > 25 < 29.99kg/m2) and obesity, a number of countries showed greater than 75% levels in both males and females.

The WHO regards childhood obesity as a serious public health issue. In the UK, where the National Child Measurement Programme measures the height and weight of around one million children in England each year, 18.9% of 10-11 year olds were obese in 2012/13 and a further 14.4% overweight.  For 4-5 year olds the figures were 9.3% obese and 22.2% overweight plus obesity.

Overweight and obese children are more likely to become obese adults and with the consequential higher risk of morbidity, disability and premature mortality. Although many of the more serious consequences are not seen until adulthood, raised blood pressure, lipid deposits in arterial lining, and Type 2 diabetes are now common in children and adolescents. Very recent data from the United States shows a 35% increase in Type 2 diabetes in children from 2001 to 2009.

People in the UK now in the over 60’s age group, will often have photographs of their whole school.  In schools of 600 plus 11-18 year olds, the number of overweight children would be less than 20 and obesity was a rarity.  Even in school photographs from the 1980’s overweight plus obesity rates were only 10-20%.

So, who is to blame?

Is it mother’s fault?

The prevalence of obesity is greatest among children from obese parents with maternal BMI associated with offspring BMI, coronary heart disease, blood pressure, plasma lipids and insulin resistance. Several studies have demonstrated a causal relationship. For example, bariatric surgery to reduce weight of obese women reduces the risk of obesity, insulin resistance and hypertension in her offspring born after surgery compared to those born before surgery, suggesting that the environment experienced during critical in utero development influences long term health. Studies in rodent animal models show that feeding an obesogenic diet to dams resulted in offspring obesity, insulin resistance, hypertension, non-alcoholic fatty liver disease and left ventricular hypertrophy. The mechanisms of this effect is clearly not a classical genetic effect, but much attention is being focused on epigenetic programming through DNA methylation and changes in microRNA expression.

Is it father’s and even grandfather’s fault?

Studies from Australia using rats showed that paternal consumption of a high fat diet inducing paternal obesity and diabetes resulted in glucose intolerance in the offspring though impaired insulin secretion. Follow-up studies showed that F2 grand-offspring from high fat diet fed grandfathers (FO) developed a higher body weight, fat mass and defects in glucose and lipid metabolism when fed on a high fat diet. These studies suggest epigenetic modification by diet, impacting grandfather’s sperm, resulting in epigenetic modifications in tissues of the F1 generation that are then carried forward into the F2 generation.

For both paternal and maternal obesity effects, it is likely that epigenetic modification will make the offspring predisposed to obesity. It is not clear as yet whether the paternal and maternal effects are additive. Nevertheless, it would appear that the development of diabesity in offspring is still affected by the diet of the offspring.

Is sucrose/fructose or saturated fat to blame?

There has been a constant battle in the blame game about the impact of sugars and fats on diabesity.  Studies in rodents clearly show that:

1)         A 60% high fat diet (by calories) with a composition by weight of protein 26%, carbohydrate 26%, fat 35% has been used in hundreds of laboratories to produce obesity and insulin resistance.

2)         A 45% fat diet (by calories) with a composition by weight of protein 24%, carbohydrate 41% and fat 24% has also been used in many laboratories to produce obesity and insulin resistance.

3)         The addition of sucrose or fructose to drinking water or diets with 60-70% by energy of sucrose or fructose induces hypertriglyceridaemia, insulin resistance and fatty liver.

Thus, the data from rodent studies suggest that high energy diets whether predominantly fat containing or sugar containing will induce unfavourable metabolic effects including obesity and diabetes. There is evidence that saturated fats and fructose are particularly damaging. In the case of fructose this author many years ago induced measurable (reversible) adverse changes in insulin sensitivity in young men as measured by the hyperinsulinaemic euglycaemic clamp procedure by feeding a 250g diabetic chocolates per day for 10 days. [At that time fructose was used in many products for diabetics as a sucrose replacement – thankfully no more.]  Fructose, unlike glucose, has no rate-limiting steps on its metabolism. Fructose is generally metabolised in the liver, leading to fatty liver and excessive inflammatory cytokine production.

Are Governments and the World Bank to blame?

In the early 1980s high-fructose corn syrup replaced sucrose in soft drinks. Agricultural policies in the US by subsidy payments have skewed markets to the overproduction of commodities that are the ingredients of energy dense foods. These commodities include high fructose corn syrup and soya bean oil.

The palm oil industry is an important driver of economic growth in SE Asia and Central and Western Africa and is the most important tropical vegetable oil in the global oils and fat industry. It is the cheapest major vegetable oil and hence it is the most commonly used by poorer households. Whilst originally used as cooking oil, it is increasingly being used in packaged foods such as margarine, ice-cream, cakes, biscuits and chocolates. The global demand for palm oil has risen from less than five million tons in 1970 to over 50 million tons in 2010. The production of palm oil provides income for poor farmers and workers in many countries and is actively supported by the World Bank. However, is diabesity the unintended consequence of an abundance of palm oil in everyday foods? The cheapness of the oil means that its intake is likely to be highest in the lower social economic classes.

Are food manufacturers to blame?

There has been a dramatic move over the last two decades from using basic ingredients in the preparation of meals to pre-packaged meals. A consequence of this is people are not really aware of what they are eating. Labelling of the pre-packed meals is often poor and in small print on the underside of the pack. Food composition only usually gives broad data such as fat, protein and carbohydrate content with perhaps salt content and is given per 100g ignoring the pack size.  Sometimes carbohydrates will be split into simple sugars and polysaccharides and fats into saturated and unsaturated, but detailed composition is not given.

Of course even if the food industry was forced to give the details, would it be understood by the general public? But surely the general public would know if on an iced fruit cup drink it said ‘contains the equivalent of 28 lumps of sugar’ and that a Big Mac and fries contained the equivalent of nine teaspoons of oil.

Is the individual to blame?

The simple answer is yes, but it is clearly a complex issue, with many adverse factors supporting an obesogenic environment. These include:

Breaking the obesogenic diabesity cycle

It seems self-evident that this cycle must be broken but it needs to be addressed at many levels. There is not one simple solution. A major factor has to be education and that should start at a young age. Mothers need to be helped more with dietary information and weight targets of babies. If all mothers try to bring their offspring to the 90th percentile then clearly target weights will increase year on year.

Schools could ban soft drinks, including fruit juice, from the premises and compulsory nutritional advice, including the potential consequences of being obese, becoming part of the school syllabus. After school games and exercise programmes could be more supported.

Food companies and restaurants could be forced to provide understandable nutritional information so that this becomes part of people’s choice mechanism. Government could impose a tax on sucrose and fructose containing drinks. Supersizing and all-you-can-eat restaurants could be outlawed. Whilst libertarian principles suggest that people should have a free choice at what they do, historically (e.g. smoking, car seat belts, motorcycle helmets, telephone use whilst driving) changes that people generally perceive to be for a person’s good have only been successful following legislation.

Obesity and its prevention need to be treated seriously as does the potential consequences of diabetes, cardiovascular disease and cancer. Research is needed to identify better the molecular mechanisms leading to obesity and the development of the diabesity syndrome, and to find drugs that will reverse/prevent obesity and its consequences.

Mike Cawthorne
Director of Metabolic Research and Head of Medical School
Clore Laboratory
University of Buckingham
tel: +44 (0)1280 820309
[email protected]
www.buckingham.ac.uk/bitm