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ventricular hypertrophy. The mechanisms of this effect are 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 through

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%, and 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; and

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

them 250g of diabetic chocolates per day for ten days. (At that

The diabesity epidemic:

whose fault is it?

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/m

2

) 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/m

2

) 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 60s 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

1980s 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 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

The Buckingham Institute of Translational Medicine

The University of Buckingham