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
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
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
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?
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
) 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 <
) 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
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