Could the high consumption of high glycaemic index carbohydrates and sugars, associated with the nutritional transition to the Western type of diet, be the common cause of the obesity epidemic and the worldwide increasing incidences of Type 1 and Type 2 diabetes?
Introduction
Our ancient genetic profiles are in the affluent societies of today challenged by exceptionally rapid changes in nutrition and life style. Simultaneously a panorama of non-communicable diseases is growing which can indicate a mismatch between the present-day human genetic profiles and current living conditions. Due to genetic heterogeneity human individuals and populations may have different risks for this.
T1DM and T2DM are two clinically defined diseases where such a mismatch may be involved. Their prevalence is now increasing epidemically in many parts the world [1], [1](b), [2]. They were, like obesity, rare during the 1800s and to the middle of the 1900s, but in the decades following the second world war (WWII) their incidence started to increase. Their concomitant rise could indicate common triggering factors.
An increase of T1DM was observed already in the 1950 s in Scandinavia, the U.K., the U.S. and Sardinia [3] and an increase of T2DM in the U.S. [4] and in some U.S. and Pacific island indigenous populations in the 1950s–1960s [5], [6]. The epidemics run in parallel with rising rates of overweight and obesity in adults, adolescents and children beginning around the same time in most high income countries [4], [7], [8]), and with the increased prevalence of new, more palatable, easy digested, sweet and energy-dense types of food and beverages which exploded in the U.S. and Western Europe after WWII. This new type of diet has subsequently through trade and marketing spread to other countries around the world in connection with their increase in wealth and per capita income [8b].
Section snippets
The post-war trends in carbohydrate consumption
A significant change in the Western food habits after WWII has been in the carbohydrate consumption. The traditional food was, as in other parts of the world, largely based on products as they occur in nature, i.e. unrefined, starch- and fibre-rich vegetables like whole grains, legumes, roots, tubers and whole fruits - all characterized by a slow release of glucose during digestion.
In the U.S. carbohydrate consumption decreased during the 1900s. In 1909 it contributed 56% of the food energy,
Sucrose
The increase in refined beet and cane sucrose consumption was impressive in many countries during the last century but started earlier. In England the yearly average intake of sucrose per capita was estimated to be 6,8 kg in 1815 which rose to 54,5 kg in 1970 [21]. Similar trends for refined sucrose consumption have been reported during the industrial era for Sweden, Norway, Denmark, the Netherlands and the U.S. [22]. A remarkable alteration in the food of mankind demasking an instinctive
Fat-carbohydrate intake and weight gain
The current average fat intake in the U.S. is around 32% of total calories – a considerable decrease from around 45% in the 1960s. But between 1970 and 1999 there was a modest increase in the per capita availability of added fats and oils caused by an increased intake of vegetable oils. (After 1999 the statistics of oil availability are difficult to interpret due to a large number of new manufacturers reporting oil production coming into the market). Of total added fats in the diet 86%
Carbohydrates in children’s food
Industrially produced food for infants and children has become a profitable global market after WWII which has grown into a multi-billion-dollar business and plays an increasing role in meeting the nutritional demands of infants and toddlers worldwide. The products include alternatives to breast milk, follow-on formulas and complementary baby and infant foods. Other foods are directed to older children.
Despite the WHO recommendation that babies be exclusively breastfed for the first 6 months of
Sugar, acceleration of growth and weight gain
Eugene Ziegler was the first to suspect a relationship between the secular trend of modern sugar (sucrose) consumption increase and the secular trend in the stature of adults, as well as a gradual increase in both pregnancy weight gain, birth weight and accelerated growth in children and adolescents that had occurred in specific populations in the 1900s [22], [74]. His idea about sugar as a driving force for growth identified sugar metabolism and the demand for insulin supply as central to this
Weight gain, acceleration of growth and diabetes risk
There is an association between body weight gain in adults and the risk of T2DM, which may be of a dose-response type [90]. But the T2DM risk is not necessarily bound to obesity. Studies have shown that weight gain can increase T2DM risk even among lean individuals [91]. Studies in the Japanese population have observed that long term weight/BMI gain since the age of 20 years and through adulthood, even within the normal weight range and independently of attained weight status, is a significant
Sugar, obesity, acceleration of growth and diabetes risk
A recent study at the population level found sugar intake to be uniquely correlated to T2DM prevalence independently of the overweight and obesity prevalence rates. The duration and degree of sugar exposure correlated with diabetes prevalence in a dose-dependent manner [103]. A dose-response relation of dietary glycaemic load to T2DM risk was also observed in a meta-analysis of prospective cohort studies [104]. Another study including 165 countries has presented results showing independent
Genetic assumptions
The full picture of the genetic risks for T2DM and T1DM is not known. For T2DM a large number of genetic susceptibility loci have been identified. The known risk variants are however calculated to collectively account for only 10% of the overall hereditary risk [115], [116]. There are also indications of a considerable genetic heterogeneity among the diabetic diseases. [117].
In T1DM genetic factors in the HLA system are considered to account for the major part of the disease risk. There is
Oxidative stress as a possible damaging factor in T1DM and T2DM
In T1DM oxidative stress is present at onset in children and adults [130], [131], and may have been present already before the clinical onset of the disease, as markers of oxidative stress have been demonstrated in non-diabetic family members of T1DM patients having shared the same diabetogenic environment [132].
Seroconversion to islet antbodies has a peak at 9 months to 2 years of age in most children with HLA-related risk for T1DM [133]. Rapid weight gain during this period of life is a
Hyperglycaemic complications
Oxidative stress caused by hyperglycaemia is the most significant factor in the development of the diabetic complications that are observed several years after the onset of the diabetic illnesses [154]. The increase of rapidly absorbed glucose to the blood, associated with the transition to the Western type of nutrition can also involve β-cell oxidative stress which may be a factor in causing β-cell complications in individuals adapted to a lower level of glucose load from their available food.
Conflicts of interest
None to declare
Acknowledgements
Thanks to Dr Alan Chester for valuable comments and for revising the English.
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