A cluster of metabolic abnormalities characterises the metabolic syndrome or syndrome X. They include raised blood pressure, atherogenic dyslipidemia, glucose intolerance or insulin resistance. The metabolic syndrome culminates in the development of diabetes, central obesity, and cardiovascular disease. The syndrome has become increasingly common in the world. It is estimated that about 20-25% of American adults and 16 % of European adult are suffering from it, and it is anticipated that the syndrome will become a epidemy in the next 20 years. For instance, 194 million of people have diabetes in 2004. This number is expected to rise to 333 million in 2025. One hundred percent increase is also expected for cardiovascular disease and obesity over the two future decades.
Programming of Syndrome X
A growing number of independent epidemiologists in different countries have shown evidence for strong links between foetal and early growth retardation and degenerative diseases later in life, suggesting that the risk of disease is programmed early in life. Poor intrauterine growth, most often due to deficiencies in maternal nutrition, but which also could be due to other maternal health problem, is associated with subsequent clinical development of hypertension, cardiovascular diseases, dyslipidemia, obesity, glucose intolerance, and Type 2 diabetes mellitus. Adult life, however, adds to the effects established in early life. These observations have led to the “Thrifty Phenotype” hypothesis, which suggests that during times of nutritional deprivation, the foetus diverts nutrients to critical organs such as the brain, at the expense of other organs such as the muscle, liver, pancreas and kidneys.
In contrast to type 2 diabetes, there is little epidemiological evidence to suggest a relation between poor nutrition in early life and the occurrence of type 1 diabetes later in life. However, as we demonstrated that the altered beta cells originated from foetus from dams who were deprived in protein are more prone to be destroyed by molecules that are responsible for type 1 diabetes, the foetal origine of type 1 diabetes deserves to be proposed.
Experimental research in animals supports these notions of causal link between malnutrition or adverse events in utero and early life, leading to alterations in foetal growth and increased risk of chronic degenerative diseases. Mechanistic studies aimed at determining the key factors involved in these correlations are obviously impossible in humans. Therefore, rodent models of maternal malnutrition in rodent have been established as the major paradigm for finding mechanisms of early programming of adult disease.
From a biological point of view, the concept of foetal programming of adult disease is not surprising. In fact, corresponding to critical periods of cell growth or regulation, differential vulnerability of different organs to teratogens has been known for many years. The same would be true for nutrient and hormonal supply to the embryo, foetus, and child. Appropriate supply of bulk nutrients must not only provide raw material for the construction of the organism, but specific nutrients may interfere with the precise regulation of development.