**5. Thrifty hypothesis**

The thrifty gene hypothesis indicates that certain populations may have genes that determine increased fat storage, which in times of famine represent a survival advantage, but in a modern environment result in obesity and type 2 diabetes. An example of the thrifty hypothesis showed by Dutch famine study which has shown that the offspring of mothers who were pregnant during the famine have more diabetes and those who were exposed in early gestation have more atherogenic lipid profile, altered clotting, more obesity, and a threefold increase in cardiovascular disease. Explanations for the heritability of these syndromes and the environmental contribution to disease susceptibility are addressed by the "thrifty genotype" and the "thrifty phenotype" hypotheses [27]. The underlying scientific hypothesis has been developed by epidemiology studies and emphasized by Dr. David Barker in the United Kingdom. During development fetuses respond to severe malnutrition by favoring the metabolic demands of the growing brain/CNS and heart at the expense of other tissues [31, 32]. In addition, the growing brain/CNS and heart tissue may

**43**

**Figure 1.**

*Excessive energy supply to the fetus or infant also has adverse consequences.*

*Fetal-Neonatal Lifestyle Basis of the Adult Metabolic Syndrome Patients*

not, however, escape entirely unscathed. The fetus is protected from death and is live-born but is more prone to diseases later in life [33]. Various studies have sup-

Epidemiology studies have shown that markers of malnutrition such as frank intrauterine growth retardation (IUGR), low birth weight, or small for gestation age (SGA) strongly predict the subsequent occurrence of hypertension, hyperlipidemia,

It has been shown that fetuses that are growth retarded during the first trimester of development are three times more likely to be obese as adults. In the case of premature infants, at the age of 4–10 years, these children who had been born prematurely had an increase in their acute insulin response, which compensated for insulin resistance. This decrease in insulin sensitivity may predispose premature infants to type 2 diabetes mellitus in adulthood, as already demonstrated among infants born at term who are SGA [33, 34], that compared with young people from the same region of Finland who are born after a pregnancy, and young people who ranged from 18 to 27 years of age who were preterm infants have become higher in chronic insulin resistance and more prone to glucose and high blood pressure [35]. Preterm births happen on their own early means that some of what would be the third trimester is lost. This is typically a sensitive period for programming and certainly a time during which the final aspects of organogenesis occur. This is explained by spending in the more difficult environment of a hospital setting in which there are many toxic substances as well as nutritional challenges. Now that many more extremely premature babies are surviving to adulthood, ensuring their health is crucial [36]. On the other hand excessive energy supply to the fetus or infant also has adverse consequences so a U shape works similarly at the tow ends of

Maternal hyperglycemia may lead to fetal hyperinsulinemia and fat deposition that influence the fetus. Offspring of obese women or women with diabetes are at greater risk for developing metabolic disorders themselves, even during childhood [37–39].

insulin resistance, type 2 diabetes, and ischemic heart disease, in adult life.

*DOI: http://dx.doi.org/10.5772/intechopen.84218*

ported barker hypothesis.

**6. Epidemiology studies**

the malnutrition (**Figure 1**).

not, however, escape entirely unscathed. The fetus is protected from death and is live-born but is more prone to diseases later in life [33]. Various studies have supported barker hypothesis.
