Have you heard of the Thin-Fat Phenotype?
It has been noted that Indians, for a given BMI have a higher percentage of body fat especially visceral fat than individuals of different population groups. The continual rise in Type II Diabetes and cardiovascular diseases among Indians poses questions on the potential causes for the same. Sixty-Two million Indians today are diabetics making our country the Diabetes capital along with Coronary Heart Disease (CHDs); which is one of the leading causes of death in our country. Is it only the food or the lifestyle? Or there is more to the story? Let’s find out!
Fetal origins hypothesis
Human life initiates as a single cell and more than 75% of cell division is complete in-utero. The growth and development inside the mother’s womb mediated by gene expressions is dependent on the environment provided to the fetus- which is further majorly dependent on the mother. Barker proposed that under nutrition during stages of crucial fetal development can cause permanent changes in the function and structure of the fetus.
Low birth weight babies and especially those of Indians- Babies of whom, are among the smallest in the world; are at a higher risk of developing Type II Diabetes and CHD’s. Intra-uterine under-nourishment and post-natal over-nourishment is responsible for major structural and functional changes in the fetus.
The limited nutrient supply inside the womb is directed towards developing of major organs such as the heart and the brain at the expense of growth and there is found to be beta-cell hypoplasia and eventual insulin resistance due to endocrinal changes. In the post-natal phase, the sudden exposure to nutrition results in catch up growth; which is an accelerated growth of the baby following a period of inadequate nutrient supply, eventually causing higher depots of fatty tissue. Higher adipose tissue in the early years of growth is responsible for insulin resistance and higher risk of developing non-communicable diseases. This weight gain/ fat accumulation that occurs on an otherwise thin poorly muscled body frame is often therefore referred to as the thin-fat phenotype.
Nutrition & Lifestyle transition
The growing economic and nutrition transitions, reduced physical activity and consumption of highly processed and packaged foods are equally responsible in aggravating the situation. Following a combination of high fat and high sugar dietary habits and constantly being in a state of positive energy balance through higher intake of food or zero energy output causes deposition of fat especially in the abdomen region.
Migration
Migration especially that of rural to urban for financial prospects was responsible to cause a rapid increase in fat percentage for at least the first 10 years. This was especially due to the sudden urban exposure, sitting jobs which reduced physical activity levels, availability of packaged foods, heightened purchasing power and surge in stress levels.
Other factors
Smoking, tobacco consumption, alcohol intake, stress, inflammation etc. have all been linked to obesity and insulin resistance.
Metabolic effects
Increased deposition of fat especially on the abdomen triggers an inflammatory response with the release of C-Reactive protein (CRP) that eventually inhibits insulin signaling. CRP is one inflammatory factor that is linked to the whole spectrum of metabolic syndrome with the strongest relation to central obesity.
The risk of developing Type II Diabetes and/or other non-communicable diseases is related to the deposition of fat on a thin frame through intra-uterine changes or migration or the recent nutrition and lifestyle transition. In a world of growing epidemic of such diseases, it is important to keep check on nutrition habits, physical activity levels, and overall lifestyle. This is the least that can be done to prevent these diseases.
Mihira A R Khopkar
Sports & Clinical Nutritionist
ESA Faculty