Sangita Yadav is the Head of the Department of Pediatrics, Maulana Azad Medical College, a premier institute of University of Delhi. She has more than 35 years

of teaching experience. She is also the Head of Department and a recognized PhD Supervisor. She is currently the Joint Secretary Liaison of Indian Academy of

Pediatrics. Chair Person of Adolescent Health Academy of IAP. Her area of interest is pediatric and adolescent endocrinology. She was awarded WHO Fellowship

for training in USA. She is one of the Founder Member of Indian Society of Pediatric and Adolescent Endocrinology. Her interest is in adolescent health. She is the

Founder Member of Adolescent chapter in 2000 and its task force. She has published more than 100 papers/articles in books and journals. She is an active and

enthusiastic Member of Indian Academy of Pediatrics.

Growth is a sensitive indicator of a child’s health, nutritional state and genetic background. Growth of a child is not only

controlled by hormones but by many other factors like nutrition and chronic systemic illnesses like hypothyroidism,

chronic liver disease, diabetes mellitus, malabsorption, etc. Principal hormones influencing growth are Growth Hormone (GH),thyroid hormones, adrenal androgens, sex steroids, glucocorticoids, vitamin D, leptin and insulin. Growth hormone promotes longitudinal bone growth. GH mediates its effects on target tissues via stimulation of hepatic Insulin like Growth Factor (IGF-1) production. IGF-1 is a single chain polypeptide hormone with structural homology to proinsulin, produced from liver. IGF-1 is at least in part GH dependent and mediates many of the anabolic and mitogenic actions of GH. Alternative hypothesis is the dual effector theory, which is based on the premise that growth is a result of the differentiation of precursor cells, followed by clonalexpansion. GH directly promotes the differentiation of cells and the development of IGF-1 responsiveness. Clonal expansion

of these differentiated cells is mediated by local production of IGF-1 in response to GH. IGF-1 appears to be critical for fetal

and postnatal growth. Levels of IGF-1 are inversely related to Body Mass Index (BMI). Inadequate calorie intake and/or protein intake is by far the most common cause of growth failure. Protein energy malnutrition is frequently characterized by elevated basal serum GH concentration. In generalized malnutrition i.e. marasmus, GH levels may be near normal or even lower. In both the conditions, serum IGF-1 concentrations are typically low. Malnutrition is a form of GH Insufficiency (GHI) in which serum IGF-1 concentrations are reduced in presence of normal or elevated GH levels. Elevated GH levels represent an adaptive response whereby protein is spared by the lipolytic and anti-insulin actions of GH. Reduced serum IGF-1 concentration is a mechanism by which precious calories are shifted from use in growth to survival requirements. Rare causes of IGF-1 deficiency

leading to severe growth failure are hypothalamic dysfunction, pituitary GH deficiency and primary or secondary GHI. Hence

these patients with growth failure are evaluated by careful auxologic assessment and appropriate measures of GH-IGF axis. Establishment of deficiency of IGF-1 and IGFBP-1, IGFBP-3 then necessitates a thorough evaluation of hypothalamic-pituitary-IGF function. Hence along with all other factors regulating growth, insulin like growth factors has a crucial role in growth attenuation.

K M Yacob is a Practicing Physician in the field of Healthcare, Kerala, India. His interest is in basic research, fever, inflammation and back pain on which he has

printed and published 9 books. He has written many articles in various magazines.

When the disease becomes threat to life or organs blood circulation decreases, temperature of fever rises to increase

prevailing blood circulation and it acts as a protective covering of the body to sustain life. When blood flow decreases

to brain, the patient becomes fainted-delirious. If the temperature of fever decreases, the blood circulation reduces. Blood circulation never increases without the increase in temperature. Delirious can never be cured without increase in blood circulation. The temperature of fever is not a surplus temperature, or it is not to be eliminated from the body. During fever, our body temperature increases like a brooding hen’s increased body temperature. The actual treatment to fever is to increase blood circulation. There are two ways to increase blood circulation: (1) Never allow body temperature to lose, and (2) Apply heat from outside to the body. When the temperature produced by body due to fever and heat which we applied on the body combines, the blood circulation increases. Then the body stops producing heat to increase blood circulation. And the body gains extra heat from outside without any usage of energy. If we do any type of treatment by assuming that the temperature of fever is to increase

blood circulation, the body will accept it; at the same time the body will resist the treatment to decrease blood circulation. No

further evidence is required to prove the temperature of fever is to increase blood circulation.