21: Lecture Environmental Eating II Part I I. Genetics: -def play a role (22 different strains of genetically obese mice and 6 of genetically obese rats) almost every species demonstrate clear differences from normal mice/rats. All have: higher food intake but in humans: obese and non-obese intake not much different lower resting metabolisms humans no one able to distinguish large difference in obese and non-obese metabolic rate Less motor, or physical activity consistent w/ human literature (larger you are less movement occurs) all became diabetic b/c increased adipose tissue : become less sensitive to insulin several endocrine abnormalities (not necessarily true in humans) sluggish/depressed sympathetic nervous function (not necessarily true for humans) II. Human Studies observe relationship b/w weight of a parent and weight of child : studying correlations if neither parents overweight: .3 chance children will be overweight 1 parent overweight : 0.6 chance children overweight (2 x) 2 parents overweight : 0.8 chance children overweight strongly suggests genetics plays a big role grandparent-child and sibling correlations also show similar results correlation: monozygotic twins (identical) reared together: 82% chance of having same weight (100% same genes) monozygotic twins reared apart: 70% chance same weight height correlation in monozygotic twins goes a little down if reared apart dizygotic twins reared together: correlation in height goes down abit height less affected by environment than weight magnitude of difference in correlation of monozygotic twins reared apart : 0.7 how variation much in body weight contributed to these genetic factors? half of total variability of obesity attributed to genetics (half of variation contributed to environment) III. Evidence: Biological Theory of Eating no feedback from fat has been identified (leptin appears to be signal that there is fat in body biological signals not specific for eating behavior small yearly energetic error not mean physiological regulation intake and weight is normally distributed and as weight increases energy expenditure increases humans don't respond to food deprivation by overeating or overfeeding by eating less half of the variance of body weight due to genetics (other environment) little evidence that early nutrition affects adult body weight little evidence that adipose cells are the primary determinant of eating behavior environmental factors must also play a role IV. Early Development another strong argument for biological factors determining intake adipose cells remain constant across a life time lose weight or go on a diet: fat cells reduce in size; some adipose cells more sensitive than others
# adipose cells remains fairly constant 2 kinds of obesity: Hypertrophic (adult onset) most common type of obesity commonly linked to diabetes characterized by increase in size (not necessarily number) of adipose cells (they expand) expansion is what increases risk of diabetes Hyperplastic (child onset) starts early in childhood : born with a large # adipose cells: if you try to keep them at normal size leads to increased weight much more resistant to weight change than hypertrophic obesity