FRHD 2060 Lecture Notes - Lecture 4: Rheumatoid Arthritis, Programmed Cell Death, Varicose Veins

• School: University of Guelph
• Department: Family Relations and Human Development
• Course: FRHD 2060
• Professor: Scott Maitland

Document Summary

Why do we age: cellular theory. Limited number of times a cell can divide. Hayflick limit, has to do with shortening of telomeres. Related to oxidative stress: programmed cell death. Brain structure changes: death hormone theory (?) Aging due to the three lifecycle forces biological, psychological, and sociocultural forces. Slow the fundamental processes of aging to increase life space. Arrest or revers aging by removing the damage caused by the metabolic process. Pigment changes, age/liver spots, moles, varicose veins, lipofuscin: hair. Destruction of pigmentation production and germ center damage. May be normative, but abrupt changes could point to pathologies: body build. Sarcopenia: loss of muscle as a natural aging process. Metabolism slows down, but diet does not. Women gain weight in hips and back. Bone density begins in late 30s, accelerates in the 50s. Slight gender differences; more prevalent in women: especially during menopause. Osteoporosis: extreme loss of bone density, cause of broken bones.