147. Obesity Etiology Flashcards
Epidemiology of Obesity
- what percent of adults are obese
- what is the trend in prevalence among ages and race
- where in the world is obesity prevalent
42% adults obese, 75% overweight
Prevalence: higher in blacks, then hispanics, then whites, then asians (due to bio/genes, enviro, SDoH)
Increasing prevalence over time in adults and kids (kids esp hispanics #1 then blacks #2)
Global: US epicenter; higher rates in Mid East, S Africa, Venezuela
What increases RMR?
How does TEE change in obesity?
How does obesity change FFM and FM, and TEE (HOW)? Why do obese people gain weight in the first place?
How does the body respond to an energy surplus (high intake)
RMR: increases with more lean mass (higher FFM) - obese males have highest FFM and RMR (lean females have least FFM, lowest RMR)
Obese: higher TEE - burn more cal doing same task than lean people due to energy demands
Obese: higher FFM and higher FM, higher BMR, higher PAL, higher EE but lower NEAT (non-exercise activity thermogenesis - obese spontaneously less physically active)
Energy surplus: intake higher than EE
causes increase in total weight (higher FM and FFM)
results in PLATEAU: new increase in FFM increases RMR to meet extra energy intake (new stability at higher weight)
List determinants of obesity
complex multifactorial chronic disease from interaction of genetics, environment, social, behavioral, cultural, physiological, metabolic factors
More Energy In: pressures to eat more (high portion sizes, low cost, good taste, high added sugar)
Less EE: pressures to be less active (more sedentary, more drive-throughs, more elevator use)
What are the genetics of obesity?
Most obesity is polygenic - more likely to have higher BMI with more risk alleles (single gene disorders - leptin deficiency and POMC deficiency rarer)
BMI closely related within families
Primordial factors of obesity
Effect of duration of obesity
Hypothalamic response to high fat diet
Effect of microbiome on obesity
Primordial: maternal BMI assoc with child risk of obesity, epigenetics (intrauterine enviro modifies gene expression); obese pregnancy = fetal lipid exposure, insuline resistance = more risk of obesity/inflammatory changes
Duration: more time spent obese = harder to return to non-obese
High fat diet = inflammation in ARC = less response to leptin
Microbiome transplant of obese twin = increases mouse adiposity
Microbiome transplant of lean twin = lean mouse
Influence of gut microbiota on host metabolism
What are some metabolic adaptations to severe weight loss?
Weight Loss: done by increasing PAL, results in lower RMR
Adaptation: lower EE (even with more PAL, less cal/kg burned due to weight loss) - persists years after weight loss = no change in FFM and increase in FM
Now pts have lower RMRs = risk of even more weight gain
Muscles become more efficient with less weight = use less energy
Fight increased efficiency by increasing work load and weights
