Prelim #1 Flashcards
what classifies someone as overweight?
defined as having excess body weight for a particular height from fat, muscle, bone, water, or a combination of these factors
what is obesity?
having excess body fat
what leads to being overweight and obese?
result of caloric imbalance, too few calories expended for the number of calories consumed - and are affected by various genetic, behavioral, and environmental factors
How to calculate BMI?
BMI = (weight in kilograms)/ height in meters^2
what are the strengths of BMI?
gives an overview of body structure; weight to body load
what are the weaknesses of BMI?
does not take into consideration: fat mass, bone mass, lean mass (muscle); genetics
true or false, obesity can affect everyone?
true
what is the overall trend of obesity in the US among adults?
rising/high rates of obesity
how much has worldwide obesity increased since 1975?
tripled
what percent of adults aged 18 and over were obese/overweight?
42%
true or false, most of the world’s population live in countries where overweight and obesity kills more people than underweight?
true
true or false, obesity is preventable?
true
childhood obesity stats?
- more than doubled in children and quadrupled in adolescents
- 19.1% of children and adolescents were overweight or obese
- globally: 41 million infants and children under 5 are overweight or obese in 2016
why should we care about obesity?
obesity is either a risk factor or associated cause of death for most of the leading causes of death including heart disease, cancer, respiratory diseases, etc.
thermodynamics of weight?
intake vs expenditure. if we eat too many calories we will gain weight, if we burn more calories than maintenance we will lose weight
true or false, our bodies are evolutionarily designed to be energy efficient
true
do primates burn more or less energy/day than other mammals?
less
do primates burn more/less energy/pound than other mammals?
less
why do we burn less than other mammals?
species with greater energy expenditure per pound tend to grow faster, reproduce more, and die at earlier ages than those with lower energy expenditure per pound. Primates (including humans) burn much less energy each day than other mammals, which corresponds with primates’ slow life history schedules and long lives
do humans differ from our Ape primate ancestors in energy balance?
humans combines social and foraging efforts, sharing surplus food energy with other members of their group. Sharing increases the energy available for all tasks including reproduction and maintenance, leading to longer lives, larger families, larger brains, and increased activity. Humans burn more energy each day than other apes to fuel these traits. this favors fat storage to survive periods of energy shortage
true or false, our bodies have been evolutionarily designed to store energy in the time of plenty?
true, our bodies are primed to store fat
what factors influence this evolution to be good at storing energy and rapidly mobilizing?
- hunter-gathers to civilizations (farming and animal domestication)
- modernization of food products (energy dense) and availability
what is metabolism?
the work your cells do; total energy expenditure
what do our cells do?
pumping molecules into and out of cells
- converting molecules/making DNA/activating enzymes (ex. ovarian cells convert cholesterol into estrogen)
- all of this work requires energy: energy consumed equals the combination of work done, or heat gained:
(ex. throwing a baseball. the kinetic energy of the ball leaving your hand is equal to the amount of work needed to accelerate it)
what is a calories?
one calorie is defined as the energy needed to raise the temperature of 1 milliliter of water by one degree Celsius
is a food calorie the same as the defined calories?
no when talking about food we are talking about kilocalories or 1000 calories. Cheerios have 100 calories but it actually means 100 kcal or 100,000 calories
what are macronutrients?
carbs, fat, proteins
what are micronutrients?
water, minerals, vitamins
about what percent of our calories consumed per day come from carbs?
half
what are the three basic forms of carbohydrates?
sugar, starches, fiber
what happens to sugar and starches?
digested and either burned or stored as glycogen and also can be converted into fat once glycogen stores are full
why do we need to break down fats?
fats are hydrophobic but our body is water based
what do bile acids do?
emulsify lipids into fatty acids and glycerol
how are dietary fats shipped around?
chylomicrons
where do chylomicrons deliver dietary fats?
through the lymphatic system, delivered to target cells such as adipocytes, muscle and liver for repurposing; cell repair and membrane building
is protein a primary source of energy?
no
what do proteins do?
build and rebuild tissues and muscles that break down per day
what are proteins broken down into?
amino acids
how many amino acids are there and how many are essential?
21 amino acids and 9 of them are essential
what do amino acids do?
absorbed into blood and travel to target cells. used to make proteins (enzymes)
how do tissues and molecules breakdown?
breakdown daily and are converted to amino acids and travel to liver and get converted to ammonia then into urea and secreted
how many grams of protein do we need per day?.
around 50 grams of protein each day. exercise increases this amount. we should only eat enough grams of protein to replenish this loss
what happens to excess protein consumed?
the protein is converted into amino acid to ammonia, then urea and then excreted as pee
what is basal metabolic rate?
this the energy your body burns when no physical work, digesting, or temperature regulation is in effect
how does size affect basal metabolic rate?
the bigger you are, the bigger the organs and more cells, and as such more work needs to be done – higher BMR
what has the lowest energy expenditure?
fat
do muscle skin and bone contribute heavily to BMR?
make up the largest organs but are the quietest- muscle accounts for ~42% of body weight but only 16% of BMR
what is the largest contributor to our BMR?
the brain! 60% of BMR
how fast does our heart pump blood?
per minute our heart pumps nearly all the blood in pour body just at rest. can triple during exercise
how does the liver affect BMR?
site of glycogen storage, metabolizes fructose, makes lipids and cholesterol molecules, and performs gluconeogenesis (20% of BMR)
what are the three basic components of energy balance?
- basal metabolic rate (BMR)
- thermic effect of food (TEF)
- activity
How to calculate resting energy? (resting exchange ratio)
CO2 produced/ O2 consumed
what can the resting exchange ratio tell us?
can calcualte the respiratory quotient - fuel metabolism. Can tell what nutrient we are burning
how long can a 250 lbs obese human survive in a fast?
150 days
what was learned from the Hamzda tribe experiment?
Hamzda tribe had higher daily activity, lower blood pressure, and lower BMI. However, when the double-labeled water technique was performed, it was concluded that the Hamzda tribe had the same total energy expenditure. Why?
- people become metabolically efficient
- reduced caloric expenditure on background biology
- hamzda had less inflammatory diseases - lifestyle when not exercising
- when they don’t exercise, they rest, sleep so their activity level drops dramatically
does obesity alter energy expenditure?
yes, as you get bigger you have more energy demand
how do the results change when we account for fat-free mass?
there is no correlation between BMI and energy expenditure
so does obesity affect BMR?
no, it does NOT affect BMR. The number of calories must increase as you get bigger to support body activity and biological processes. Yet the metabolic rate is not changed meaning the rate of how metabolic substrates are broken down are the same. Remember BMR is different than fuel consumption
can exercise change total energy expenditure?
yes, but there is an energy expenditure cap. In response to exercise our bodies become efficient! You can’t overcome obesity
describe the Minnesota starvation study and the conclusions drawn?
- study with 36 participants-military conscientious obejctor
- the goal was to understand the physiological effects of severe and prolonged dietary restriction on body composition
- body weight dropped drastically at the beginning, then remain stable through the starvation stage even when the caloric intake kept decreasing
- after 24 weeks of starvation, body tissue weights and organ weights reduced signifcantly along with higher fluid composition
why is the concept of critical energy needs?
energy HAS to come from a source. So if not from food, it comes from other sources such as fat, tissue, muscle, etc. Thus there is a balance in daily energy expenditure. Too much and we cut into essental reserves
what are nutritional labels based off of?
2000 calories/day recommendation
what was the nutrition labeling and education act of 1990?
extensive surveys done by USDA found men ate about 2000-3000 calories/day and women about 1600-2200 calories/day but NOT accurate. Ignore the complexities of indivudal metabolism and digestion
what are the percentage breakdown of macronutrients that should be consumed?
60% from carbohydrates, 30% from fat, 10% from protein
what are the two main techinques for measuing metabolic rate?
- double-labeled water technique
- direct calorimetry: utilizing an enclosed system to measure the amount of heat this is produced from an individual
what is the mifflin st. jeor equation?
formula that predicts the average dietary intake needed for maintaining energy balance. accounts for age (in years), gender, weight (kg), height (cm) and physical activity (PA factor)
what is the mifflin st. jeor equation for men and women?
men: (10 x weight) + (6.25 x height) - (5 x age) + 5
women: (10 x weight) + (6.25 x height) - (5 x age) - 161
what does the st. jeor equation measure?
used to calculate essential energy: minimal energy needed to maintain metabolic needs
what are the PA factors (physical activity)?
- 1.200 = sedentary
- 1.375 = lightly active
- 1.550 = moderately active
- 1.725 = very active
- 1.900= extra active
how does age affect REE?
as you age and grow older the requirement for energy decreases
- to maintain the same weight, you need to eat less than what you normally consumed
- age is dependent on the number of calories you consume
- as we age our metabolism slows and changes – need to compensate the amount of energy we take in
how does physical activity affect REE?
increased activity/increased expenditure means we need more energy to maintain weight
if calories consumed = calorie lost, body weight is maintained
what calories/day should you set to lose wieght?
reduce the number of calories between BMR and BMR with P. A. DO NOT GO BELOW BMR because of critical energy needs
how did unrestrained eating of Mcdonalds differ from restrained eating?
unrestrained led to gaining 24.5 pounds, 13% body weight increase, increased his cholesterol to 230 mg/dL, experienced mood swings, sexual dysfunction and fatty liver
sticking to a 2000 calories daily diet (below total caloric need), lost 37lbs, lost a total of 21 inches from waists, hips and chest, improved blood chemistry
if you are losing weight rapidly (faster than 1-2 pounds a week) what is normally the cause of this weight loss?
water loss
what is the take-home from the Biggest Loser water experiement?
caloric intake needs to be restrained to maintain a balanced energy regulation
calorie maintenance?
if an individual who was overweight lost weight, he/she would need to consume less calories than that of an individual who is the same body weight to maintain the current weight they are at… this is 20% less calories than the calculated calories
factors that contribute to energy dysregulation?
genetics, social + economic factors, environmental, high intake, low expenditure
social + economic factors?
- income gaps and social class
- limited access to certain foods (more likely nutritious)
- disadvantaged social status can lead to chronic stress which can cause psyiological changes
- stress can also be associated with emotional eating – increased energy consumption/intake
- weight bias + stigma
- modern day ideologies on the ideal body type can induce further stress
reduced energy expenditure?
reduction in the level of physical activity
- decrease in amount of acrtive transportation
- reduced work-related physical activity = more sedentary work life
- less exercise occurrences in leisure time
environmental factors + increased intake
food accessibility
- larger portion sizes
- high availability/convenience of food
western diet & highly processed foods
- higher caloric intake associated with more processed foods when compared with unprocessed ones
increased sedentary lifestlye
lower levels of sleep
what percentage do diet and exercise each make up of weight loss?
70% diet, 30% exercise
true or false, all calories are the same?
true all calories are the same, but not every calorie is created equally (differences in satiety(
what happens when someone is obese and they lose weight?
they’re calories need to decrease by 20% due to metabolic rate changes after weight loss. Reduce calories by 20% or exercise 20% more!!
ex. never obese Bob needs 2000 calories. Obese Rob (250lbs) loses 50 lbs now needs 2000 calories based on BMR and TEE calculation. However, Rob acatually needs 1800 calories to maintain weight. If Rob eats 2000 calories, his weight will increase
how does environment affect our food and obesity?
- food availability
- adaptation to food type and amount
- physical excursion
- temperature
do animals in nature become obese?
great whales
- natural fluctuations in habit and food availability
- accumulate huge fat stores prior to migrating to warmer water to deliver offspring - use this energy while lactating when food supplies are low
- examples of changes in adiposity but no changes in metabolic performance (heart disease, diabetes)
grizzly bear
- during hibernation accumulate huge fat stores prior to colder weather. use this energy while asleep but also for arousal out of hibernation. but again NO change in metabolic perfromance
cavefish
- live in low nutrient environment - total darkenss
- long bouts of starvation and reduced metabolic rate
- insatiable diet when food is available
- do not become obese or metabolically dysfunctional
- mutation in MCR4 gene leading to overeating - human mutation leading to obesity
lionfish
- limited nutrient-stressed environment. eat uncontrollably
- intestinal fat deposits
- liver damage
how can we separate the environemnt grom genetics?
Pima native americans study.
- agriculture-based society, low dietary fat
- trent towards having a higher BMI compared to other cultures
- two distinct populations of Pima Native Americans; one group in mexico one in the United States. creates an environmental difference
- isogenic = pretty much homologous genetically
- arizona pima become obese but northenr mexican Pimas did not
WHY?
- sedentary lifestyle
- western diet
Conclusion: environment plays a role!!
can twin adoption studies help us identify environment vs genes?
genetics:
- found that if biological parents were overweight, children tend to be overweight as well regardless of environment
- correlation of adoptee’s BMI to biological parents not adoptive parents
CONCLUSION: Independent of environment
are we stigmatized into buying or not buying certain foods? for example, is buying local produce/foods is better for you?
benefits
- reduce carbon footprint
- support local business and agriculture
- in season eating
- potentially organic
- less food processing
disadvanatge??
ex. two carrots grown in two separate locations? whats the difference. One imported from mexico, one from upstate NY.
- not many things that are genetically modified
- soil compostition and micronturent composition
iodine deficiency?
- iodine is needed for thyroid hormone production
- body does not make iodine
- before the 1920s, iodine deficiency was common in the Greatlakes, Appalacian MT chain, and NE USA
- goiter = abnormal enlargement of the thyroid = inflammation
What is the solution?
- fortified salt
rickets?
- softening or weakening of the bones due to vitamin D deficiency
- delayed growth, bowlegs, weakenss and spine and bone pain
- decided to supplment milk
Vitamin D
- active form comes from UV sunlight exposure
- fish and eggs
- lack of sunlight
- poor diet due to environment
why is rickets going up again?
- we don’t drink milk as much anymore. prevalence of soy, oat, almond, coconut, cashew milk
- now alternative milk beverage are supplemented with Vitamin D and calcium
- juices are supplemented too
eggs carton labels?
brown eggs cost more money. Why?
- no nutritional differences between shell color
what is the difference between free range and cage free?
- free range: vertical and horizontal movement, access to fresh food and water, continous access to outdoors during laying cycle, enrichment for natural behavior
- cage free: vertical and horizontal movement, access to fresh food and water, enrichment for natural behavior
- USDA organic: free range + organic diet
how does this affect obesity?
- being an informed consumer
- understanding the rationale behind labels and nutrients
- this is our environment
do nutrients play a role in obesity?
- nutrient-poor correlate with obesity
does egg consumption correlate with serum cholesterol levels?
the biggest influence on blood cholesterol level is the mix of fats and carbohydrates in your diet - not the amount of cholesterol you eat from food
meat labeling?
no hormones added
- hormones are NOT allowed in raising hogs or poultry, thus label no hormones added can only be used if followed by the statement that federal regulations prohibit the use of hormones
antibiotic raised meat, poultry, and dairy animals. good or bad?
- raised antibiotic free: the mother can receive antibiotics and the newborn can receive antibioitcs for 1 to 2 days postnatally but never recieve antibiotics again
- but it is against the law to sell meat containing antibiotics so antibiotic free is a misleading term
pasture (grass fed) vs grain fed
- the animal food source could allow for different muscle fat (marbling) type storage. changes in fat types could have different biological utlility in humans
- but dietary research has not shown this nor the food labels articulate a difference
what percentage does research suggest variation in obesity is genetic?
~65%
is there one gene that makes humans obese?
there is no one gene that makes humans obese!
what is the most common gene deficiency related to obesity?
melanocortin 4 receptor deficiency
how can genes control/make fat tissue?
the main idea: DNA genetic material and information is transferred to offspring. changes in the DNA code or gene expression can favor fat storage
what changes our genetic material?
the genetic code and gene expression are impacted by our environment and diet
what is the thrifty gene hypothesis?
evolutionary selection of genes that favor obesity
- exceptionally efficient in the intake and/or utilization of food
what are the reasons for the thrifty gene hypothesis?
- famine has been an ever-present selective pressure on human populations
- it was not unusal for ancestors to undergo periods of feast intermixed with periods of famine
it was assumed that individuals that could store fat in the time of plently could better survive periods of famine and reproduce
- if true then modern humans in a food rich environemnt would become obese
is the thrifty gene hypothesis flawed?
- not enough evolutionary time for natural selection of obese inducing genes
- famines are infrequent and only have occured since civilization (12000 yrs)
- reproduction is low during famines or food scarcity (high mortality and low birth rates)
- why would obeisty genes, knowing that it causes metabolic disorders, be benefical? metabolic orders are a new thing
are famines a strong enough selection? what are the actual effect of famines of metabolic performance?
Dutch Hunger winter:
- Germans food embargo on the Netherlands
researchers examined offspring conceived during this period
- increased likelihood if obesity, type 2 diabetes and early mortality
- 10% increase in mortality by 68 years old
Does this support the thrifty gene hypothesis?
- adverse fetal environment followed by plentiful food in adulthood may be a recipe for adult chronic disease
- but if they were still in famine would this have happened?
ukraine famine: terror famine or holodomor
- millions of peasants were stripped of food
- regions of famine. different levels based on location from severe to non famine regions
- same conclusion: examined offspring conceived during the famine had higher cases of type 2 diabetes
- but way higher in the areas of severe famine
- 1.5x increase in the odds of developing type 2 diabetes in adulthood in individuals born during the famine in the first 6 months of 1934 (tail end of the famine)
- timing points towards early gestation as a critical time window for determining risk of type 2 diabetes
- can transcend generations
do you agree or disagree with the famine data suggesting obesity and metabolic disorders can be inherited?
unsure, maybe we need another generation of the offspring.
dutch hunger winter:
- found changes in methylation statuses (epigenetic regulation) of genes involved in metabolism
what is epigenetic regulation?
above genetics, the branch of biology that studies the casual interactions between genes and their products, which the phenotype into being
- gene regulation independent of DNA base pair sequence changes
DNA strands wrapped around histones
- how tight determines whether chromatin is open or closed which turns on and off gene expression/transcription
- epigenetic marks such as DNA methylation influence the transcription potential of genomic regions and once changed, can result in long term effects
centra dogma
- linear flow of DNA/RNA/protein is overly simplistic
- gene and protein expression is regulated by several layers of epigenetic mechanism resulting in an intricate combination of chromatin accessibility and transcription factor recruitment to coding sequences
- addition of methylation groups which changes the status
How does epigenetics relate to obesity?
lots of epigenetic site implicated in obesity
true or false, nutritional status and diets also impact epigenetics?
true, also composition of diets (high fat, etc)
is obesity inheritable?
evidence for SNPs causing obesity (single nucleotide polymorphism)
- a genetic variation when a single nucleotide is altered and kept through heredity
- depending on the location of the SNP, it could alter gene expression and/or alter protein function
example of an obesity inducing SNP: FTO
- fat mass and obesity associated gene (FTO)
- FTO demethylates RNA
- changing the methylation status on mRNA alters the amount of protein made
- SNPs associated with obesity risk and higher BMIs
- dysregulates genes involved in energy metablosm and adipose tissue homeostasis
but the CDC says: genetic changes in human populations occur too slowly to be responsible for the obesity epidemic
what percentage of type 2 diabetes can be attributed to genetic heritability?
only 10-15%
why focus on taste?
taste changes our preferences and decisions on why we eat
the importance of taste?
- feeding behavior
- palatability of food
- taste preferences - sweet vs bitter
- genetically encoded (taste cues: nutrient density, malady or death)
- learned experiences not innate (exposure reshapes taste sensation)
What can we taste?
- bitter sensing of natural toxins
- sweet energy-rich foods
- sour - taste of acids
- umami- amino acids meat and cheese
- salty electrolyte balance
anatomy of taste of mammals: taste buds
-taste receptors that are bundled into taste buds
- taste receptors that communicate with nerve fibers in your brain
-when taste cells are stimulated, the receptors depolarize and this depolarization is transmitted to the taste nerve fibers resulting in an action potential that is ultimately transmitted to the brain
focus on sweet receptors
T1R2 & T1R3 are activated by a diverse set of stimuli including carbs, sugar alcohols, sweet peptides and proteins, and other small molecule sweetners
mechanism of sweet receptors
- chemoreceptors detects sweetness
- activates G-protein coupled receptor (GPCR)
- GPCR activates the second messenger PLC-B2
- intracellular Ca2+ is released
- opens TRPM4 & TRPM5, leading to membrane depolarization and release of ATP to send signal to brain
- gustatory cortex in the brain is activated
yogurt example: food manufacturers use sugar to enhance flavor and repeat consumption
create an addiction !!
how do sweet taste signals activate reward circuits in the gustatory cortex?
sweet taste signals activate reward circuits int he gustatory cortex and are associated with dopamine release in ventral striatum
What is dopamine?
- a neurotransmitted synthesized de nove in our nervous sytem. feel pleasure; focus; think and plan, strive and interest
- the dopamine system plays a central role in food seeking behaviors, food preference and in the motivation of eat
-chronic exposure to obesogenic diets has been linked to impairments in dopamine syntehsis, release, and receptor function particularly in the striatum
what happens to mice lacking dopmaine?
- decreased survival but could be rescued with L-DOPA (increased body weight)
- dopamine regulates food intake. This study highlights that dopamine is responsible for feeding
do we think obesity induces changes in dopamine altering food perception and eating behavior?
in the obese state, the release of dopamine in response to eating is diminished. Less satisfaction from eating. Thus, you would need to eat more to feel the same satisfaction.
dopamine receptor availability
repression of dopamine receptors in obese people
less dopamine = less reward
- feeling less desired after sweet and salty food
- but this does not mean obese humans are dopamine deficient (like the mice)… what might these data suggest instead
- sensitivity in altered
dopamine and obesity
- less activation of the receptor - could be fewer receptors or less dopamine released
- could mean dopamine receptors are not activated the same way as normal BMI patient
- neurological reprogram that leads to less dopamine release and sensation
do obese humans perceive taste differently?
- for salty foods, the amplitude is similar but obese people do not sustain the sensation for as long as healthy individuals
- for sweets, the amplitude is smaller/depressed
OUTCOME: reward of eating sugar and salty food is dampened
- could cause obese individuals to crave more sweet and salty foods
- could only alter the amount of overeating and not necessarily food preferences
what are the outcomes of what main circuits may be disrupted?
- reward -saliency
- motivation - drive
- learning - conditioning
- inhibitory control - emotional regulation - executive function
What is the Mayer glucostatic theory?
changes in glucose regulate appetite and feeding behavior
Blood glucose experiment
- a decline in blood glucose levels influence appetite
- particularly when arteriole and venous blood glucose levels reach equilibrium
- argues that inadequate delivery of glucose to the brain activates the neurocircuits that drive feeding along with wide-ranging neuroendocrine and autonomic responses
- However, this theory has lost support because of the lack of evidence of any suppression of eating by high glucose availability
what are lower dips in glucose associated with?
associated with hunger and energy intake in HEALTHY individuals
are artificial sweeteners associated with obesity?
- obesity keeps going up and consumption keeps going up
can artificial sweeteners change blood glucose or insulin levels?
no, the consumption of calorie-free beverages sweetened with artificial sweeteners have minimal influences on total daily energy intake, postprandial glucose and insulin compared with a sucrose-sweetened beverage
WHY?
because artificial sweeteners activate your taste buds, this process primes your body for sugar causing your pancreas to secrete insulin… but no sugar ever comes
WHAT COULD THIS MEAN FOR YOUR BODY?
body thinks its in fed state so turns off glycolysis so converts glucose to fat. more hungry/eat more
thus can artificial sweeteners increase the risk for T2D?
depends often on who pays for the study. It is MIXED
age-related weight gain?
- gain 10-25kcal/day
- steady weight gain from 18-24 to 60
levitsky’s law
change in weight = calories in - calories out
is it eating too much or exercising too little?
eating too much!!
obesogenic environment
inducements that create an environment that makes it easy to eat food/gain weight
Search for the hunger and satiety stimuli
GI track
1. ghrelin
2. CCK
3. PYY
4. GLP-1
5. Insulin
6. Leptin
stretch the stomach you feel full and you don’t eat as much (stretch receptors)
- balloons
is eating behavior really controlled by a biological signal?
- eating behavior is modulated by many neurochemicals
- these neurochemicals are not behaviorally specific to eating
- biological theories of eating are based on concept of homeostasis (no evidence that this is accurate)
- rise of hedonics as a major cause of eating behavior (parts of brain light up when you eat foods you like, especially parts of brain that control eating behavior)
- neurochemicals involved in hedonics are similar to eating behavior
- if eating behavior is determined both by a biological stimulus AND hedonic stimuli, how powerful can the biological stimuli be
- biological theories cannot account for:
1. secular trends
2. migration effects - pharmaceutical industry profits
how much do people compensate when you alter away from homeostasis?
mean absolute compensation = 24.5%
- you can change anything about your eating behavior within 25% and you don’t feel a difference
weight scale freshman experiment
the control group gained weight but the experimental group did not
- experimental group were given scales and asked to log weight every day
two-year study of members Cornell wellness center?
lost weight as well
- adult population
how does it work?
reduces the effects of food primes that make us consume a little more energy than we expend
- changes the way we perceive things
testing the effect of negative food primes
- put bowl of popcorn in front of participants
- examine effects of different advertisements
- 1 was car commercial, 1 was food commercial
- negative food prime
- if you watch a food commercial you eat food!
- less than when watching the non-food video
testing stepping on a scale on the effect of positive food primes
- when you had people weigh themselves before seeing the videos, the effects of the commercials are inhibited
priming theory of age-related weight gain
- imprecise energetic compensation
- food priming
positive food priming
a stimulus in the environment that makes us eat
- food is fundamental, if its there you should eat it
how does priming cause overeating?
- seeing food
- portion size
- variety
- social facilitation (more people you eat with the more you eat)
are food primes the cause for age-related weight gain?
- foods eaten at home has gone down and the amount of foods eaten away from home has gone up
- The fat content of food is higher away from home
- portion sizes are larger at restaurants
- eating with more people
- A variety of foods is greater
- more advertisements
hummingbird metabolsim
- one of the fastest metabolisms on the planet
- at the end of each day 40% of the hummingbird’s body weight is fat
- it has fatty liver
- it becomes diabetic with concentration of 700 mg/dl in blood
- but by morning everything is normal
- at night hummingbird goes into hibernation
- sugar is the trigger for hunger, storing fat and becoming diabetic. may be a survival switch
are artificial sweeteners an effective glucose alternative?
- artificial sweeteners primes our body as IF it had glucose and prepares you for your next meal making you overconsume spiking your insulin levels
Does high fat diet (HFD) alter taste?
- mice were fed a HFD for 8 weeks and taste bud abundance was measured
- less taste buds in obese mice (HFD)
What could be happening?
- related to HFD induced inflammation
- less taste receptor stem cell proliferation
- more cell death in response to HFD
Limitations ?
- done in mice not humans
- inhibiting inflammatory pathways could protect against taste bud loss
- could taste buds be restored?
- could allow investigators to test if taste buds control energy intake and food preference?
why do we have taste receptors in gut?
act as nutrient receptors making sure our body has everything we need
- regulate glucose sensitivity: sweet receptors
- sweet receptors in the gut correlate with diabetes
sweet receptors in the gut
sweet taste receptors control peptide secretion which will regulate intestinal glucose uptake and pancreatic insulin release
- sweet taste receptors are located on enteroendocrine cells of the gut
- senses sweet substances and causes the release of Glucagon-Like-Peptide 1 (GLP-1)
- GLP-1 targets the neighboring enterocytes to stimulate glucose uptake from the intestines
- GLP-1 then targets pancreatic beta cells to secrete insuling in response to sweet substances
what do sweet taste receptors mean for artificial sweeteners?
- sweet taste receptors will be activated by artificial sweetners
- causes the release of GLP-1
- GLP-1 targets the neighboring enterocytes to stimulate glucose uptake from the intestines but no sugar to be taken up
- GLP-1 then taergets pancreatic beta cells to secrete insulin in response to sweet substance but again no glcuose to be taken up. might cause a decrease in glucose causing you to eat more next meal
- insulin signaling promotes lipid storgae and lipid biogenesis in the liver
sweet receptors in the gut correlate with type 2 diabetes?
- taste receptors are negatively correlated with blood glucose
- sweet receptors decline
WHY?
- sweet taste receptors recognize glucose
- prepare pancreas for insulin secretion
- if reduced, then less control over insulin therby elevating blood glucose levels
what else do taste receptors do in the gut?
- bitter taste receptors are going to regulate cholecystokinin (CKK) which regulate toxins and food intake
- CCK stops food intake and depends on the CCK-receptor
- when bitter taste receptors, located on enteroendocrine cells, are activated they release CCK
- activates the CCK-receptor located on enterocytes that activate pump transporters that remove toxins for the enterocyte and moves it back into the intestinal track
- activates CCK-receptors located along the vagus nerve which sends a signal back to the brain to stop eating
in mice without CCK, they keep eating but they don’t gain weight… why?
- additionally blood glucose levels don’t change
there must be other things that control food intake besides CCK
ghrelin
- ligand
- ghrelin is produced in the gut
- stimualtes growth hormone (GH) release
- responsive to feeding/fasting state. High levels in fasted state, low levels in fed state
-injections of ghrelin increases weight and promotes hyperphagia, stimulates food intake - ghrelin alters respiratory quotient but not TEE
- respiratory quotient tells what macronutrient we are burning
does ghrelin stimulate food intake in humans?
- measured eating behavior in humans after ghrelin infusion
- when looked at how much food consumed at buffet, the ghrelin patients consumed more food
- ghrelin patients felt more hungry
where in the gut is ghrelin synthesized?
-enteroendocrine cells within the stomach
- post-translationally modified to be secreted
- acylation allows it to leave the cell and have its effect
GOAT (Ghrelin O-acyl-transferase)
- essential for ghrelin acylation - this form of Ghrelin is thought to control food intake
- the GOAT enzyme acts as a nutrient sensor
- in response to fatty acids GOAT becomes activated and modifies Ghrelin
- GOAT uses dietary lipids as substrates for ghrelin acylation
How does ghrelin work?
- circulation and hypothalamic regulation
- crosses blood brain barrier
- binds to neurons of the median eminencne
- activates neurons which induces food intake - vagal nerve stimulation within the gut
- receptors on vagal nerve is bound to ghrelin and supresses electrical activity of the vagal nerve
- this electrical signal reaches the NTS where the signals are transferred to ARC neurons to stimulate food intake
is ghrelin altered in obesity?
obese people have less ghrelin! reduction in blood ghrelin levels.
why?
-obesity is associated with elevated insulin and leptin levels which have been shown to disrupt ghrelin production
- loss of ghrelin reduces growth hormone in obese individuals whcih could be negative feedback onto ghrelin regulation
- physiological adaptations to a positive energy balance associated with obesity could reduce ghrelin levels
would ghrelin mimetics be a good pharmaceutical target?
for type II diabetes to try to change eating behavior
- doing a lot of other things
denotation
descfribe or characterize meaning
connotation
provide positive and/or negative meaning
frame
interpretation that organizes and structures meaning
terms for body weight
- body weight is a complex and dynamic concept with many labels carrying diverse connotations. choosing terms is problematic
person-first language vs. identity first language
a person who is heavy vs. a heavy person
what upstream factors shape energy intake?
psychosociocultural world: thoughts, interactions, relationships, groups, values, organizations, institutions, cultures, societies, etc.
physical world: spatial distances, form of objects
food choice process model
food activities – personal food sytem (value, negotiations, stratgies) – influences (culture, social factors, personal factors) – life course
what are food activites?
the thoughts, feelings and action associated with selecting and consuming food
- not just what people do but also what they think and experience
what are personal systems?
mental processes whereby people translate influences upon their food choices into how and why they eat in particular situations
- personal systems consider and weight values, such as taste, nutrition, convenience, price, relationships, ethics, and other values
what are influences?
factors from past experiences and current situations that shape eating
- types of structural influences include: culture, personal factors, resources, contexts, and social factors
food choice summary
-food choices are made within food systems
- individuals have personal agency to make choices
- systems are structures that determine what foods are available to choose
- structure versus agency is a major dilemma in food choice
food system: subsystems and stages
producer subsystem, consumer subsystem, nutrition subsystem
producer system
food production, processing, distribution
- the food industry focuses on economic profits for providing food to consumers
consumer system
food acquisition, preparation, consumption
-households focus on satisfaction of members by providing foods to eat at meals
nutrition subsystem
food digestion, transport, metabolsim
-people and health professionals focus on keeping their bodies healthy
food insecurity
limited or uncertain availability of nutritionally adequate and safe foods, or limited or uncertain ability to acquire acceptable foods in socially acceptable ways
food insecurity and body weight
- adults who are food insecure have higher weights, especially women
- adults who are severly food insecure have low weights
built environment
are the physical world that is modified by humans including buildings, spaces, and objects
- eye height in grocery stores
- farmers market: healthy choices
