Mid term 1 Flashcards
what is the conversion of kg to lbs
2.2
What are the 2 aspects of energy balance
EI - macronutrients ingested and absorbed Carbs protein fat and alcohol
EE - RMR, TEF thermic effect of food (10%) caloric intake, EEA - energy expenditure of activity
Energy intake - what is the energy content of food calorie and how it is measured
Unit of energy
kcal is kg calorie and is teh energy needed to increse temo of 1 kg of water by 1 degree
energy kcal provided from foods
measured via a direct calormeter
burn food in a bomb calorimeter and see the increase in water temp
Energy content of food - what do we actually care about
I do care about the amount of energy ingested, just about how much of it is available, and useable trackers software like my fitness pal
Pros and cons of software tracking
cons - people lie about what they have had ie social desireability - nutrition facts of food is very different between programs and places hard to standardize - not everyone can metabolize foods the same ie individuals with celiac disease
pros - very convinent and easy dont have to weigh foods dont have to do crazy shit
Atwater factors
the system allocates energy values to food based on the heat of combustion of each group and is corrected for energy loss in digestion absorption and excretion through urine and feces
very debated as lots of variability between the grouyps and different types of CHO PRO FATS in terms of kcal but there is no other alternative
CHO - 4kcal/g - dietary fiber is subtracted from cho before the calorie calulation
Pro 4kcal/g
fat 9kcal/g
alc - 7kcal/g -
these numbers are averages most meals are mixed that include most of them
Atwater specific factors
just understand that content of macronutrients according to thetype of food class ie veg vs animal research is out there and variable reflects that foods of teh same macro can have differnt heat combustions and as a result digestability but we use the average
Coeff of digestability is the energy available/energy of combustion
for CHO and fats its consistently above 90%
for protein its lower as 20% is nitrogen which is excreted and does not contribute to energy
also cant digest fiber so there is less available is not absorbed becuae of fiber or excreted as urea
This is too complex for the general public, so we just use the water factors to estimate
what is an exeption to the atwater fiber thing
know that there is a thing of solunble fiber which is partially fermented and variable which provides some energy when broken down and absorbed in canada its about 2kcal/g or lower with evidence
Food labels
use Atwater factors daily value calculated at an average of 2000 calories a day
Food label intake
take your values Fat pro cho and multiply it by atwater factors to get a breakdown of macros dietrary fiber is already accounted for so do not subtract
summary - additional information fiber energy availibility
dietary fiber can affect the digestability of fats and carbs in a meal
energy availibility can also change due to otehr factors including things like obesity and energy balance that affect gut microbiots
Gut microbiota
good baceria in gut mode of delibery is through vaginal cavity in pregnancy where they deposit onto baby and csection
shown in ultraclean enviroments compared to the past showing changes in gut microbiota less healthy in years to come meaning that eating dirt is good for you
change microbiota via probiotics or stool like poop pills increse in pa means increse in gut microbiota too
Oxidative hiarchy
essentilaly just what gets prioitised to metabolism
intake-expenditure equals what
know that alcohol has 0 ability to store so it gets metabolised first
intake
alc carb pro fate
expendture
alc carbs pro fat
stores
nothing, glycogen , body protein, adipose tissue
autoregulation
perfect, exellent, exellent , poor
Energy intake hiearchy - Carbs
intake and oxidation
tightly controlled need for brain limited storage as muscle glycogen increse muscle and in liver
oxidation influenced by intake more carbs means oxidation goes up
8 hrs following 500g carb intake RER is 1
incresing plasma including increses your carb oxidation and storage and decresed fat oxidataion wont burn as much
Energy intake hierarchy - protein
intake and oxidation
tightly controlled
need
poor capacity to store extra amino acids
increse in protein intake leads to increse in proteiin oxidation
Energy intake hiearchy - fats
- dietary fat is transported by plasma chylomicrons with the FAS found in TG and cleared by adipose tisue via enzyme of LPL
increse in fat in a meal up to 40-50 g does not mean increse in oxidation
need but has a unlimited capacity for storage
energy intake hiearchy - alc
Intake coupled to oxidation
no essential need no storage capaicty
suppresses other duel oxidation
Energy intake hiearchy summary
Alc burned first no storage suppresses others especially fat
excess pro or cho results in crese in their oxidation lim storage and tight control regs
fat is last no reg oxidatioon controlled by ingestion of otehr macros
Does it matter which macronutrients energy come from what about from a EE perspective
prentice study
when in perfect energy balance does not matter fat oxidation is suppressed and carb is incresed and as carb drops fat oxidation will increse
From an EE perspection
-EE is similar no matter what you are using without change in marcro stores but the respiratory quotient does change to reflect which macronutrients are being metabolised
What if you are not in energy balance does it matter then?
- a study we already know - if you overfeed then underfeed carbs or overfeed and underfeed fats, we already know increased carbs increase metabolic decrease fat oxidation. The same goes the other way if you decrease carbs, increased fat oxidation but not to the same extent carbs as a result of this you start to use up your glycogen stores resulting in fatigue over time
What if you are in a positive energy balance
the system is effecivly blind ot the differeence in fat intake when you eat more fat there is slightlky higher metabolism but overal most is stores as you are eating more than expending
Energy intake summary
does it matter where it’s coming from no if it is in balance, but it could influence the respiratory quotient and could have an influence on energy intake, which could influence EE, i.e. feeling less full with cho vs fat, leading to increased intake of you overeat better to overeat carbs than fats
Efficiency of the macronutrient storage
The macronutrient source matters as storage of fat is very efficient if the body has an opportunity to store it will.
What are the 3 things that make up your TDEE and amounts they make up
RMR makes up 60-75% of your TDEE but has low variability this number also goes down the more athletic you are
TEF or DIT thermic effect of food or dietary induced thermogen - makes up about 10 percent of your TDEE
EEA - energy expendiiture of activity made up of your TEE which is your thermic effect of exercise plus your NEAT non exercise activity thermogensis and makes up about 15-30% of your total TDEE but is highly variable
EE in gen is very variable
in peak EE in your 20s and starts to go down as you as a result of decresed muscle mass decresed activity levels
How do we measure TDEE
Many ways best is the doubly labeleed water technique in qhich we substitute water for water isotopes h2 and o18 hydrogen which gets found in your sweat and urine and oxygen as co2
you look at the ratio between hydrogen and oxygen in the urine as the ratio goes down concentration goes down and you are expending more energy
need to have a complete diet record and also you cant replace more than 25% of the bodies water but doing it in small amounts is safe
it is useful in any sporting enviroment as you have equasions to account for themic effect of exercise but they dont take into account contact and hits
another way is direct calorimetry, which is the caloric chamber. the problem with that tho is that it’s not really a free-living situation, as you don’t get to do whatever you want
Low energy availibility
In sports, a lot of the time, your intake will be less than your TDEE, which leads to low energy availabilities, meaning you are not eating enough to combat expenditure, which impacts performance not bad in the short term but does have a lasting effect
RMR vs basal metabolic rate
BMR measurements are taken in dark room upon waking after 8 hrs of sleep and fasting for 12 hrs to ensure digestive system is inactive with subject in reclined position
RMR is taken under less strict enviroments and do not require the individual to spen the nigh sleeping in the test facility
How to measure RMR
Overnigh fast
subject awake
controlled the phase of menteral cycle as it is higher in luteal phase
abstinence from exercise for 12 hrs
resting in a supine positing (laying down) as muscles need to be relaxed
Thermoneutral conditions - temp as close to body temp as possible
What is RMR
The energy needed to sustain life function which at rest
How is RMR measured
Direct calorimitry - heat production = metabolism
indirect calormitry based on analysis of expired gases
can also use preduction formulas but these are not very effective for a single indiviudal
Factors that influence RMR
Weight - increse RMR with an increse in weight - more muscle more RMR as muscle is more metabolically active
age - 1-2 percent decline per decade after 20
gender - higher in ales
genetics
ethnicity
body temp - every 1 degree increse in body temp there is a 12 percent increse in resting RMR
Fitness levels in trained vs untrained athletes, as well as EPOC
Adpative thermogenesis - effect of temp
Thermogenesis - heat production - made up of obligatory and facultative means they both influence metabolic rate
Obligatory hermogenesis - energy required to digest absorb and metabolicze nutrients and is also independent of ambient temp
Faculative thermogene - speciaized form of thermogen that is activated only as a cold defencse mechnanism to maintain body temp
- extra heat produced on demand ot maintain body temp
- shivering (skeletal muscle) switched on and off via nervous system
- brown fat metabolism 0 contains mitochondria that produce energy
Starvation
starvation or what the body thinks starvation is decreses RMR to compensate for it, for example when. dieting fasting or overeating
Your first first loosing weight, RMR and BW are linearly related, if you decrese by 10lbs there is similar known decrese in RMR
However after subsequent weight loss periods there is a drop in RMR that is much lower that what you would expect from the loss of tissue
in a 15 week study using caloric restruction and weight loss drugs they predicted the resting energy expendtiture but in actuality it decresed way more than expected
one short cycle of body weight loss and regain can induce a reduction in TDEE that is much lower than predicted by body weight
what can we conclude about RMR from weight loss interventions
Does it come back? nope not usually after weight loss the decrese in RMR will not come back after you regain the weight, it will stay low
Incresed risk of future obesity, how fast you lose weight is importat
Effect of PA on RMR
Does chronic or acute exercise affect RMR
There is inconsistent data research that has shown increse decrese or equal on the effect to RMR - wont chnage it chornicaaly unless you do it for extended periods of time
RMR and lean body mass
Heart liver kidneys brain make up only about 6 percent of body mass however 60% of your RMR there is also impact from muscle which depends on several factors
chnages in FM and FFm rather than change in heart etc
increse the size of heart steroid preg etc
EPOC
Effect of duraction and intensty of exercise EE increse in first few hours after exercise but can persist for up 2 48 hrs think protein synthesis
if this can last 48 hrs then despite being rested and in a post absortive state RMR will and can be elevated with exercise about a 5 percent increse
TEF or diet induced thermogenesis
The energy needed to digest, absorb, and store is measured via indirect calorimetry or predictive equations, which we don’t like
What influences TEF to change
type of macronutrient - protein requires the most energy because it has to break protein to metabolize it, which requires additional energy TEF will go up with a high protein diet, not by a huge amount, but it will play a role
- exercise - does it rly affect it much no one rly knows the amount of DIt is proportional to the energy protein content less food less DIT
Glycogen depleting exercise may elevate DIT but there are inconsistent reports of that too
we also used to think that obesity was caused by DIT being obstructive or broken but this is not the case
Other factors that may influence DIT Think obligatory
50-75%. of DIT is obligatory so have to have it
it is also higher with protein compared with cho and fats
CHO 5-10%
Fat 3-5%
Pro 20-30 % will be used as energy
also as we get older metabolism slows
also depnds on energy balance, if we are in energy balance, metabolise energy if in positive enegry balance take it and store it how muych energy it takes to store depends on the type of macronutrient ( will be protein as it has to be broken down, carbs can also be stores as body fat, once glycogen stores are full- but needs to change
If 50-75 % of DIT is obligatory the rest can be blockde with adrenergic blocades via the sympathetic nervous system to prevent faculatative
Other factors influencing DIT ( sympathetic nervous
Influences DIT shown that when you block the SNS when earting your RMR goes down about 12 percent
What is EEA
Energy expenditure of activity- made up of the thermic effect of exercise TEE and non-exercise activity thermogenesis - highly variable but around 15-30% of your TDEE
So what is EEA - def of all how is it measured what does it include
Energy needed for all activities (skeletal muscle )
from planned workouts
spontanous activity from NEAT like occupation leaisre sitting standing ambulation
measured via indirect caloirmetry
includes Activity and EPOC
EE for activity how to measure
Many differnt ways for EEA
indirect calorimetry
HEart rate
pedometers accelerometers
questionaires METS
PAL ratio of TDEE: RMR
How to estimate EEA
MET times BW, then multiply it by time in hrs find what the MET equivalent is
Where did MET come from
- Met is 3.5ml/kg/min and is what you are at, at rest
it was done by one single male oen size does not fit all when research was done not a single group had a resting MET of 3.5 no matter the RMR and BMI found that 1 MET is very significanly overestimated
body comp accounted for about 60% of the variability
The energy cost of PA is actually underestimated based on METS
- Met is 3.5ml/kg/min and is what you are at, at rest
What is EEA dependent on and what should we not forget
Freweuncy intensity time type
You also get improvements in efficiency with training so will use Less METS
also EPOC plays a part
and exercise may also affect NEAT - people doing higher levels of activity show potentially that they have lower levels of PA the rest of teh day
NEAT
The energy expended for everything that is not sleeping eating or sports exercise like activities typing yeard ward walking at office fidgeting very variable and large component of TDEE
Best way to measure TDEE
doubly labeled water tech
Study of overfeeding Effect of NEAT
- showed that is was variability in amount of weight gain - increse in fat mass was not related to BMR there was a strong relationship to an incresed activity lto lower change in fat mass but no change in activity led to more fat mass -
Kind of shows the body tries to regulate itself by increasing NEAT as you increase intake to compensate and prevent fat gain, but if that doesn’t happen, then easy fat gets gained
Can you quickly estimate EEA or TDEE
PAL - TDEE/BMR
Lfestyle based prediction for activity levels ie if you are chair bound PAl of 1.2 or things like super strenous work or active leaisiure time up to arounf 2-2.4
Regulation of body weight are we every in balance
No, never - you wake up in the morning you are hungry, then you feel good, then later you are hungry again, so tracking balance in short periods of time doesn’t work only over longer periods
How is balance achived? (theorys 1)
Set point theory
feedback control system that is designed to regulate a particular variable to match a specific target
hypothesis that the body has an internal control mechnism that is a set point that regulates metabolism to maintain a certain level of body fat
Biological control of genes hormones etc
changing one side of the eqasion will lead to a change in the other ie decrese EI body decreses EE to maintain fat mass
theroy has not been proven
How is balance archives (theory 2)
Focused on enviroment and behavior
- a system without active feedback control of food intake and energy expenditure
- The settling point theory was proposed to help explain why overweight and obesity are more than just problems of metabolism, weight loss and gain in most humans are. more related to the patterns of diet and PA that people settle into as habits based on the interaction of their genetic dispositions, learning and environmental cues to behaviour
Steady state - increse in inflow = increse in outflow
Theory - think of like water in a reservoir increse in inflow increse in outflow
Decrese water means decresed outflow where you can resiste continous perturburations within a certain range
perturbations in the components of energy intake or expenditure result in a compensatory change in these components
- passive compensatory changes such as increse in EE with an increse in body size
- active compensation such as change in food intake after expersie
occurs over the longer term and accounts for much of the variability in weight loss with intersice interventions and how individuals compensate for an increse in exercise
Regulation of the system adding a sensory to the system when flow drops turn on
Negative feedback - sending information backwards to the input to close the tap or intake as the float rises
positive feedforward - using that same information, a rising float, the response is to turn up the outflow or expenditure
Body weight regulation
Although generally stable we often see an increse in body weight or fat with age up to a certain degree
variables associated with body fat that may be regulated include:
- body weight fatness
temp
energy intake expenditure and balnce
Homeostatis - maintaining one of the biological reasons we eat or spend energy why do we eat
- long term homeostasis vs short term satiety - meal initiation vs termination when your hungry vs when your full
pleasentness of food - hedonics - reward or conditioning vs avoidance - christmas vs eating shit you dont like so you dont eat
Emergency circuits - hypoglycaemia, stress, inflammtion
body weight regulation Regulation of energy balance does it function in isolation think biological mechanisms
_ doesn function in isolation can be overwhelmed by other needs ie envioromental like going out to drink and someone orders nachos and you eat
What are the issues with the two theories and what is the answer
set point issue - doesnt explain why the worlds set pints have increse over the last 50 years - causeing an obesity epidemic - also contradicted by studies showing that starvation and subsequent refeeding results in even higher body and fat mass
Setting point issue - doesnt take into account biological regulation of weight control
combo of the two, some of the set point, some, but can be ove of the settlingrwhelmed by environment and behaviours and other shit too
How do we measure appetite - Hunger , Satiation, Satiety, Orexigenic, anorexigenic , agonist , antagonist definitions
Hunger - sensations that promote food consumption and is a multidimensional attribute with metabolic sensory and cognitive facets
Satiation - Following initation of a meal eating hunger subsides while satiation which is the sensations that govern meal size and duration become incresingly dominant, feelings of satiation will contribute to cessation of eating and begin a period of abstinence from eating
Satiety - sensations that determine the interval period of fasting are termed satiety
Orexigenic - have a stimulating effect on appetite like ghrelin
Anorexigenic - cause loss of appetite
Agonist - drug of other chemical that can combine with a receptor on a cell to produce a physiologic reaction typical of a naturally occuring substance
Antagonist - a chemical substance that interferes with the physiological action of another, especially by combing with and blocking the nerve receptor
How to measure hunger and appetite
Brain imaging
Biomarkers
Food intake - but doesnt rly reflect appetite
questionaires
all these suffer from limitations
the most common way is the visual analouge sclae or VAS
VAS
measuring appetite most common way - questionaire
How hungry are you right now
how strong is your desire to eat right now
how much could you eat right now
how full are you right now
how strong is your desire to consume sweet or savory food
how thirsty are you right now
its a scle from full to not full at all
Problem: there is a lot of difference between quantification of food between how much inidviduals are when they are normal and between humans there is also social desireability say what they think interviewers want and its also not very standardized so the correlation between VAS and EI are weak/moderate at best
The brain adapts to maintain fat stores
integrates signals from meals and signals from fat stores to regulate EI and EE to maintain stable fat stores
Eating food inhibits the rewarding properties of food
when you starve, the rewarding properties of food increase and the satiety signals decrease
Energy balance regulation
Signals from the body we need to know
What is it, where is it secreted, when is it secreted, and how does it affect EI and EE
Energy balance regulation - leptin
- protein decresed from adipose tissue
leads to a decrese in food intake (anorexigenic) and weight loss
most obses individualsa are leptin resistent - satity hormone that inhibits hunger
Decrease in body fat decreases in leptin increse in body at increse in leptin - if leptin deficient they will lose weight but resistence wont work
But leptin treatment could potentially help with weight loss maintenance eg satiety weight loss may result in insufficient leptin
Energy Balance regulation Insulin
- secreted by the bcells o fthe pancreas and rises in response to glucose load
- crosses blood brain barrier to reduce appeitite or increse EE
if it acts in the brain it would increse EE or reduce appetite but if done in the peripheral can cause hunger and weight gain
less effective in diabetes
Can it regulate appetite or body weight then? - yes depends on things like glucose and where its injected
as weight loss is achived your REE decreses and blood glucose drops and insuling decreses ie lower satiety so its complex that the body has to regulate
Energy balance regulation Ghrelin
- peptide in stomach
- stimulates growth hormone that rises with fasting and falls with feeding
increses your food intake
lack of sleep also promotes ghrelin
Energy balance regulation Peptide YY PYY
- small and large bowel decretion
released after feeding and leads to reduced food intake
as BMI increases, PYY drops obese individuals are deficient
Glucagon like peptide
type 2 diabetes treatment
increse in insulin
now its also approved for weight loss
decrese food intake by incresing satiety
stimulates insulin release and inhibits glucagon release lower blood blucose
secreted with PYY and inhibits feeding
Incretin - increase in the amount of insulin released when glucose levels are normal or particularly when they are elevated stim a decrese in glucose levels
enhance insulin secretion supresses glucagon raises glucose concentration after a meal
surpasses gastic emptying ie delay in amount of time the contents f stomach go into bowel and increses satiety
Cholecystokinin CCK
- gut hormone that inhibits feeding
stimulated digestion of fat secreted by duodenum or small intesine
may synergize leptins action and decrese food intake
shorter-term effect of 30-60 min
What is energy availibility
= dietary energy remaining after exercise availible for other psysiological functions like growth
KNOW
EA = dietary energy intake (kcal-exercise energy expenditure (kcal) /FFM
Why is energy availibility important in sport
- In sport your EE increses but intake usually doesnt usually match this increse for ablance which leads to REDS if not corrected in long time. This results in low energy availibility and also has implications on fertility
sufficient energy availibility and quality of nutrition are essential to support health and desired adaptations
Poor EI is usually the problem for low energy availability it is essential
What is considered LEA (low energy availibility
20kcal/kg/Fm chronicaally gives issues
Moderate is 30kcal/kg/ffm
Adequate is anything 45 adn over
Incresing amoung youth because of body image issues leading to lower EI
LEA
- associated with majority of consequences of REEDS and the feale athlete triad in addiiton to health and performance consequences
Risk factors for developing LEA
- aesthatic weight making or endurance sports
- not incresing intake with incresed training
- attempting to lose weight while training is high (VERY VERY BADshould already be done pre and post season
- inadequate food availibility ie via financial reasons hectic travel schedule and cramped living and cooking spaces
= very busy lifestyles where food is of low priority or disordered eating - lots of others
What sports are at risk for LEA
- sports where athletes aim for comp weight or weight classes
- aesthetic sports like gym and figure skating
- sports where food is excluded ie low fat vegertarian or vegan - things like body building
- most sports can be at risk
cutting must be done very slowly due to RMR
How does LEA occur 2 things
- intenstionally - body weight concerns due to aesthetic or performance related concerns restricted eating can lead to eating diorders energy demand for trainer lowers need enough for all body processes including menstruation
- unintentionally - poor biological regulation that matches intake to EE increased load decreased intake usually appetite suppression
Influence of LEA masking
- effects of LEA on performance may be masked by the huge effect of body weight on performance or may also even result in slight performance gain or stagnation even in LEA lower body weight can imporve performance cuz you are lighter but this is only acutely
LEA can occur at the upper and lower limites of EE
- ie think about the tour de france - who expend 9000-11000 calories per day those athletes have a 8-10 times resting exnergy expentidture than most so how is it possible to eat that much when stren exercuise supresses hunger leads to gi distress - EI higher than amoung they are EE
- elite gynmastics - gynmnasts have menstrual issues - ei well below EE - Belwo sedentary indivduals even through training
reducing EI will also reduce TED and RMR
makes body more effcicent and harder to lose weight
weight cycling loss of muscle mass and REDS
S and S of LEA
- reduced trinign capacity
- repeated injury or illness
- delayed or prolonged recovery time
- change in mood
- failure or loss in weight, reduced low bone density, reduced libido cessation or disruption in the menstrual cycle, and excessive fatigue
Obesity
- excess adiposity in adults lead to metabolic consequences we are not startting to move away from BMI
- it is a increse in body weight due to excessing accumulation of fat this is the definition in canada but now starting to classify it as a disease in some places the
- new def in some places is - a disease in which excess body fat has accumulated such that health may be adversely affected should be able to measure fat content and health status
What did obesity used to be classified as causing what is the reality
- directly causes disease like diabtes hypertension CVD causing PA nutrition and others
- the reality is its a 2 way street - obesity develops subsequently to other diagnoses aswell can cause disease but can also be caused by diseases
Obesity and type 2 diabetes - strong correlation
- T2D- insulin resistence with relative insulin deficiency to a predominate secretory defect with insulin resistance - increse cases of kids with this now
- gestatioal diabetest mellitus - refers to glucose intolerance with onset or first recognition during pregnancy. a key risk factor of it is incresed weight before - 5-20 percent of all preg women
How is t2d diagnosed
- FPG (fasted blood glucose) - changes day to day has a high variability but is it is above or equal to 7mmol/L considered to have it - no caloric intake for atleast 8 hours
HBA1C- is average blood sugar over the last 2-3 months it is more stable than FPG more than or equal to 6.5% - 2HPG in 75G oral glucose tolerance test if more than or equal to 11.1 mmo/L after 2 hrs
- random or tested at any other point in the day if it is more than 11.1Mmol/L
what is diagnoses for pre diabetes
- ust under diagnosis values
- FPG 6.1-6.9
2hPH - 7.8-11
A1c % - 6-6.4
Exercise is the first line of defense against diabetes
Obesity and T2D risk factors
- low PA
aging - risk factros come along with increse in age like sarcopenia less PA and incresed BW - genetics
- obesity (abdominal obesity
- gestational diabtees is a major risk factor for T2D post pregnancy higher risk for next 10 years
- 5-10 % of the population have T2D that have a normal BMI of 18-24.9 this number doubles to 10-20% as they become an overweight or obese population of a BMI over 25
POroposed explination that link obesity and T2D
- occurs chonrically and over time
- increse in adipose tissue across body - adipose tissue is metaboliccaly active and breaks down at same time (not same rate) as it builds up
- when it breaks down it releases more FFA into blood stream
- the more adipose tissue the more FFA gets released which are essential but too many of them starts to impact the liver
- elevated FFA interferes with liver and insulin uptake by liver meaning the liver cant take in as much insulin
- FFA will go into liver to get broken down which would consequently also raise gluconeogenesis so incresed glucose that gets released into system
- increse in glucose in bloodstream means the pancrese will secrete addiitonal insulin to reduce blood glucose back to normal but over time if this occurs for a long time the pancrese gets overworked and the beta cells releasing insulin in the pancrese fail means they cant release as much - leads to hyperglycemia over time then T2d develops
- additionally skeletal muscle has an increse in insulin resistence aswell as a decresed glucose uptake
Obesity and hypertension
- hypertension is systolic bp more tha or equal to 140 and diastolic is above or equal to 90
- obesity and hypertension incresingly recognized as a subtype of hypertension in canada and the EU
- very responsive to weight loss and salt restirction
40 percent of overweight and obese have hypertension
16 percent of normal weight have hypertension
New update for hypertension AHA - systolic above or equal to 130 diastolic above or equal 80 the values stated before are liekly ihgher now too
Hypertension primary secondary
primary - essential like high bp with no obvious underlying cause like aging 90-95% of it
Secondary - caused by other conditions affecting kidneys, arteries or diseases, renal failure, or preg like preeclampsia
Mechanisms of linkage between obesity and hypertension
Sympathetic nervous sysem
- High SNS activity more likely to have hypertension as more signals sent from brain blood vessels to constrict and increse stiffness increse in Bp overall as increse pressure in tube
- people with hypertension have 2 times higher SNS activity
- also higher body weight and fat increses the SNS system - signals still come from brain but they are enhaned by leptin FFA angiotestion from the increse in FFA which all increse the SNS activity
- adipocytes - in a normal person, always have some construction signals and some dilation signals with higher adipose signal to brian via leptin to increase construction signal, but also higher adipocytes also send inflammatory markers like CRP to impact the inner lining of blood vessels that send the dilatory signal because of the inflammation - so you have increase stiffness from SNS that construct it then inflammation because of the adipose tissue over time it degrades thels so you don’t get as much endothelial dialation
Obesity and risk for cancer
cancer - study done starting with no cancer trakc then look to see what they passed away from compare BMI BMi over 40 and normal BMI over 40 risk for cancer death incresed by 52 percent for men and 88 percent for women risk for mortality
Obesity and risk for osteoarthritis
number one preventable risk factor- is it purly mechanical? no cuz its also found in hands fingers etc not just overloaded joints so what is it because of then
- inflammatory enviroment - not due to loading alone.
cytokines lepin adiponectin and strong associations with glucose and lipid disregulation
sedentary lifestyle impacts PA = vicious cyles PA prevents all of this shit
Obseity - abdominal viceral fat and ectopic fat
abdominal - individuals w same BMI can have vastly different health risks - excessive viceral fat around stomach has built up apple or beer belly and carries significant health risks
- viceral fat - hidden stores deep in belly around organs intestines and liver
Ectopic fat - excess adipose tissue not classically associated with adipose tissue storage ie heart and kidneys - significant increse in risk of cardiometabolic disease but it is responsiev to exercise
SLeep and obesity
- as number of hrs of sleep goes down BMI goes up and opposite is true too
study - less than 7 hrs sleep have higher BMI but also some studies show more than 9 also have higher BMI not as proven so stick with the other one
another study - sleep deprivation increses food intake in rats and humans shorten sleep for 2 days led to increse in appetite especially for sweet salty and starchy foods by a lot
Sleep and obesity - apnea
- associated with poor cardiovascular health wake up multiple times a nigh and end up being very tires less healthy food intake and less active during the day obesity also leads to it because of an increse in weight so it is bidirectional
shortened sleep also led to an increse in apetite especially in foods that were startchy salty or sweet by a lot
Sleep and obesity - biological mechanisms
- shorter sleep decreed leptin and incresed ghrelin led to hunger just after 2 days of sleep deprivation - measured hunger via the likehart sclae
aslo a positive correlation as hunger goes up biological mechanisms that are leading incresed in appetite are also going up
Stress and obesity - cortisol
- stress hormone short term can be beneficial like saise the SNS raise heart rate raise bp fight or flight but not good long term
- it is also the most potent glucocorticoid and casues insulin resistence
can be measured with saliva samples or through blood, but the blood draw can increase cortisol artificially for the short term, so saliva is better to measure better using a hair sample, but it can died
Stress and obesity - Cushing syndrome - cortisol
- excess cortisol of any cause stuff like stress from exams or life not likely to cause it but more so like medications that raise cortisol levels as you start to produce higher levels of coritsol over time and high levels of cortisol is associated with abdominal obesity over time incresed for hypertention dislipidemia hyperglycemia and insulin resistence which all leads to cardiovascular disease T2DM
Stress and obesity - cortisol - reduce it
- Exercise and sleep best way
- not everuone responds to stress in same way 40 percent gain weight 40 percent lose and 20 stay stable theere are biological mechisms behind these if yo uare someone that already obese than more likely to dall into the weight gainer category
study = - control group no stress high reactor day and low reactor or cortisol ate same amoutn but those that underwent stress the high reactor cortisol group raised their caloric inatke and low reactor group ate less shows a functional response and those that were in the high reatcor section shower a greater preference for high fat and higher sugery foods
high vs low reactor is a biological mechanism that can slightly change that, but it is hard
Epigenetics and obesity
- expression of genes through the enviroment
there is a genetic component but it is much less than we originally though
study - offspring of both obese one obese and adopted parents if both not them lower BMI than if both obese
but there is also a big enviromental component if they were raised by adopted then it stayes relatively the same
study - MZ twins - genetically identical - assessing ECWN - calories needed to maintain gaigh gave them surplus kept sedentay body weight incresed and RMR incresed but there were differences in the twins some gained half of what the oteher gained which suggest behavioral factors like NEAT was incresed in the ones that gained less
- they did see more genetic influence on viceral fat in both twins tho so visercal fat very heavily linked ot genetic CVD etc
Same study but deficit - tight relationsip in weight loss but a stronger relationship of viceral fat loss so shows that you can reduce viceral fat by exercise and it is one of the best ways to reduce this fat the reason its much tighter is beacuase if you are already exercising a lot NEAT becomes less of a factor
Genetics and epigenetics terms
- mendelian disease - direct transmisison
Oligiogenes - a gene that significantly affects a hertiable charectistic
poly gene - a gene that has small effect heritable charectistcs
Gene - gene interactions
- another level of complexity in biological individuality and takes place at the interaction between genes
expression of one gene affects the expression of another gene if you have two genes that predispose you to obesity, they can interact and make your chances higher
Gene - enviroment interactions
- constant interactions are taking place between genes and sequence variations in such genes including all kinds of factors in enviroment which necessitate a cellular response
- very clear that such interactions exist for obesity phenotypes even though few studies have actually addressed the issue
Predisposiotion to obesity in an obesogenic enviroment
- high availibility of food leads to less exercise more predisposed to obesity
Epigenetics
- the study of cellular mechanims that modify gene expression without changing the underlying DNA sequence
- may occur during a lifetume or can be passed onto the next generation
- enviromental influences changing expression of that particular gene
- often done through pregnancy
Obesity in youth
- how to define it - youth classification systems differ most now use BMI center for disease control and prevention growth charts age and sex based percentile cut off points
- 85 centiles of BMI at risk for overweight and 95th centiles of BMI overweight
- you look at the growth curves y axis of bmi and age of years is x where the children start off vs where they end up and track over time
- dont give kids a specific BMI look at percentiles as they shoot up in height and extreme growth occurs
- slightly diff for males and females
The critical period for obesity in youth - prenatal infancy
- affect epigenetic expression of different of different genes.
- birthweight
- birthweight early life nutrition - relationship between birth weight and adult BMI is j shaped or U shaped, ave birthweight associated w average adult BMI born heavy or super ligh incresed risk
-breastfeeding - may be associated with slightly lower BMI throughout life also improved health outcomes - also good for mother reduced risk of CVD
- birthweight early life nutrition - relationship between birth weight and adult BMI is j shaped or U shaped, ave birthweight associated w average adult BMI born heavy or super ligh incresed risk
- smoking higher BMI in childhood
- exercise - lower rates of high birth weight but longer term studies are still needed
- preg complications GDM - vs preclampsia incresed BP and organ damage
Dutch famine study
- events occuring in pregnany have lifelong effects on the child showes that child exposed to famine in trimester 1 or 2 incresed risk of obesity at 19 years where as ifther exposed during trimester 3 that had a lower rate of obeisty
- there is also recommended amounts of weight gain during differnt points in pregnancy
early excessive weight gain may alter utero envorment to promote obesity early GWG has been linked to gestational diabtes post partum weight restention and childhood obeisty
exercise is associated with a large decrese in risk of large baby
Obesity guidelines (prevalance
- large prevalance of obesity in canada and only growting more over time
What has changed in obesity since 2007
- declaration of obesity as a chornic disease because it is a very complex medical condition
because there is significant bias stigma and weight discriination
advances in the sciirnce f obesity and weigght regulation like how does it occur
advances in obesity treatent and therapies bariatric surgery meds etc
recognition of petient centered care and outcomes beyond weight loss different people can be different weight and be different levels of health
Definition of obesity
- previously defined as BMI and not health
- defined as a prevalent complex progressing and relapsing chronic disease characterized by abnormal or excessive body fat adiposity that impairs health
- BMI and waist circumference can be used as screening tools
diagnosis shoul dbe based on the presense of functional mediucal or psychosocial impairmenrs related to presense of abnormale or excess body fat rather than on antropometrics alone
- BMI and waist circumference can be used as screening tools
- should be managed using evidence based chronic disease management pronciples validate patients lived experiences move beyond the simplistic approaches of just eating less and move more and address the root drivers of obesity
- people who are living with obesity should have access to evidence-informed interventions, which should include medical nutrition therapy, PA psychological interventions, and pharmacotherapy
recognizing and addressing weight bias
- people living w obesity face substantial bias and stima which directly impacts their health and well being as well as access to care
- health care providers should assess their own beliefs and attitudes towards people lying with obesity and how these may influence health care delivery
health care providers should be aware that internalized weight bias ie the attitudes of people living with obesity towards themselves can adversley affect behavior and health outcome
- health care providers should assess their own beliefs and attitudes towards people lying with obesity and how these may influence health care delivery
- avoid using judgemental words images and practices when working with patients living w obesity
- avoid assumptions that an ailment of complaint a patient presents w is related to their body weight
What is success in weight
- prevention of weight gain - gian about 1 lb per yea r
- losing weight
maintaining weight - success is based on each person all three goals you need to understand energy balance
What is clinically significant weight lsos
- more than 5 percent of baseline body weight
- leads to reduction in CVD and T2DM and achive this by diet exercise meds surgery or combo
general guidelines for weight loss
- min threshold to prevent weightgain according to ACSM is 150-250 min of PA a week to preevnt weight gain greater than 3 percent
= need to ensure that there is not too much of an energy imbalance so with increse of EE and decresed EI to a extent
= resistence training is not effective for weight loss but it is important for lowering adipose tissue and keeping muscle mass you never want to lose muecle as you cant get it back as easily - it is possible to maintain energy balance in a state of low energy fluc ie low EI or low EE as you get satiety signals and with too much of an energy imabalnce leads to preference for sweet and high fat foods
can also be influenced by outside factors like social thinking, going out, and getting offered food
Weight loss vs fat loss study
- know that diet leads to large decrese in body weight and fat mass butu also large decrese in muscle mass not good
exercise alone leads to decrese in body weight fat mass and a matienence in muscle
diet and exercise toegther leads to lower body weight decresed fat mass and less muscle mass lost overall
How is exercise often described
- FIIT
- in addition to someones body weight the total volume of PA determines the amount of EE volume as frequency times time
Incresing EE for weight loss
Works because
- effect on energy baalnce is proportional to increse in EE
- increase in fat and CHo oxidation would be expected to have favourable health consequences
Would not work becasue
- achiveable amounts of exercise leads to just a small increse in EE
- adhereance to changes in exercise and PA is poor
- increasing EE could also be linked to a compensatory increase in EE
Increasing EE for weight loss studies - volume and bouts
- Research shwon that as more volume and more intensity that there is a greater reducion in body weight - as volume activity and EE increse concurrent reduction in fat mass occurs both groups lost weight but they also maintained their mucslce mass meaning its high quality weight loss and it is greater when volume of activity is greater
- another study for short and long bouts of activity to lose weigth resulted in similar amount of weight regain after but making it adhereance is very important so make it accesable
Increasing intensity for weight loss
Why it works
- same EE in less time
greater imporvments in fitness and other risk factors
greater preservation of FFM
decresed appetite after high intensity exercise
variety and more enjoyable for some
Why it would not work
- less enjoyable
less acceable
greater risk and saftey concersn
less self-efficacy - belief in the ability to perform such activities
Incresing intensity for weight loss what is that best
- low intensity exercise maximises fat oxidation vs high intensity exercise like HIIIT influences EPOC factors metabolizing primarily CHO
intensity that leads to highest EE
The proportion of glycogen triglycerides FFA and glucose changes as intensity changes the relative amount is the percent of total EE at low intensity the highest relative fat oxidation is at 25 % of max intensity but for absolute the greatest fat oxidation is at 65% intenisty and the greatest caloric expenditure is at 85% - overall vol of activity is the same for both groups but intensity changed and showed a greater decrese in fat with vigourous but also a greater increse in lean muscle mass with vig intensity exercise
HIIT loses more weigh than moderate factors like EPOC endorphin release and evidence that HIIT causes a decrese in appetite after high intensity affects this
What really matterns in terms of weight loss
- adhereance to the plan - if you dont do the work nothing will happen have to stick to it most important part minimize cost remove barriers simplifying plans and reminders
Role of resistance training in weight loss
- increse in muscle mass is the number 1 predictor of function in later life
- it would work because you get increses in RMR increses in fat oxidation increse EE increse in muscle mass if you have that muscle you can walk up stairs you can stay active for longer incresed TDEE lose body FFM
why it would not work - effect on FFM is small
- effect on FFm during energy restriction dieting is even smaller therfort effect on RMR is not meaninful
- energy cost of resistence training is small
- there is not much evidence BUT it may be more important in certain pop like older adults to prevent the FFM loss that comes with dieting
- critical to maintaining function as diet alone has a high risk of muscle mass loss, which is hard to get back once it’s gone
Resistence training for weight loss
- not very effective for weight loss alone
- can contribute to change in body comp
- can be important for certain populations
- imporved metabolism
- maintence of function
Exercise for class 2 and 3 obesity why it works
- why it works
- contribute to negative energy balance
- imporve health and the QOL
- imporved response to bariatric surgery
why it would not work - fitness too low to achive meainful EE
- too many comorbidities that could be worsened by exercise like joint pain
- time for exercise and fatigue from exercise could interfere with other activities
Not everyone responds the same to weight loss for classes 2 and 3
- becasuse of adherence compensatory factors and otehr factors
Things to consider for exercise for class 2 and 3
- access to facility
access to equipment
adapted exercise
adapted places to sit and changing facilities
PA for clas 2 and 3 obesity
- aerobic activity 30-60 min for small amounts of body weight and fat loss
- reduction in abdominal viceral fat weight matienence incersed cardio and fitness
Beyond weight loss what are the other advantages for PA
- fitness stay functional longer
- QOL independecnce imporvements in fat distribution or quality
- prevention of weight gain from body comp
- in individuals w low fitness have twice the risk of feath
exercise capaicty was the strongest predictor of death VO@max - increse of 1 MET meant an increse of 12% improvemnt in survival
absolute fitness is a better predictor - it doesnt matter how you lost the weight but it does matter how you keep it off to prevent regain
Sport performance - why its important
- tailored nutrition
energy management
recovery and growth
Weight management and disease prevention
- not just cal in vs cal out - metabolic impacts and pa and nutrition on disease
Communication for research
- research publically funded most scientists have limited training and do it poorly
theres lots of different types of science communicators and ways to distribute infomration sport and wellness is huge but based on limited infomration fad diets harming health
How to spot bad science 12 ways (1-6)
- sensationalised headlines - simples headlines that can get misinterpreted
- misinterpreted results - news articles distort info for story read original research
- conflicts of interest companies employ people to publish research can be for personal or financial gain
- correlation and causation - correlation not equal causation
- unsupported conclusion - speculative language needs to be clear
- problems with sample size - smaller the sample lower the confidence
