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Health at every size
weight inclusive framework that supports health promoting behaviours equitable care for people of all body sizes without weight loss being the goal of care
emphasis on care, anti-fat bias, bodily autonomy, social determinants of health
Weight centric approach
goal for weight loss and bmi in normal range
measures change on scale
views weight as controllable through individual effort
practitioner role is to perscribe an energy deficit and monitor weight
concerns are weight cycling, stigma and disordered eating
Weight inclusive approach
focus on health behaviours and well being
measures clinical markers, function, quality of life and eating behaviours
views body weight as genetic, environmental and social and economic factors to shape
practitioner role to collaborate on goals the client chooses
main concerns raised is that it might underaddress the weight relaated risk if applied ridgidly
4 principles of HAES
access
healthcare is a right at all sizes
wellbeing
care, healing are collective and deeply personal
bias free care
care provided only when free from anti-fat bias
Context
sociopolitical construct reflecting on societies values
bais and stigma
document among health professionals including dietitians and nutrition students
associated with
results in delaying or avoiding healthcare
shorter visits and less patient education
poorer mental health
physiological stress and weight gain
HAES take home message
produced similar cardiometabilic and anthropometric outcomes
the individual needs different approaches
susceptibility to hunger improved with HAES
Disordered eating
range of unhealthy thoughts and behaviours related to food, exercise, body image
restrictive eating
food and excecise routines driven by feeling unworthy
obsessive food thoughts and feeling out of control around food
binge eating
emotional distress when food or exercise rules are broken
Between normal eating and diagnosed EDs
Difference between disordered eating and eating disorders
frequency and severity of symptoms
Physical signs/symtoms of EDs
disiness
fainting
hair and skin changes
weight fluctuations
dental problems
seizures
chest pains
Compromised organ systems of disordered eating
digestive issues
immune dysfunction (sick often)
irregular menstrual patterns
CVD dysfunction
orthostatis hypotension
bradycardia (slow heart rate)
Biochemical signs of disordered eating
low iron, anemia
hormonal imbalances
electrolyte disturbances
hypokalemia from purging (loss of potassium)
Blood sugar irregularities
Mood changes of disordered eating
irritability
low mood and anxiety
undernutrition will exaxerbate depression and anxiety symptoms
complications of mental health treatement
Cognitive changes with disordered eating
food preoccupation
difficulty concentrating or brain fog
socially withdrawn especially from food events
Behavioural cues of disordered eating
skipping meals, diet pills etc
binge eating with a loss of control around food and marked emotional distress
strong need to control food and avoiding non homemade foods
compensatory behaviours to make up for eating
extra excercise, food restriction, purging
body checking
rigid food and excercise patterns
frequent discussion of weight, shape and diet
self worth attached to food, exercise and body image
Risk factors of ED
trauma
copign mechanism to feel in control after feeling helpless
emotional distress and limited healthy coping skills and starvation can numb, binging to soothe, purging and stress
gender dysphoria to minimize unwanted physical changes
perfectism, strong drive and competiveness
mental health
family history
occupationa nd activities whcih push for physical attributes
cultural ideas that promote certain bodies as more worthy
Avoidant/restrictive food intake disorder (ARFID)
food behaviour not driven by weight or body concerns
Low interest in eating
eating feels liek a chore and meals can be forgotten and unfinished
Sensory sensitivity
strong aversions to smells or looks of food which can limit the range of foods they want to eat
Fear of consequences
fear of chocking, vomiting, allergic reactions etc
Clinical significance of ARFID
limited intake or variety can cause nutritional gaps, reliance on supplements or impared daily life
presentations can overlap and treatment is specific and supported food exposures
Inpatient ED treatment programs
Highest level of care
based on medical instability and rate of weight loss and overall risk
bradycardia, hypotension, electrolyte abnormalities
Structure: supervised meals and snacks, medical monitoring, individual and group therapy
Goal: medical stabilization and interruption of symptoms
limited psychoeducation at the time
Outpatient ed treatment
appropriate for medically stable individuals with ongoing medical monitoring
group based cognitive behavioural therapy for eating disorders with nutrition guidance from RD
Goal: To improve the relationship with food, eliminate symptoms, learn healthy coping skills and body image work
Child and adolescent family based treatments
parents and caregivers are active responsibility for meals and weight restoration
Phases
full parental control
gradual return of control to adolescent
focus on normal adolescent development and relapse prevention
evidence: strongest research for anorexia adapted for other disorders
empower family to be primary support system and reduce blame
Nutrition education for ED
plate by plate approach
why diets dont work
understanding body needs
reframing unhelpful thought patterns around food
Set point theories
understanding weight regulation in bodies
explaining weight restoration goals
Center for clinical intervention is a good set point resource
Energy expeinditure
energy expended in one day is the total energy expenditure divided into resting energy expenditure (REE) Thermic effect of food and physical activity
Resting energy expenditure
what is required to sustain life keeping vital organs functioning
60-75% of 24 hour energy expenditure
around 1 kcal/kg body weight / hour
most significant determinant is the lean body or fat free mass
REE is higher in those with higher lean body mass
can be measured as long as the subject has rested for 30 minutes before the test
Basal energy expenditure
lowest rate of energy expenditure in an individual
measure din a post absorptive state (no food in 12-24 hours)
lying motionless on your back
Factors affecting resting energy expenditure
lean body mass (muscle and tissues are more metabolically active than adipose
Male sex is higher than females
body temperature
increases REE with elevated body temperature
age
REE decreases by 2% every decade after 30 years old even after adjustign for changes in lean body mass
Energy restriction
after several weeks of energy restriction the REE declines whcih is the reason for plateau with diets
Genetics and endocrine
hypothyroid and hyperthryoid decrease or increase REE
metabolic stress and just can increase REE
Factors effecting regulation of energy balance
nervous system and hormones produced by gut pancreas and fat
genetics also influences energy balance and body weight
decrease in energy intake and loss of fat mass is orexigenic neural and hormonal stimuli that increases appetite and decreases REE
increase in energy intake and body fat results in anorexigenic stimuli to decrease appetite and increases energy expenditure known as adaptive thermogenesis
Adaptive thermogenesis
the increase in energy expenditure that occurs with increased body fat
Neurochemicals that decrease appetite and food intake
cholecyclokinin
GLP-1
Peptide YY
glucagon
insulin and amylin
Neurochemicals that increase appetite and food intake
ghrelin
Prader-willi syndrome
genetic disorder that presents with voracious appetite and massive obesity
ghrelin levels are increased significantly
Adipocytes
large round cell filled with triglyceride
cytoplasm containing nucleus, mitochondria and organelles is small below plasma membrane
when found in large aggregations in conjunction with fibrous connective tissue they form adipose tissue
Adipose tissue
storage site for over 90% of the body energy reserves
fills body crevices and provides thermal insulation to body
surrounds organs and forms shelter
White adipose tissue
primary form of adipose
light yellow colour due to carotenoids
comes from dietary fats through lipogenesis
Brown adipose tissue
more mitochondria causing darker colour and blood vessels
responsible for diet induced thermogenesis
Adiponectin signals
that the body has the capacity to store fat
increase as body fat content decreases
improve body sensitivity to insulin increasing capacity to store fat
high levels associated with lower risk of coronary artery disease
low levels associated with obesity and comorbidities
Leptin signals
there is adequate fat stored
increase as the body fat mass increases
regulate reproduction by promoting fertility and initiating puberty when body energy stores are adequate
Adipose tissue mass increasing
when mature adipocytes increase in size
hypertrophy
accumulate more tyiglyceride when there is energy intake above expenditure
Increase in number
hyperplasia
immature adipocytes divide to produce more cells
Body fat distribution
abrominal and central fat
primarily around abdomen surrounding organs
often in males
android
Lower body fat distribution
mainly in lower region
hips and thighs
more orgen in females
gynoid
Abdominal fat placement
surrounding intestines and liver increases risk of T2D
fatty liver, hypertension, dyslipidemia, CHD, metabolic syndrome
even if BMI is within healthy range
Lower body fat distribution
not associated with the increase health risks
some data showing that it is inversely related to CVD and diabetes
Obesity redefining
before defined as BMI > 30kg/M²
now defined as chronic, progressive and replapsing disease characterized by presence of abnormal or excess adiposity that impairs health and social wellbeing
Obesity causes
genetic components
hypothalamic regulation affected by
genetics, microbiome, gut hormones
adipose tissue hormones
enviornemnt, medication, chronic stress
Genetic and weight factors
40-70% of variation in weight gain
50 genes are associated with weight gain
appetite regulation
satiety cues
energy expenditure
fat tistribution
Congenital causes of obesity
genetic disorders with obesity as a feature along with developmental, neurological or structural abnormalities
prader-willi, downsyndrome
Bardet-bidel syndrome, cohen, carpenter
Neuroendocrine disorders
hormonal/metabolic conditions where dysregulation of cortisol, thyroid, reproductive or growth hormones contributes to obesity
cushings syndrome
hypothalamic disorders
hypothyroidism
PCOS
growth hormone deficiency
Medical causes
antidepressants
anti-diabetic medicatins
insulin promoting fat deposition
antipsychotis
anticovnulsants
contraceptives
projesterone medications
chronic inflammatory conditions
glucocorticoidsd
AIDS treatement
Mental health and weight obesity prevelence
25-60% for bipolar
30-60% schizophrenia
20-50% depression
Mental health and weight
screen for mental health in individuals working on weight management
look at medication side effects
severe mental illness who gain weight on anti-psychotics
GLP-1 agonists have the most safety and efficacy amond medications indicated for chronic obesity management in canada
Weight bias
negative attitudes and views abotu obesity and people with obesity
weight stigma
labellign people livign with obesity based on deep rooted social stereotypes
makign assumptions about people with obesity
Weight-based discrimination
treating people different or unfail based on weight
verbal, physical and relational discrimination
Widespread bias on weight discrimination
belief that obese people are lazy, noncompliant, undisciplined, lack of willpower and self control
impacts:
hiring decisions
education opportunities
health care decisions
housing selection
adoption selection
airline policies etc
Reducing weight bias in obesity management
assess own attitudes and beliefs regarding obesity considering how their attitudes and beliefs can influence care delivery
recognize internalized weight bias (towards oneself) in people living with obesity can affect behavioural health outcomes
healthcare providers avoid usign judgemental words, images and practices with patients with obesity
avoid making assumptions that an ailment or complaint a patient presents is related to their body
Obesity canada practice guidelines 2020
BMI not used for diagnosis
comprehensive medical assessment required
not all people with high BMI have obesity
everyone should practice healthy behaviours
weight loss is not the main goal
no longer recommending caloric deficite amoutns
recommending individual nutrition interventions
healthy eating focus
health based outcomes
recognize the harm of weight stigma, bias and discrimination
recommends healthcare professionals assess theri own bais
Weight spectrum practices
weight centric
fad diets, extreme weight loss plans, weight loss for thinness
Non-weight weight inclusive approach
HAES
critical fat studies
health improvement regardless of weight
4 Ms of obesity
mental health
mechanical health
metabolic health
monetary health
FACTORS CONTRIBUTING TO PREDISPOSITION
4Ms of obesity Mental health
cognition
depression
ADHD
addiction
psychosis
ED
Trauma
Insomnia
isolation/social spport
Therapy access
4Ms of obesity Mechanical health
sleep apnea
osteoarthritis
chronic pain
reflux disease
incontinence
thrombosis
inertrigo
plantar fasciitis
injury
4Ms of obesity Metbaolic health
T2D
dyslipidemia
hypertension
fatty liver
Gout
PCOS
gallstones
cancer
medical side effects
Malnutrition
4Ms of obesity Monetary health
education
employment
income
disability
insurance
benefits
bariatric supplies
weight loss programs
access to therapy
food environment
5 As of obesity assessment
Ask
is client interest in nutrition changes
Advise
provide key nutrition messages for all adults
individuals preferences, values, goals culturall acessible affordable and sustainable
person first language, weight inclusive non diet approaches
Ask and assess
does patient want to make more changes
Agree and assist
explore options, collaborative care
monitor and evaluate health related outcomes
health behaviours, nutrition status quality of life, CVD, metabolic and functional status
Reassess intervention, plan, readiness, barriers and supports
Explore and assist other options with patient and client as needed
General assessment of people living with obesity
comprehensive history to identify root causes of weight gain and complications of obesity and barriers to treatment
recommended blood pressure measurement in both arms
fasting glucose or glycated hemoglobin and lipid profile to determine the cardiometabolic risk and where appropriate ALT test to screen for non alcoholic fatty liver disease
EOSS: Edmonton obesity staging system
used to determine severity of obesity
shows stages related to risk of comorbidities
better predictor of all cause mortality when compared with BMI or waist cricumference measurement alone
Micronutrient deficiencies
B12, iron, vitamin D
because of restrictive diets, medications or bariatric surgery
Mindful eating practices
lower food cravings
reduce reward driven eating
improve body satisfaction
improve awareness of hunger and satiety
Nutrition physical exminatino
look for edema, skin, hair, eyes, oral cavity
Nutrition assessment weight history
age of onset obesity and major weight trajectories
previous weight loss attempts in response to interventions
highest and lowest weight
major life events associated with weight change
current phase of weight
height
current weight
IBW and ABW are only used in critically ill populations
Nutrition assessment nutrition history
assess nutrition literacy
assess energy intake
identify nutritional restrictions (celiac, allergies)
24 horu recall, FFQ
focus on portion sizes, meals away from home, preparation methods, energy density
Alcohol, vitamin, mineral supplements
previous weight loss methods
nutrition education and nutrition therapy
food restructuions and eating patterns
Estimating energy and protein needs in general non-critically ill patients
indirect calorimetry = gold standard
if not available
Predictive Mifflin- St Jeor equation usign actual body weight
greater error at higher BMI
individualize based on clinical condition, goals and response
protein estimation using actual weight
Estimating energy and protein needs in critically ill adults with obesity
BMI 30-50: 11-14kcal/kg actual BW/day
BMI > 50: 22-25 kcal/kg IBW/day
Protein
BMI 30-40: 2g/kg IBW/day
BMI >40 up to 2.5g/kg IBW/day
Micronutrient of concern Vitamin D
deficiency risks
elevatid adoposity (could be in adoipose)
medical conditions assoicated with fat malabsorption
chrons, ulcerative colotis
celiac
liver disease, CF, short bowel syndrome
previous bariatric surgery
low intake of calcium rich foods
limited sun exporusre
darker skin pigments
Drug interactions
corticosteroids
orlistat
cholestyramine
phenobarbital
phenytoin
Vitamin B12 nutrient of concern
deficiency risks
elevated adiposity
Medical conditions
IBD, T2D
GERD
Pernicious anemia
alcoholism
Restrictive eating patterns
Previous bariatric surgery
Drug interactions
metformin
proton-pump inhibitors
Iron nutrient of concern
Deficiency risks
elevated adoposity
medical conditions
chrons disease, ulcerative cholitis
celiac, liver disease, peptic ulcrs, chronic kidney disease
Restrictive eating patterns
frequent blood donatino
blood loss
previous bariatric surgery
Biochemical assessment
Vitamin D commonly low in obestiy
iron studies: risk of deficiency, poor intake, inflammation, bariatric surgery
Vitamin B12, folate
low with metformin, baratric surgery, anemia, neiropathy risk
Diet therapy
recommended that a non dieting approach is taken to improve the quality of life and psychological outcomes
choosing dietary patterns and food approaches based on best long term adherence
Nutrition intervention
follow individualized care
food based approaches
dietary patterns
intensive lifestyle interventions including behaviour modification
Diet therapy calorie restriction
emphasis on variable macronutrient distribution ranges
lowerm moderate or higher carb with variable protein and fat
achieve body weight eduction over 6-12 months
can achieve short term weight reduction but is not sustainable long term
set point theory
Very low cal diets have not been shown to be sustainable and VLCDs are effective onlywhen used with behaviourla support
oftne regain at 12 months
may permanently impact neurobiological pathways affecting appetite control and weight regulation
Healthy eating pattern: Med diet
meet nutrient needs
promote weight loss
include physical activity
no supplement requirment
promote behaviour change
scientific backing
reduces risk of CVD and T2D and increase reversion of metabolic syndrom with little effect on body weight and waist circumference
DASH diet
low in
sat fats
cholesterol
total fat
sodium of 2300mg
emphasis on fruits and vegetables
low fat diary
whole grains
fish, poultry and nuts
improving blood pressure, established lipid targets
glycemic control and reduced risk of T2D, CVD, coronary heard disease and stroke
Glycemic index
ranking carb foods based on how much they increase BG Levels
green
low GI 55 or less
Yellow
Medium GI 56-69
Red
high GI of 70+
GI foods
focus on quality carbs
whole grains, legumes, vegetables and fruuits over refined carbs
pair carbs with protein and fats to lower the GI
encourage portion awareness
The portfolio diet
cholesterol focus
45g nuts daily
50g daily of plant protein
20g daily of viscous fibre
2g daily of plant sterols
naturally occuring but to get this requires fortified foods as a part of meals
Improves
established blood lipid targets
blood pressure
estimated 10 year coronary heart disease risk
Special considerations
adults living with obesity and impared glucose tolerance (prediabetes) should consider intensive lifestyle interventions that target a 5%-7% weight loss
adults living with obesity and t2d should consider intensive lifestyle interventions targeting a 7-15% weight loss
Effective psychological and behavioural interventions in obesity management
multicomponent psychological interventions
behaviour modification (goal setting, self monitoring, problem solving
Cognitive therapy
motivational interview
values-based strategies to alter nutrition and activity
Support the develpment of confidence in overcoming barriers (self-efficacy) and intrinsic motivation (personal meaningful reasons to change)
Who should be considered for pharmacotherapy in obesity management
BMI > 30kg/m² or >27 with adiposity related complications
BMI and central adiposity and adiposity related complications to guide treatment decisions
will be life long treatments
starting low and going up according to when there is needs to increase
Approved Pharmacotherapy in obesity management
semagludide (Wegovy)
GLP-1 RA
Tirzepatide (Zepbound)
GIP/GLP-1 RA
Liraglutide (Saxenda)
GLP-1 RA
Naltrexone/bupropion (contrave)
Orlistat (Xenical)
Setmelanotide (Imcivree)
specific genetic obesity concerns
Principles of pharmacotherapy in obesity management
pharmacotherapy is evidence based pillar
use in conjunction with health behavioru change
individualize choice based on health goals, comorbidities, efficacy, adverse effects, contraindictions, medication interactions
focus on improvements in metabolic conditions, mechanical, mental health and quality of life not only weight reduction
GLP-1 therapy advisory
marked reductions in energy intake risk of inadequate nutrient intake and loss fo muscle/lean mass as nutrition concerns
attention should be shifted to dietary quality, adequate protein and resistance and strength exercise to preserve lean mass
Surgical procedures
metabolic/bariatric surgery considered for
BMI>40
>35 with adiposity related complications
30-34 with severe adiposity related concerns not adequately managed without surgery
Considerations before surgery
comprehensive medical, nutritional and psychological assessment
assess ability to follow lifelong nutrition, supplementation and follow-up
address active substance use and uncontrolled psychiatric illness before surgery
evaluate and treat porentially reversible causes of weight gain where appropriate
Restrictive bariatric surgery
limiting the volume of food that can enter the stomach
Malabsorptive bariatric surgery
purposefully bypass sections of small intestine to reduce absorption
Roux-en-y gastric bypass
most common procedure (60-70% of them)
creates a small pouch at the top fo the stomage restricting food intake and causing early satiety
pouch attached to the distal jejunum
Food bypasses the rest of stomach, duodenum and the initial part of the jejunum
duodenum continues to recieve bile and pancreatic enzymes which are critical to break down fats, proteins and carbohydrates

Key nutrients of concern with Roux-en-y surgery
protein
iron
bypasses the duodenum (main absorption site and no gastric acid)
B12 because of intrinsic factor and gastric acid loss
calcium
bypass of duodenum/jejunum
bone health risk
vitamin D and
fat soluble vitamins
A, D, E, K
usually need chyme be suspended and taken to the small intestine
fat malabsorption
Folate, zinc, copper
reduced absorption surface
Laparoscopic vertical sleeve gastrectomy
85% of the stomach removed so restrictive procedure
banana shaped portion left
50-150ml capacity left
no malabsorption but still concern from the small stomach
less intrinsic factor made because there are less of the cells to make it
removed area of the stomach is principle in releasing ghrelin
less ghrelin is less hunger hormone
pylorus preserved so no dumping syndrome
Key concern nutrients from laparoscopic vertical sleeve gastrectomy
protein
smaller stomach limits intake
iron
folate
less gastric acid, smaller intake capacity
B12
loss of intrinsic factor
Vitamin D
calcium
Duodenal switch with biliopacreatic diversion
combines sleeve with intestinal bypass
pylorus is preserved
substantial weight loss with significant malabsorption
Greatest risk of protein and micronutrient deficiencies vs other 2
lifelong nutrition monitoring and supplementatino
less common than others
Key nutritional concerns with duodenal switch
protein
iron
calcium
vitamin D
fat soluble
A, K, D, E
zinc
copper
Gastric banding issues
protein, b12, iron
low intake if diet is poor
mo malabsorption though
Pre-bariatric surgery
low calorie meal replacement perscribed to reduce liver size
specific regimine is determined by surgical program
those with diabeses have to follow blood sugar closely and get instruction on how to adjust medication while on the low calorie diet prior to surgery