11A- weight management and disordered eating

what is the source of fuel in food

macronutrients

• carbohydrates, lipids (fatty acids), and amino acids

what do all 3 major macronutrients converge at

• acetyl Co-A

• feeds into TCA/Krebs cycle and oxidative phosphorylation in the mitochondria

order of events to create energy

• glycolysis

• beta-oxidation

• deamination +

how is excess fuel stored

• multistep process that requires energy itself

• storing dietary fat is the most energy efficient

• 2-3% of the energy from fat is used to store it

energy balance

energy intake- energy requirements

neutral energy balance

adequate energy= no net storage or depletion

positive energy balance

extra energy= energy storage

negative energy balance

insufficient energy= depletion

how is total energy balance determined

• combination of factors

• ex. food intake (including digestive efficiency), activity level

energy balance

• consuming more energy than needed will result in energy storage

• consuming less energy than needed will result in depletion of the energy reserves

• energy needs directly impact energy balance

total energy expenditure formula

TEE= BMR + activity + TEF

• TEE= total energy expenditure

• BMR= basal metabolic rate

• TEF= thermic effect of food

how does MBMR, activity and TEF variation determine TEE

• BMR is largest proportion of TEE (75%)

• activity is the most “straightforward: to modify voluntarily for healthy people (around 15%)

• TEF is relatively stable compared to BMR and activity (around 10%)

how does TEF varie

• meal size

• meal composition (higher TEF for proteins and carbohydrates vs. lipids)

• meal frequency, timing, duration…

• factors that influence BMR may also influence TEF- body composition, age, etc.

  • TEF seems to be reduced in obese vs. lean individuals (may be related to insulin resistance.sensitivity)

how does BMR vary across individuals

varies between individuals and different points in life

• height and weight (=BMI)

• sex (% fat vs muscle mass, hormones)

• age/development/lifestage (pregnancy, lactation, infancy, childhood, adolescence, adulthood, senior…)

• hormone levels (ex. thyroid hormone)

• stress, fever, illness

• other genetic factors

• effects of medications and other compounds (ex. caffeine)

• fed, fasted, or starved energetic state

external cues that modulated energy intake

• time of day

• food availability

• food quality

• social norms and influences

internal cues for energy intake

• hunger and satiety

• emotions (ex. stress, boredom)

ghrelin

• “hunger hormone”

• produced by stomach

• increases drive to eat

vagus nerve in hunger

• connects brain and digestive system (PSNS)

• vagal stimulation be stretch receptors in the stomach decrease appetite

leptin

• “energy expenditure hormone”

• protein hormone

• made by adipocytes

• levels correlate with energy reserves (stored triglycerides)

• leptin inhibits hunger to stimulate satiety

GLP-1

• glucagon-like peptide-1

• peptide hormone produced by large intestine and ileum

• decreases blood glucose levels (+insulin and -glucagon)

• decreases appetite by slowing gastric emptying

CCK

• cholecystokinin

• peptide hormone that stimulates the digestion of fat and protein

• secreted by duodenum in the small intestine

insulin

• peptide hormone

• secreted by b=cells in the pancreas

• induces uptake of glucose into body cells (+other function)

• reduces hunger

overall overview of factors impacting appetite control

*missing vagal innervation of the stomach

anticipatory signaling

regulation of food intake begins before a meal due to anticipatory signaling over 1h before feeding

what is anticipatory signaling triggered by

sensory and internal cues: smell/sight of food, time of day, other environmental cues

how does anticipatory signaling work

• GLP-1 peaks around 1 h before a meal and return to baseline by meal start

• ghrelin builds over time adn declines with feeding

• insulin increases just before mealtime and in response to blood glucose

how does obesity vary across subpopulations

• increases with age

• economics:

  • lower with increasing education

  • lower in landed immigrants vs. non immigrants

• dietary patterns

  • 5+ fruits or vegetables per day reduces the risk of obesity

• many other factors

what chronic diseases is obesity associated with

• diabetes (T2)

• gallstones and gallbladder disease

• high BP

• arthritis

• CV disease

• colon cancer

• breast cancer

• joint disorders

• sleep apnea

mechanisms obesity increases risk of type 2 DM

• chronic inflammation contributes to development of insulin resistance in tissues

• increased use of FFA= increased toxic byproducts; damage to beta cells of pancreas and insulin deficiency

how do larger adipocytes contribute to chronic inflammation

• enlarged adipocytes attract macrophages by secreting macrophage chemotaxis protein (MCP-1)

• macrophages produce pro-inflammatory TNF-a

• TNF-a induces export of FFA into the blood

how does inflammation cause insulin resistance

• muscle imports the excess FFA from the blood, which build up as ectopic lipid droplets

• ectopic lipid droplets interfere with GLUT-4 translocation= insulin resistance

• exact mechanism unknown, but may be due to premature signaling pathway

obesity and CVD

obesity promotes appearance of unusual lipoproteins that further increase the risk of CVD beyond “just” high LDL

how does obesity cause CVD

• high levels of VLDL in obesity prevent normal metabolism of lipoproteins, leading to abnormal transfer of cholesterol and triglycerides between lipoproteins

• production of “new” lipoproteins enriched with triglycerides (VLDL-TG and LDL-TG)

• enriched lipoproteins can be converted into small dense-LDL (sd-LDL) by hepatic lipase

• sd-LDL is like “norma;” LDL but worse- better at penetrating artery walls, longer residence time in the blood, more susceptible to oxidation

normal lipoprotein metabolism vs lipoprotein metabolism when VLDL is high diagram

BMI classifications (KNOW THIS)

when is BMI effective or not effective

• useful for measuring risk in a population, but not as effective for an individual

• muscle weighs much more than fat, so muscular individuals have a higher BMI than expected

BMI limitations

• does not factor in lean muscle mass vs adipose tissue

• location of adipose tissue (visceral vs SC) varies across subpopulations and better predicts some co-morbidities

• ignores metabolic markers of disease risk and mental health component of obesity

SC vs visceral fat

• SC: around belly and outside

• visceral: around organs and more internal

waist circumference cutoff’s associated with risk and stratified by ethnic origin and sex

EOSS

• edmonton obesity staging system

• more comprehensive rating scale that includes physical adn psychological symptoms as well as functional limitations

• focuses on associated health problem adn their severity vs weight

*be able to place someone on this scale

EOSS staging

0

• obese but no risk factors present

• no action or preventative options only

1

• subclinical risk factor(s) present

• preventative options only

2+

• at least one established risk factor

• specific nutritional, lifestyle, surgical, and/or pharmacological action needed

weight cycling

• the human body has evolved to maintain survival when food was scarce and store energy efficiently in times of plenty

• adipose cells have an average lifespan of around 9.5 years

• leptin is a critical regulator of energy intake and expedenture

  • serves as an indicator of energy stores

• however, leptin’s impact on energy intake can make weight management difficult

• as energy stores are depleted, metabolic changes occur to stretch remaining stores as long as possible (“ecomode”)

  • BMR decreases

  • activity decreases

  • leptin decreases → increases hunger (increase food intake)

• these factors make it easier to regain a positive energy balance, allowing adipose cells to refill

• these factors also explain why calorie restriction alone is not a reliable weight management strategy

behavioural modification to treat chronic disorders of energy balance

• may include specific interventions like CBT

• ex:

  • preparatory phase: assess the nature and severity of obesity and any medical or psychosocial comorbidities

  • phase 1: initial weight loss including changing eating pattern, activity

  • phase 2: long term weight maintenance phase focusing on “locking in” new habits, tapering off monitoring

behavioural modification- diet

• general recommendations for dietary modifications to treat obesity reflect those in the Canada Food Guide:

  • high protein to promote satiety

  • water as drink of choice

  • nutrient dense as opposed to energy dense foods

  • reduce processed foods

  • substitutions as opposed to eliminations

weight loss diets

• low calorie (ex. weight watchers- follow canada’s food guide but reduced calorie intake)

• prepared meals/drinks

• low fat

• low carb (paleo, keto, atkins)

• intermittent fasting

• gluten-free

• commercial weight loss programs are a spectrum from fat diet to healthy diet

considerations for weight loss diets

• context and individual needs matter in diet choice

  • a gluten free diet for a person with gluten intolerance in good

fad diet

• a plan that promotes results such as fast weight loss without robust scientific evidence to support its claims

• client should be discouraged from using

healthy diet vs fad diet

weight loss pharmacotherapy approved in canada

• orlistat: pancreatic lipase inhibitors limits fat absorption

• liraglutide and semaglutide: GLP-1 agonists reduce appetite

• naltrexone and bupropion: hunger suppression

orlistat

GLP-1

once weight loss pharmacotherapy is stopped

often regained

side effects of weight loss meds

• headache, dizziness, fatigue

• GI disruption (nausea, vomiting, abdo pain, diathermia)

• hypoglycemia, gallbladder problems, pancreatitis

weight loss surgery

• bariatric surgery: gastric banding, gastric bypass, sleeve gastrectomy

• typically limited to higher obesity classes and obesity and established comorbidities

• requires lifelong changes in diet adn lifestyle to accommodate permanent to GI physiology and absorption

• good outcomes

trajectory for bariatric surgery pt.1

trajectory for bariatric surgery pt.2

DSM description of feeding and eating disorders

a disorder characterized by a persistent disturbance of eating or eating-related behaviour that results in the altered consumption or absorption of food and that significantly impairs physical health or psychological functioning

causes of feeding and eating disorders

• psychosocial and sociocultural combine to develop a distorted body image

• genetics can play a factor- ex personality traits (perfectionism, rigidity, narcissism…) “baseline” body type, hunger/satiety

• often first appear in adolescence

  • physical, social and mental changes

  • desire for control during changes can manifest in control of food intake and weight

feeding and eating disorders in canada

• PHAC: 3% of women will be affected by eating disorders in their lifetime (~1.7 million total)

• CCHS: 3.8% of Canadian girls and women (aged 15-24) were at risk of an eating disorder

  • 30% of grade 9-10 girls (~14 to 16 years old) report trying to lose weight in the last year

• Incidence of eating disorders among boys and men is increasing (up to 1/3 of patients)

Early detection is important to refer for treatment – highest mortality of any mental illness (10 to 15%)

major feeding and eating disorders similarities and differences

anorexia athletica

• “sport anorexia”

• eating disorder characterized by excessive and compulsive exercise

• not officially recognized by DSM-5 (patients likely classed as anorexia nervosa, R-type)

• typically rooted in performance vs. body image concerns

female athlete triad

• disordered eating due to pressures to maintain lean, thin, and athletic bodies

• energy restriction paired with excessive exercise can upset hormonal imbalance

• low estrogen levels can lead to amenorrhea (stopping of menstruation)

• low food intake and low estrogen can impact nutrient intake, especially calcium