1/21
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
Static energy balance
This is changing one side of the energy balance equation which results in either weight gain or loss. If energy intake = energy expenditure, then body weight is maintained.
Dynamic energy balance
This talks about the numerous biological and genetic influences that affect both sides of the energy equation. Energy intake can and does affect energy expenditure.
Factors of dynamic energy balance
Brain:
Metabolic and hormonal signaling (insulin resistance)
Cognition, reward, mood, stress, choice
Environment& lifestyle
Genetics, epigenetics, and early life events.
Intake factors:
Diet composition, i.e., refined foods, TEF
High fat diet, can increase intake
Diet energy density
Fiber intake
Expenditure factors:
Resting metabolic rate (lean mass)
Physical activity and body mass composition
Biological influences of obesity
Genetics: Studies have demonstrated the role of genetics in susceptibility to obesity, as well as influences on energy storage & energy expenditure. Even modest excess in energy intake has a more dramatic effect on individuals with obesity versus individuals who are lean.
Enzymes & hormones are factors as well.
Gut microbiome: alternation in this may impact the pathogenesis of obesity and many other diseases. Gut bacteria may alter how we store fat, balance concentrations of glucose in the blood, respond to hormones that make us feel hungry or full.
Fat cell development: Number of fat cells increases (hyperplasia) most rapidly during late childhood and early puberty. Cells also expand in size (hypertrophy); after max size is reached, more cells develop to store more fat. Fat cells are capable of increasing their size by 20-fold and their number by several thousand-fold.
Sleep and circadian rhythms: Short sleep associated with obesity and poor cardiometabolic health. Alters regulation of hunger and appetite (lower leptin and higher ghrelin). Every hormonal process in your body has a circadian rhythm and disruptions can be metabolism altering.
Stress: Chronic stress can lead to appetite changes via cortisol.
Inflammation: Adipose tissue secretes cytokines that influence health. Chronic overeating tends to “turn on” inflammation leading to weight gain and insulin resistance. There may be a direct relationship between obesity and inflammatory diseases.
Viruses/pathogens: There is a hypothesis that obesity can be caused by pathogenic organisms.
Enzyme & hormone factors of obesity
Lipoprotein lipase: enzyme that promotes fat storage in fat & muscle cells
Increased levels of LPL seems to increase fat storage efficiency.
Leptin: hormone produced by fat cells under direction of (ob) gene
Decreases appetite & increases energy expenditure
Gain in body fat stimulates production of leptin, resulting in appetite suppression & increased energy expenditure
Obesity is associated with leptin resistance
Ghrelin: protein synthesized & secreted primarily by stomach cells
Promotes positive energy balance by stimulating appetite & efficient energy storage
Powerfully triggers desires to eat
Carbohydrate-insulin model:
Increasing fat deposition in the body resulting from the hormonal responses to processed, rapidly digestible carbs.
Drives positive energy balance.
Cycle of biological influences of obesity
Increased appetite; increased food intake → adipose tissue → pro-inflammatory state → hormonal
White vs brown adipose tissue
Energy storage vs. heat production
Insulin sensitivity/modulation vs. enhancing glucose & lipid metabolism
Androgenic hormones, adipokines vs. uncoupling protein 1 (UCP1) [thermogenesis-related]
Environmental causes of obesity
Learned behaviour: appetite vs. physical hunger.
Physical activity: too little energy expenditure. Modern environments foster inactivity.
Neighborhood obstacles to PA and healthy foods: environments that lack opportunities for safe physical activity and access to fresh, nutrient-dense food linked to obesity. What is the built environment of a community? Food deserts: low-income areas with limited access to affordable and nutritious food.
Obesogens: environmental pollutants that are foreign to the body and disrupt metabolism/energy balance (endocrine disruptors). Increased exposure may be associated with insulin resistance, altered lipid metabolism/increased fat storage, altered regulation of satiety/appetite. E.g., BPAs and phthalates.
Medical complications of obesity
Mainly driven by excess visceral fat! Adiposity releasing inflammatory cytokines around the organs which affects everywhere else in the body.
Pulmonary: abnormal function, sleep apnea, hypoventilations
CVD
Brain: stroke
What is inflammation
This is a normal protective reaction of the immune system to injury, infection, physiologic, or metabolic stress. Local vs. systemic, acute vs. chronic.
Chronic = prolonged/sustained, low-grade inflammation contributing to increased risk for chronic disease.
Cardiometabolic consequences of obesity
Referring to CVD and T2DM related to increased body fat and abdominal obesity. Exacerbated by physical inactivity, poor diet, poor sleep, and stress, all contributing to increased chronic inflammation.
Visceral adipose tissue is metabolically active, i.e., secretion of hormones/cytokines
Increases insulin resistance
Markers of cardiometabolic inflammation: increased Tg, glucose, insulin, HbA1c, CRP-high sensitivity, homocysteine.
Metabolic syndrome
Cluster of risk factors related to obesity, insulin resistance, and visceral adipose tissue. A proinflammatory state, and increases risk for CVD and T2DM.
Diagnosis established by at least 3 of the following:
Abdominal obesity (waist circumference): M >40in, W >35in.
Triglycerides >150mg/dL
HDL: M <40mg/dL, W <50mg/dL
BP >130/>85mmHg
Fasting glucose >100mg/dL
Treatment for obesity
Comprehensive lifestyle program of healthy eating, physical activity, and behaviour therapy. Prescription medication use, surgery.
Goal setting for weight management
Weight loss advice does not apply equally to all individuals!
Reasonable goals help achieve the desired result in managing weight. Unreachable targets ensure frustration and failure.
<2% weight loss per week (1-2 lb per week). Reduce body weight by about 5-10% over 6-month period, but even 3-5% decrease can lower blood glucose, lipids, and BP and improve overall health and control of chronic diseases.
Some lean mass will always be lost, but we want to lessen the amount of lean mass lost. At a minimum, prevent further weight gain.
Healthful plan: energy intake goal
Consider slight kcal deficit ~ 250 - 1000 kcal/day. Intakes <1200 kcal/day typically not recommended. Ensure that there is not too significant of a deficit to the point where one is starving and their physiological cues kick in.
Healthful eating plan for obesity
Individualized, nutritionally adequate, balancing macronutrients
How to assess underweight/undernutrition?
% weight change over time and duration
Females: is menstruation regular?
Biochemical data:
Proxy for macros
T3: proxy for CHO intake
Triglycerides: proxy for fat intake
Look at
Approaches to underweight nutrition care (in patient)
Oral & PA
Fortification
Supplementation
Enteral feeding
Strategies for weight gain
Incorporate physical activity: primarily weight training to build muscle. As activity increases, energy intake must be increased to support the activity. Must ensure that it is medically safe and appropriate.
High energy diet: energy dense foods, large or extra portions, small, frequent meals (>6 “meals” / day), high-calorie drinks. Gradually increase portions, add about 500kcal/day every 4-7 days. Monitor for fluid shifts and refeeding syndrome. Using EER or 30kcal/kg or up to 40kcal/kg.
Food fortification
This is boosting the nutrient content of food & fluid (without affecting volume) by adding protein and/or calories. Examples: cheese, butter, avocado, oil, jams,
Food supplementation
These are ready-to-feed nutrition products that assist with weight gain and increasing total energy & protein intake.
Advantages: convenient, nutritionally complete, disease-specific ones are available.
Appetite stimulants/enhancers can be helpful, e.g., megestrol acetate (Megace). Collaboration w team to determine need for psychiatric medication, can support appetite stimulation by decreasing anxiety. A lot of SSRIs don’t work effectively if someone is not taking in enough nutrition.
Enteral feeding
The provision of nutrients using the GI tract. Used if the patient cannot consume enough food or drink to meet nutrient needs. Tube feeds delivers nutritionally complete formula directly into the stomach or intestine. Short term: nasogastric feeding, or long term: gastronomy, PEG feeding.