Obesity and Eating Disorders Flashcards
What are the BMI classifications?
“Underweight <18.5
Healthy weight 18.5 - 24.9
Overweight 25- 29.9
Obese 30 - 39.9
Severley obese >40”
What are some contributing factors to obesity?
Portion size, convenience foods, snacking, processed foods and drinks, emulsifiers, colourings, alcohol consumption, energy density of food
What calorie deficit is required to lose weight?
500-700kcal
What does exercise increase?
Cellular AMPK, GLUT4 activation, glucose uptake and mitochondrial activity with enhanced ATP production
What are key drivers of obesity?
“Sleep disruption
Chronobiology
Processed foods
Long term stress
Microbiome
Genetics”
Discuss how sleep impacts obesity and how this can be supported
“Insufficient sleep creates a hormonal imbalance which drives overeating and weight gain
Dysregulates hunger hormones - increases ghrelin promoting hunger and unhealthy food choices
Disrupts blood sugar regulation and insulin sensitivity
Activates inflammatory pathways - further contributing to obesity
Support: Sleep hygeine - no blue lights, epsom salt baths, deal with route cause - stress management. Mg, B6, valerian, passionflower, chamomile, rescue remedy night spray”
Discuss how chronobiology impacts obesity and how this can be supported
“Shift work, sleeplessness and bright light at night increases adiposity. Shift work is associated with obesity, dysreg of triglycerides and cholesterol, abdominal obesity. Eating late at night is associated with an increase in post prandial glucose levels, reduced lipolysis and dysbiosis and circadian disruption. Irregular eating patterns are associated with weight gain and obesity.
Support: Try to maintain regular eating patterns. Avoid eating sweets/ drinking caffeine in the evening if possible. Eat nourishing snacks”
Discuss how processed foods impacts obesity and how this can be supported
Palatability is a key factor to controlling appetite. Highly palitable food combined to hit bliss point causes dopamine craving for more. Stimulators include sugar, fat, salt, alcohol, caffeine. Artificially-sweetened drinks have 47% risk of increased BMI. HFCS is linked with obesity, NAFLD and metabolic syndrome
Discuss how the microbiome impacts obesity and how this can be supported
Mounting evidence for dysbiosis and obesity and diabetes. Traditional diets produce SCFA producing bacteria but modern processed shift the microflora towards mucus-utilising bacteria. Lack of Akkermansia muciniphilia is linked to obesity which can contribute to damaged mucosa barrier, metabolic endotoxaemia, disrupted insulin signalling and low grade inflam
Discuss how chronic stress impacts obesity and how this can be supported
Cortisol is a catabolic hormone which breaks down fats and protein in gluconeogenesis. It also prohibits glycogen synthesis. It can also suppress beta cell insulin production and insulin mediated cellular glucose uptake Therefore the additional blood glucose response gets stored as adipose tissue which contributes to obesity. As the glucose isn’t actually getting into the cell hunger signals are sent to the brain. Cortisol also drives appetite for highly palatable food further leading to over eating.
Discuss how genetics impacts obesity and how this can be supported
“FTO fat mass gene SNP - strong predictor of obesity
VDR SNP associated with inflammation - gut permeability and bacterial translocation
ADIPOQ SNP associated with adiponectin deficiency and metabolic distruption
SLC2A2 SNP = habitual consumption of sugar - T2DM predictor”
What is adipose tissue? What does it produce?
“Metabolically active organ that is made up of:
WAT - SAT & VAT - long term energy storage
BAT & Beige-white AT - abundant in early life
Adipocytes produce peptide hormones, steroids, lipids, inflammatory cytokines. An increase in no and size of adipocytes = WAT expansion = obesity”
Discuss hyperplasia and hypertrophy of adipocytes - when does it happen and what is it linked to?
If there is excess energy available adipocytes will either increase in size (hypertrophy) or increase in number (hyperplasia). Hypertrophy is strongly linked to dyslipidaemia, IR, T2D and NAFLD. Hyperplasia associated with fewer health effects. Consider fasting (800 kcal/day)
What is satiety and what factors are involved
“Stomach stretch by vagus nerve
Hormones such as ghrelin, leptin, adiponectin, Glucagon-like peptide (GLP-1), CCK, thyroid hormones, oxytocin, cortisol, insulin and glucagon
Neuropeptides and transmitters such as Neuropeptide Y (NPY), serotonin and dopamine
All play a role in appetite regulation”
What is Leptin and Leptin Resistance - what does this lead to?
Leptin is a satiety hormone produced by adipocytes which sends satiety signals to the CNS. LR is reduced sensitivity or failure of the brain to respond to leptin. In obesity, leptin levels are usually high but cannot function. This can lead to changes in metabolism, abdominal weight gain, metabollic disorders, chronic fatigue which results in increase adipose tissue and increased leptin resistance
What is ghrelin?
Ghrelin acts as an appetite stimulating signal which plays a role in short term feeding behaviour and long term regulation of energy metabolism. It increases before a meal and is at its lowest 1 hr after eating. In obesity there is usually low ghrelin but this increases with a reduction in weight (dieting)
g
What is adiponectin, what is reduced levels linked to and how can you increase it?
“Most abundant circulating adipokine. Increases glucose uptake and beta-oxidation of fats. Increases insulin sensitivity and anti-inflammatory.
Reduced levels leads to insulin resistance and T2D, inflammation, obesity, CV disease. Low adiponectin:leptin ratio increases oxidative stress and inflammation. BMI & visceral fat are strong predictors of adiponectin levels.
Increase by Blueberries, Turmeric, O3, 40-50g fibre, green tea, cold water therapy and HIIT daily”
What impact does IR and inflammation have on each other and what are causes/ risk factors for IR
“Inflammation causes IR and IR drives inflamm
High oxidative stress - poor sleep/ toxins
Reduced physical activity - increases GLUT4 expression
Chronic stress - increases glucose and inflammatory cytokines
Mitochondrial dysfunction - increased ROS, low ATP, reduced GLUT4
Poor methylation - high homocysteine
Dysbiosis - increases circulating LPD”
What are S/S of IR
“Fatigue
Increased hunger
Brain fog
Overweight
High hip: waist ratio
High BP, chol, trig
High blood glucose”
How do you improve insulin resistance?
“1. Balance blood sugar (3 well structured meals), focus on protein esp breakfast and healthy fats, lots of fibre reduces glucose release, low GL, Mg, Chromium, Cinnamon, Berberine, cal restriction if appropriate, avoid processed foods and artificial sweeteners
2. Reduce inflam - avoid inflam foods/ drinks, trans fats, alcohol, sweetened drinks, processed foods. Increase AO intake - eat rainbow - anthocyanins, green tea, cruciferous, greens, O3:O6 balance, quercetin, turmeric, prebiotics. AO: glutathione, ALA, Vits A,D,E,K. Priritise sleep (deprivation can increase CRP)
3. Optimise insulin sensitivity - meal timing and frequency key to insulin and glucagon secretion. TRF - eat earlier, fast overnight, increase mod exercise. Mg, Vit D, chromium, Zn, ALA, CoQ10. Prebiotics”
What is the fasting glucose levels linked with mortality high or low
“5.6-6.9 mmol/L - each 1 mmol increase increased risk of mortality by 32%
4.4-5.2 linked to lowest mortality”
What steps can you take to help address over-eating?
“CNM naturopathic diet
3 meals/ day no snacking
Focus on protein esp breakfast
Smaller portions - from dinner plate to side
Keep meals simple
Fast and leave at least 4 hrs between meals
Chew food well
Mindful eating
Address micronutrient def - Vit D, C, A, B9, Zn, Fe, Ca”
