Obesity and Eating Disorders Flashcards
What is obesity? BMI?
Overweight and obesity are defined as abnormal or excessive fat accumulation that presents a risk to health. A body mass index (BMI) over 25 is considered overweight, and over 30 is obese
Explain why sedentary lifestyle is a driver for obesity?
Exercise increases cellular AMPK (Activated Protein Kinase), increasing GLUT 4 activation, efficient glucose uptake and mitochondrial activity with enhanced ATP production. Energy as a result of exercice is efficient and will delay aging. We need to produce energy to get better energy.
Explain why sleep disruption is a driver of obesity?
Sleep disruption creates a hormonal imbalance in the body that promotes overeating and weight gain:
* Associated with reduced glucose tolerance and insulin sensitivity
* Disrupts the balance of ghrelin and leptin with increased ghrelin levels promoting hunger and unhealthy food choices. You get hungrier and get less satisfaction from food. People who are overwight have unbalanced ghrelin, leptin and insulin making the to want more food and getting less satisfaction from it. The desire is there, and the enjoyment is not. Sleep can be a starter of the chain reaction.
* Proposed that inflammatory pathways may be activated by insufficient sleep contributing further to obesity.
* Sleep is affecting appetite – if sleep is disruption and gut regulating hormones are disrupted and leptin dysregulated it makes it very difficult for them to stay on a protocol.
* Sleep apnea
Good sleep hygiene for overweight people?
- Sleep hygiene: Epsom salt baths; avoid Blue Light; deal with root cause of sleeplessness; stress management; magnesium (people larger will need more magnesium, combine a powder form (magnesium threonate or glycenate) with an Epsom salt bath for example) and B6 supplement during the day; valerian, vervain, chamomile or passionflower teas, lemon balm; Rescue Remedy Night Spray; lighting; natural fibres etc.
- Good sleep environment – no WIFI (more susceptible to wifi in sleep mode), dark cool room, no noise, protect the room, earthing matts to reduce levels of radiations.
Explain why Chronobiology is a driver for obesity?
Chronobiology: Shift work, sleep deprivation and exposure to bright light at night increase the prevalence of adiposity.
* Shift work is associated with obesity, dysregulation of triglycerides (hyperlipidaemia) and cholesterol, abdominal obesity, T2DM and CV disease. Central adiposity and CVD that runs alongside.
* Irregular eating patterns are associated with weight gain and obesity. Late-night eating causes higher peak post-prandial glucose levels, reduced lipolysis, circadian rhythm misalignment, together with microbial dysbiosis.
How to help client on night shifts?
- With clients on night shift try to adhere to a regular eating pattern, whether on day or night shifts. Avoid eating sweets / caffeine on nights as much as possible; look to nourishing snacks.
- The idea of one meal in, one meal out is the rhythm you need to assist weight loss => help regulate appetite to have meals at the same time each day and bowel movement at the same time each day.
- Caffeine affects blood sugar levels and we are likely to see a dip in blood sugar levels.
- Blue lights deplete us of melatonin which helps us get to sleep but is also an antioxidant – depleting antioxidant of someone being inflamed.
How processed foods is a driver of obesity?
Processed foods: Palatability is a key factor in controlling appetite.
* Strong dopamine stimulators (fat, starch, salt, free glutamate, alcohol, caffeine) activate rewarding brain circuits to trigger anticipatory cravings for ‘more’. Overstimulation from food but no satisfaction => dopamine effect and food addiction theory around obesity.
* Reward value and palatability of food can override satiety signals. The food industry combine fat, sugar and salt to create a ‘Bliss Point’ to maximise dopamine release. Chemical food is tricking the brain for the bliss point but you still want more because you are not satisfied nor satiated. Encourage possibly a binge! Even as treat food do not recommend them.
* Artificially-sweetened drinks have a 47% higher risk of increased BMI. High fructose corn syrup (HFCS) has a strong association with obesity, NAFLD and the metabolic syndrome => potentially toxic for the liver. HFCS is 100x sweeter than sugar and more toxic. Associated with the increasing rate of obesity. Low fat food contain preservatives and HFCS…
* Fast food: you eat them fast but the consequences on health are fast too especially for someone who is vulnerable.
How LT high cortisol is a driver for obesity?
Long-term high cortisol exposure plays a major role in the development and maintenance of obesity:
* Cortisol levels (overactive HPA axis) are elevated in obese individuals and associated
with enhanced abdominal fat deposition.
Factors influencing HPA-axis include high GI consumption, chronic stress, chronic pain,
alcohol, chronic sleep deprivation, and night-eating syndrome.
* Stress can alter eating behaviours for 80% of individuals of which 50% consume more food. Stress enhances preference for energy dense ‘comfort foods’.
* If you have prolonged cortisol exposure it will affect the conversion of T4 to T3. And that will make someone sluggish and effect their appetite.
* Managing and addressing stress levels is important. Stress affects eating behaviour. When you expose animals to stress their appetite goes away, But obese people when expose to stress turn to food as a way of self-soothing. Eating behaviour need unpicking.
* When HPA access is dysregulated, you are more prone to consume alcohol and have sleep disturbance. Alcohol is anti-nutrients, affect appetite and sleep.
* If HPA axis is out so is the appetite and the sleep.
How the microbiome is a driver for obesity?
Microbiome: There is mounting evidence for a connection between a disrupted microflora, obesity and diabetes:
* ‘Traditional’ gut flora produces carbohydrate-active enzymes to digest complex polysaccharides as found in plant fibre.
* A by-product is production of SCFAs, used as fuel by intestinal cells.
* The low plant fibre content of an industrialised diet has shifted gut flora towards mucus-utilising bacteria. Due to the lack of production of SCFAs regulating appetite and gut functions.
* Lack of Akkermansia muciniphilia has been linked with obesity => lack of mucous producing cells see in individuals that are overweight. This can contribute to a damaged mucosal barrier→metabolic endotoxaemia→ disrupted insulin signalling and low-grade inflammation. => resistant weight loss
* The mucosa is important from a protective point of view – otherwise we see inflammation.
* Is it the damage from the diet that cause the gut dysfunction or damage to the mucosa, or the species as a result of a poor diet.
How genetic is a driver for obesity?
Genetic factors play a role in obesity:
* SNPs in the fat mass and obesity-associated (FTO) gene are a strong predictor of obesity.
* VDR SNPs play a role in obesity associated with ongoing inflammation. This may be due to altered gut permeability and microbial translocation.
* Mutations in the ADIPOQ gene are associated with adiponectin deficiency which may predispose to metabolic disruption.
* Polymorphisms in the SLC2A2 gene are associated with increased habitual consumption of sugar and is a predictor of T2DM.
* Knowing your clients genetic profile may be helpful in understanding the predisposing environment.
* SNP can be a strong predictor of obesity => gut permeability and inflammation => many people want to know the why they have gained weight and genetic vulnerability can be an answer
What are the 7 drivers for obesity?
Genetics
Chronobiology
Sleep disruption
Microbiome
LT high cortisol
Processed Foods
Sedentary lifestyle
What is adipose tissue
Adipose tissue (AT) is a metabolically active organ which regulates whole-body energy homeostasis.
What are the 3 types of adipose tissues?
o White adipose tissue (WAT): Long-term energy storage => these are usually set in life, so what can change them?
Subcutaneous adipose tissue (SAT): Situated under the skin.
Visceral adipose tissue (VAT): Intra-abdominal.
o Brown adipose tissue (BAT): Abundant in early life. Some people have greater ratio of BAT to WAT. People that are obese have more WAT than brown. BAT has a better fuel burning capacity than WAT. Ratio can change through life.
o Beige-white adipose tissue: Similar actions to BAT.
What can adipocytes produce?
Lipids, steroids, inflammatory cytokines and peptide hormones (e.g., leptin).
Persistent energy surplus can lead to WAT increase in size and number, how to name these mechanism?
- Chronic energy imbalances with increased storage results in increased adipocyte numbers (hyperplasia) and size (hypertrophy). Your genetics will determine how efficiently you can have adipocytes that increase and enlarge. To some degree ability to store fat of some people is greater. Hormonal stimulus can also increase this process, puberty, pregnancy and menopause can increase the number of adipose tissue cells.
- Hypertrophy is strongly associated with dyslipidaemia, IR, T2DM and NAFLD.
- Hyperplasia tends to be associated with fewer serious health effects.
What to do to reduce WAT and increase BAT?
- Consider fasting as a starting point for all obese clients. Research for 800 kcal / day. Increase metabolic rate and decrease body weight.
- BAT is more efficient as burning calories as fuel as WAT. People with more BAT are more efficient are using fat as fuel vs. individuals with greater % of WAT. Cold exposure can be helpful to boost WAT to burn fat.
What is satiety? What factors are involved in satiety?
Satiety is the physiological state at the end of a meal when further eating is inhibited by ‘fullness’.
Many factors are involved in satiety:
* Mechanical stretch of the stomach via the Vagus nerve => if you constantly eat large portion the mechanical mechanism becomes dysregulated and only respond to large portion.
* Adipocyte hormones: Ghrelin, leptin and adiponectin. When WAT cells become a certain size they start to release hormones => adipocyte hormones.
* Hormones and peptides: Glucagon-like peptide (GLP-1) and cholecystokinin (CCK).
* Neuropeptides and neurotransmitters: Neuropeptide Y (NPY), agouti-related peptide (AGRP), serotonin.
* Other hormones such as thyroid hormones, oxytocin, cortisol, insulin and glucagon and neurotransmitters (e.g., dopamine and serotonin) also play a role in appetite regulation.
* When thyroid is dysregulated it affects appetite and metabolic rate => ability to breakdown and utilise food will be broken and will affect weight gain.
* Excessive cortisol due to stress, caffeine, etc. you don’t get the same satiety from food
* Insulin is really key in satiety and BS regulation.
Satiety does not work properly for obese individuals as BMI gets higher. The less satisfatction from the same meals.
What is the satiety hormone produced by adipocytes? How does it work?
Leptin is a ‘satiety’ hormone produced by adipocytes as it becomes enlarged.
* Acts as a signalling factor from adipose tissue to the CNS (hypothalamus telling no more food is requires), regulating food intake and energy expenditure.
* Released in a diurnal pattern.
* Overtime when there is an abundance of leptin produce it becomes insensitive and stops working, What causes it to stop working is an imbalance of insulin and glucose => blocks leptin at the receptor.
* Overtime leptin resistance cause individuals to become poor in energy and in a chronic fatigue sort of state.
How to regulate leptin resistance?
- To make the leptin work more efficiently: physical activity (the best), fasting (challenge with people with dysregulated blood sugar levels).
