Obesity Flashcards
Overweight and obesity
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
Obesity pandemic - reasons
- increased portion sizes
- food abundance / exposure
- rise of convenience food
- Food palatability
- increased use of colours / flavour enhancers
- energy density
- alcohol consumption
- snacking
- speed of eating
How exercise effects the body
Exercise increases cellular A increasing GLUT 4 activation, glucose uptake and mitochondrial activity with enhanced ATP production.
How sleep disruption effects the body
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.
- Proposed that inflammatory pathways may be activated by insufficient sleep contributing further to obesity.
Sleep hygiene
Epsom salt baths; avoid Blue Light; deal with root cause of sleeplessness; stress management; magnesium and B6; valerian, vervain, chamomile or passionflower teas; Rescue Remedy Night Spray; lighting; natural fibres etc
How Chronobiology effects the body
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 and cholesterol, abdominal obesity, T2DM and CV disease.
- 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.
- 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
How Processed foods effects the body
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’.
- 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.
- 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
Bliss Point = The amount of salt, sugar and fat to maximise deliciousness
How Long-term high cortisol exposure effects the body
- 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’.
How Microbiome effects the body
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.
- Lack of Akkermansia muciniphilia has been linked with obesity. This can contribute to a damaged mucosal barrier → metabolic endotoxaemia → disrupted insulin signalling and low-grade inflammation.
How Genetic effects the body
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.
Adipose tissue
Adipose tissue (AT) is a metabolically active organ which regulates whole-body energy homeostasis.
- AT changes in quantity and distribution with age.
- Adipocytes and other cells of adipose tissue produce lipids, steroids, inflammatory cytokines and peptide hormones (e.g., leptin).
- ↑ number and size of adipocytes = WAT expansion = obesity
White adipose tissue (WAT)
Long-term energy storage.
- Subcutaneous adipose tissue (SAT): Situated under the skin.
- Visceral adipose tissue (VAT): Intra-abdominal
With persistent energy surplus, white adipose tissue can continue to grow.
- Chronic energy imbalances with increased storage results in increased adipocyte numbers (hyperplasia) and size (hypertrophy).
- Hypertrophy is strongly associated with dyslipidaemia, IR, T2DM and NAFLD.
- Hyperplasia tends to be associated with fewer serious health effects.
- Consider fasting as a starting point for all obese clients. Research for 800 kcal / day
Brown adipose tissue (BAT)
Abundant in early life.
Beige-white adipose tissue
Similar actions to BAT.
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.
- Adipocyte hormones: Ghrelin, leptin and adiponectin.
- 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
Leptin
Leptin is a ‘satiety’ hormone produced by adipocytes.
- Acts as a signalling factor from adipose tissue to the CNS, regulating food intake and energy expenditure.
- Released in a diurnal pattern
Leptin resistance (LR)
Leptin resistance (LR) is a reduced sensitivity or failure in response of the brain to leptin.
- Leptin acts on the leptin receptor in the hypothalamus.
- In obesity, leptin levels are high but cannot function due to leptin resistance. Over time this leads to changes in metabolism, abdominal weight gain, chronic fatigue, sleep dysregulation, metabolic diseases. ↑ adipose tissue = ↑ leptin resistance.
Ghrelin
Ghrelin — functions as an appetite-stimulating signal.
- Plays a role in long-term regulation of energy metabolism and the short-term regulation of feeding — increasing food intake and body weight.
- ↑ before a meal and ↓ to lowest levels within 1 hour of eating.
- In obesity, we usually see ↓ ghrelin, but a reduction in body weight ↑ ghrelin (hunger associated with dieting).
Adiponectin
Adiponectin is the most abundant circulating adipokine.
- Increases glucose uptake and β-oxidation of fats. Increases insulin sensitivity. Anti-inflammatory.
- Reduced adiponectin is associated with: IR, T2DM, obesity and CV disease. BMI and visceral fat are significant predictors of plasma adiponectin levels.
- A low adiponectin:leptin ratio (sign of dysfunctional adipose tissue) may increase oxidative stress and inflammation.
- Consider the following — reported to boost adiponectin levels naturally: Blueberries (anthocyanidins) and turmeric (curcumin) plus omega-3, 40–50 gm fibre per day, green tea (catechins), cold water therapy, and daily HIIT.
Insulin Resistance
Inflammation drives insulin resistance, and insulin resistance drives inflammation. Causes and risk factors:
- High oxidative stress, e.g., poor sleep, environmental toxins.
- Reduced physical activity — exercise modulates inflammatory mediator expression involved in IR and increases GLUT4 expression.
- Chronic stress — ↑ glucose, lipids and inflammatory cytokines.
- Mitochondria dysfunction — ↑ ROS, low ATP, ↓ GLUT 4.
- Poor methylation (high homocysteine), hypertension, elevated triglycerides. Low adiponectin.
- Dysbiosis — drives the inflammatory process with ↑circulating LPS
Signs and symptoms of insulin resistance
- Lethargy.
- Hunger.
- Brain fog.
- Overweight.
- ↑ waist to hip ratio.
- ↑ blood pressure.
- ↑ cholesterol / ↑ triglycerides.
- ↑ blood glucose levels.
- Acanthosis nigricans.
- Skin tags.
Naturopathic approach to insulin resistance:
- Stabilise blood glucose levels:
- Macronutrient balance: Reduced carbohydrates, increased protein, increased MUFA.
- Protein-based breakfast — helps normalise insulin secretion.
- ↑ fibre — slows gastric emptying, slower release of glucose and therefore ↓ insulin response.
- Calorie restriction as appropriate.
- Avoid processed food with artificially engineered
palatability — incl. sugar and sweeteners. fast food and snacks. - Magnesium, manganese, zinc, B vitamins, chromium etc
- Reduce inflammation:
- Avoid inflammatory foods ― refined carbs, damaged fats etc.
- Increase a rainbow of plant foods incl. blue, purple, black foods.
– Proanthocyanidins modulate inflammation, enhance anti-inflammatory adiponectin and support microbiome: ginger, turmeric, flaxseeds, tea, apples, berries.
– Green tea polyphenols ↓ fasting glucose and ↓ HbA1c.
– Foods rich in prebiotic fructans, fructooligosaccharides (FOS), inulin e.g., chicory, leeks, onions, Jerusalem artichokes.
- Antioxidants (α-lipoic acid, glutathione etc).
- Prioritise sleep ― sleep deprivation can increase C-reactive protein.
- Optimise insulin sensitivity:
- Meal timing and frequency is key to ensure appropriate insulin and glucagon secretion.
‒ Time Restricted Feeding (TRF); elimination of snacks. ‒ Eat last meal earlier in the evening then fast overnight.
- Increase moderate exercise — ↑ insulin sensitivity by acting directly on muscle metabolism.
- Vitamin D, magnesium, zinc, α-lipoic acid, CoQ10, chromium, Gymnema sylvestre, cinnamon, bitter melon, fenugreek, garlic.
- Prebiotics — inulin and FOS have been shown to modulate appetite, blood glucose and insulin levels
Tracking glucose levels
- Fasting glucose levels of 5.6‒6.9 mmol / L: Each 1 mmol / L increase gave a 32% increase in mortality.
- Fasting glucose levels of 4.4‒5.2 mmol / L: Associated with the lowest mortality regardless of sex and age.
- The Blood Glucose Awareness Training (BGAT) programme is a self-management intervention shown to be effective in improving health outcomes in individuals with insulin resistance.
- BGAT encouraged participants to observe the effect of stimuli (e.g., 30 mins exercise) and meal composition on blood glucose levels
Reducing Obesity Strategy
Follow the CNM Naturopathic Diet and address over-eating with:
- Eating 3 meals a day with no snacking.
- Smaller portions — eat from side plate vs. dinner plate
- Protein-based breakfast — eating a protein-based breakfast helps normalise insulin secretion and reduces tendency to snack.
- Protein with each meal — palm size.
- Keep meals simple — the variety of foods in a meal increases intake: The more foods differ in their flavour, the greater the boost.
- Leave 4 hours + between meals.
Fasting or a fasting window such as 16:8.
- Chew food well — 30 times.
- Mindful eating — enjoy the ritual of food vs. ‘food to survive’.
Addressing micronutrient deficiencies:
- Despite excessive dietary consumption, obese
individuals often have insufficient intake of
vitamin A, C, D, folate, iron, zinc and calcium.
Stimulating fat loss:
- Meal composition — educate, e.g., low GL; macronutrient balance.
- Breakfast is vital and should include protein and only low GL carbs.
- Protein at each meal — postprandial thermogenesis was increased
- 100% on a high-protein / low-fat diet vs. high-carb / low-fat diet. Exercise daily — 35 minutes low intensity.
Food diary and frequent practitioner contact.
