Week 2 - Obesity Flashcards

1
Q

standard definition of severe obesity

A

40kg m2

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2
Q

The world health organisation (WHO) definition of overweight and obesity

A

An abnormal or excessive fat accumulation that presents a risk to heath

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3
Q

BMI

A

Most frequently used measurement for assessing obesity (divide weight in kg by height in metres squared)
- The BMI cut-point categories were originally defined by the WHO to reflect the J or U shaped relationship which has been identified between BMI and mortality (WHO 1998).
- Given the inability to distinguish between fat and fat-free mass, BMI provides a simple way to assess obesity levels at a population scale but has limitations on a personal basis
Evidence indicates that the combination of BMI and waist-circumference can be used to improve disease risk prediction

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4
Q

Reverse causality

A

Refers to a direction of cause and effect that is contrary to a common presumption. E.g., it is likely that the inclusion of sick, elderly and current or past smokers (which are each associated with lower body weight) may have inflated the mortality risk in the healthy body weight range; therefore, masking the adverse impact of overweight and obesity.

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5
Q

Global BMI Mortality Collaboration (2016)

A

Identified a heightened risk of mortality in both the lower and upper range of overweight Furthermore, mortality risk increased progressively throughout classes of obesity.
* There findings suggest that the health risk associated with excess adiposity begin the overweight range and progress in step-wise fashion as BMI increases.

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6
Q

The Global Burden of disease collaboration (2017) identified 20 health conditions where evidence suggest an association with BMI:

A
  • Cancers: Oesophageal, Colon and rectal, Liver, Gallbladder and biliary tract, Pancreatic, Breast cancer (post-menopause & pre-menopause), uterine, ovarian, kidney, thyroid, leukaemia.
  • Cardiovascular and cardiometabolic diseases: Ischaemic heart disease, Ischaemic stroke, haemorrhage stroke, hypertensive heart disease, diabetes mellitus, chronic kidney disease.
  • Musculoskeletal conditions: Osteoarthritis, low back pain.
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7
Q

The influence of adiposity is dependant on both the quantity of fat present and the storage location:

A
  • E.g., when a person has a healthy amount of body fat, the majority is typically stored in subcutaneous regions e.g., hips, thigh and upper arms.
  • Fat in these areas’ facilities triglyceride storage’ and metabolic homeostasis.
  • Animal studies have shown the absence of this essential fat is associated with the same metabolic problems seen in obesity (Garrilova et al 2000).
    During the progression to over-weight and obesity, an increasing amount of adipose tissue s stored in central regions which is associated with poor cardio-metabolic health. This is because fat stored in ectopic regions interferes with the normal metabolic function of affected tissues (principally via insulin resistance and chronic low-grade inflammation – Fabbrini et al 2009; Schulman 2014).
  • The most important areas where ectopic far is commonly located include the abdominal cavity (visceral fat), liver, heart and pancreas.
    At any given BMI, individuals with a greater proportion of central fat possess the poorest health outcomes
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8
Q

‘thin-on-the-outside-fat-on-the-inside’

A

An individual with a healthy BMI but a large proportion of fat stored centrally (experience poor metabolic health outcomes).

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9
Q

What % of obese individuals are classed as metabolically healthy?

A

10-34%

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10
Q

Android obesity

A

Possess more adiposity in the upper body
Human adipose tissue mainly around the trunk and upper body, in areas such as the abdomen, chest, shoulder and nape of the neck
More common in men

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11
Q

Gynoid obesity

A

A type of obesity where excess body fat accumulates in the lower body, particularly in the buttocks, thighs, and hips
More common in women

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12
Q

Human physiology complies with the first law of thermodynamics:

A

energy can be transformed from one form to another but cannot be destroyed (Hall et al 2012).
- Human energy balance is determined by matching between chemical energy entering the body via food and drinks versus thermal and kinetic energy expended through metabolism and movement.

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13
Q

Energy intake (food and drink) =

A

Energy expenditure (resting metabolic rate, diet-¬ induced thermogenesis, physical activity) ± energy stored (fat, protein and carbohydrate).

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14
Q

Common techniques used to assess energy intake:

A

Weighed food record, food frequency questionnaire, 24hour recall.

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15
Q

Components of energy expenditure:

A

1) Resting Metabolic Rate (RMR):
Measurement Method: Breath-by-breath gas analysis, ventilated hood, or whole-room calorimeter.
Details: Measurements are taken while the subject is at rest in a supine position, during the post-absorptive state, over 30 minutes. The first 10 minutes are discarded to avoid habituation effects. This measures oxygen uptake and carbon dioxide production.

2) Diet-Induced Thermogenesis (DIT):
Measurement Method: Breath-by-breath gas analysis, ventilated hood, or whole-room calorimeter.
Details: Energy expenditure increases following food intake, measured using expired air analysis post-meal. Indirect calorimetry is performed before and after consuming a standardized meal. The difference between pre- and post-meal measurements is used to determine the increase in metabolic rate due to food intake.

3) Physical Activity Energy Expenditure (PAEE):
Measurement Method:
Self-report: Uses metabolic equivalents based on the type, duration, and frequency of physical activity to estimate energy expenditure.
Direct measurement: Expired air analysis using stationary or portable metabolic carts, primarily in controlled lab settings.
Accelerometery: movement sensors worn by ppts for several days. Proprietary algorithms are used to derive EE estimates from acceleration data

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16
Q

RMR

A

the rate at which the body expends energy when at complete rest. It represents the sum of each tissue’s basic energetic requirements.
- Fat-free mass, or lean mass, is the primary determinant of RMR so data suggests that lean mass drives daily energy needs.
- RMR is also a key determinant of daily energy expenditure.
- RMR is related to body size, age and sex.
In non-athletes, RMR typically accounts for ~70% of total energy expenditure each day

17
Q

The liver/brains and skeletal muscles contribution to RMR

A

Despite representing ~2% of total body mass, the high metabolic activity of the liver and brain means each contribute ~20% to RMR (Wang et al 2011).
Skeletal muscle typically comprises one third of body mass and ~20% of RMR.

18
Q

Diet-induced thermogenesis:

A

Diet-induced thermogenesis represents the energy expended in the act of digesting and processing food and energy containing drinks.
- Humans have no voluntary control over this parameter which is principally determined by the amount of energy consumed each meal and its nutrient composition
Diet-induced thermogenesis contributes only 10-15% of daily energy expenditure (under normal circumstances, differences between people are not thought to contribute to the development of obesity

19
Q

PA:

A

Movement or PA is the most variable component of daily energy expenditure which can vary from zero to several thousand kilocalories.
- This component of expenditure encompasses all forms of muscle contraction: standing, ambulation and low-moderate-high intensity physical activity (Levine 2003).

20
Q

The ‘carbohydrate-insulin model of obesity’.

A

Simple sugars foster passive overconsumption but may also contribute by altering the endocrine regulation of adipose tissue

21
Q

Adaptive thermogenesis:

A

Any deliberate attempt to induce a negative energy balance is met by several compensatory responses that seek to attenuate the energy deficit and maintain body weight

22
Q

The leptin-melanocortin signally pathway

A
  • The most well-characterised monogenic cases (phenotypes that are related to a defect in a single gene) are those relating to the leptin-melanocortin signally pathway in the hypothalamus which causes extreme hyperphagia (overeating) and severe obesity
23
Q

The study of epigenetics

A

Lifestyle-related alterations in gene expression
Maintenance of a healthy lifestyle can help mitigate against the risk of obesity in those who are genetically susceptible.

24
Q

The problem of ‘bi-directionality’ in obesity and sedentary time

A

One issue that makes the interpretation of sedentary behaviours effect on obesity even more difficult is that of ‘bi-directionality’- where the possibility exists that it is weight gain and obesity driving increasing sedentary time, rather than vice versa

25
Q

Acute effect of exercise on obesity:

A

All forms of bodily movement are fuelled by the breakdown of adenosine triphosphate (ATP)
- The ability to sustain exercise is dependent on the capacity to continually replenish ATP through a combination of aerobic and anaerobic metabolic pathways.
- The oxidation of CHO’s and fat are central to this pathway, which means that single bouts of exercise have the capacity to modulate both energy and substrate balance.
- Heavier individuals will expend more energy than lighter individuals when performing the same weight-bearing activity
- In regards to running, a linear relationship exists between running speed and oxygen update. Therefore, the energy expended to cover a certain distance is approximately the same regardless of the speed at which it is completed

26
Q

The energy expenditure of running:

A

Can be estimated as: one kilocalorie per kilogram (of bodyweight) per kilometre (distance covered).
* E.g., a 75kg individual would expend ~750 kcal running 10kms

27
Q

‘Fat max’

A
  • As intensity progresses, the percentage of fat oxidised increases to a maximum which occurs at around 64% of maximum oxygen uptake (Achten et al 2002)
  • This point = ‘fat max’ (Jeuendrup and Achten et al 2001)
  • After this point, as intensity increases further, a reduced availability of oxygen and redistribution of blood to skeletal muscle reduce the contribution of fat to energy metabolism – here the contribution of CHO’s increases.
    During steady-state exercise, the relative contribution of fat to energy metabolism will increase as the limited stores of CHO in the liver (60-120g) and skeletal muscle (200-500g) are depleted (Flatt 1995)
  • Trained subjects are able to rely more on plentiful supplies of fat during exercise
  • Metabolic adaptions are central to this shift: increases in mitochondria, capillaries and oxidative enzymes.

Although the relative contribution of fat predominates at ow exercise intensities, the absolute amount of fa oxidised (grams) will be small when low-intensity exercise is performed. Thus, increasing the intensity of exercise, and overall rate of energy expenditure, will increase the amount of fat oxidised.
After a bout of hard exercise that predominantly relies on CHO as substrate, if this is not replenished and stores remain depleted, the energy deficit will subsequently be met through an increase in fat metabolism
- For the purpose of weight loss, a focus on the overall energy expended during exercise may be more relevant than the contribution of individual macronutrients.

28
Q

The consumption of food or energy containing drinks, before/ during exercise:

A

Glucose and insulin supress adipose tissue lipolysis and skeletal muscle fat oxidation. The consumption of food or energy containing drinks, before/ during exercise, therefore suppresses fat oxidation.
- Research as shown that a habitual diet that is high in fat can augment fat oxidation

29
Q

Post-exercise oxygen consumption (EPOC)

A

Whether a single bout of exercise affects resting metabolic rate, and therefore energy expenditure in the hours afterwards is an issue often referred to as post-exercise oxygen consumption (EPOC) and it is thought to reflect a heightened rate of metabolism elicited during the post-exercise recovery process.
Although exercise of higher intensity and longer duration is more likely to influence EPOC, consensus suggests that typical bouts of exercise that most people are able to complete are unlikely to raise post-exercise energy expenditure substantially.

30
Q

Does exercise increase appetite?

A

A large body of research has shown that single bouts of exercise do not increase appetite or energy intake.
- Research has actually demonstrated that moderate to high intensity exercise suppresses appetite (however, this response is typically brief and does not influence subsequent eating behaviour).
Taken collectively, individual bouts of exercise are able to induce a relative energy deficit which may contribute to weight management

(Research weakness: Assessment of eating behaviour in controlled laboratory settings may not provide the most ecologically valid data).

31
Q

Clinically relevant weight loss in individuals with obesity/ overweight is typically defined as what?

A

Equal or greater than 5%.

32
Q

Does exercise intensity matter?

A

Research evidence shows that weight loss responses seem to be most relevant to the exercise volume and energy expenditure rather than to the exercise intensity or modality
- E.g., weight loss is typically negligible with resistance training interventions as the energy expenditure elicited is low

33
Q

‘Sarcopenic obesity’

A

Individuals with obesity who also possess a low muscle mass.
* This condition is more common in older adults and is linked to insulin resistance and chronic low-grade inflammation (Cleasby et al 2016).
Training can also protect against the loss of bone mineral density during weight loss interventions (Villareal et al. 2006) and show that a combination of exercise and diet is needed to optimise changes in body composition during weight-reduction interventions.

34
Q

obesity in remission

A

A common problem in weight management is that few people can maintain their weight loss after successful interventions. As previously mentioned, this problem occurs because the body robustly defends against negative energy balance and weight loss. This issue has prompted the suggestion that individuals who have lost significant amounts of weight should be treated as having ‘obesity in remission’

35
Q

The most widely recognised recommendations regarding physical activity and weight management are those endorsed by the ACSM:

A
  • Guidelines suggest that 150 to 250 minutes of moderate-intensity physical activity per week is necessary to prevent weight gain.
  • This amount of physical activity is equivalent to an energy expenditure of some 1200 to 2000 kcal week –1 or the completion of 20 miles’ walking/running.
  • Notably, however, it is suggested that this amount of physical activity is sufficient to induce only a modest amount of weight loss (2– 3kg).
  • Instead, >225 to 420 minutes of physical activity per week are recognised as necessary to induce a clinically relevant level of weight loss of 5 to 7.5 kg
    The ACSM state with confidence that resistance training is not an effective means of facilitating weight loss.
36
Q

Summary:

A
  • Obesity results from positive energy balance, where energy consumed in food and drink surpasses that expended through basal metabolism, diet-induced thermogenesis and movement, over a sustained period.
  • Obesity risk is a product of genetic and environmental influences which interact.
  • The role of sedentary behaviour as a risk factor for obesity is not clear at present, with the possibility that weight ain may drive greater sedentary time.
  • Convincing evidence shows that physical activity is inversely related to obesity and obesity-related traits.
  • As a therapy, the ability of exercise to influence obesity is related to the accumulated effects of each individual bout on energy and substrate balance.
  • Exercise training can provoke clinically relevant weight loss if a sufficiently large amount of energy is expended, and energy compensation does not occur.