Lecture 2 - Appetite, Energy & Obesity Flashcards

1
Q

Describe the homeostatic principles behind regulating food intake.

A

We have an internal state that our bodies are motivated to retain. This is based on physiological cues that start and stop people eating (Rosenbaum & Leibel 1998)

We eat until homeostasis is restored and are motivated to maintain the absence of hunger.

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2
Q

Outline the evaluative point regarding homeostatic principles of food intake.

A

Hunger and food intake is a combination of biological controls, external environments and psychological factors.

This has implications as learned behaviours can be unlearned.

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3
Q

Define Satiation

A

A process that stops ongoing feeding, a within-meal process that is influenced my a number of processes:

  • Social setting
  • Attention
  • How eating feels
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4
Q

Define Satiety

A

Inhibits intake after termination of a meal. Stops further food seeking behaviours for a period of time.

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5
Q

Describe how the processes of satiety and satiation are complex.

A

Forms an analogy with ST and LT memory which involves several sensory systems.

If you were to manually fill the stomach, you would still feel hungry as the sensory process has not occurred.

If satiation was just physiological there wouldn’t be a “pudding tummy”.

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6
Q

What is the Satiety Cascade?

A

Describes a series of behavioural and physiological events that occur following food intake and that inhibit further eating until the return of hunger.

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7
Q

Outline the elements in the satiety cascade.

A

Sensory - feedback on smell, texture taste etc, little effect after a while.

Cognitive - dieting, social conventions, perceptions on volume etc.

Post-Ingestive - Stomach stretch, CCK, PYY, Ghrelin

Post- Absorptive - Insulin, glucose, oxidation, amino acids, negative effects (intolerances, sickness etc)

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8
Q

Name the central biological mechanisms implicated in maintaining energy balance.

A

Ventromedial Nucleus- satiety
Lateral Hypothalamic Area - hunger
Arcuate Nucleus - integration of appetite signals
Paraventricular Nucleus - junction between orexigenic and anorexigenic neuromodulators, among side endocrinological pathways such as stress.

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9
Q

According to Wynne et al 2005, describe the role orexigenic peptides in food intake.

A

Anabolic effector pathways - substances are synthesised into complex material of living tissue. Processes and stores fat.

These pathways promote the search and consumption of food, therefore decreasing energy expenditure and increasing hunger.

NPY, Orexin

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10
Q

According to Wynne et al 2005, describe the role of Anorexigenic peptides in food intake.

A

Catabolic effector pathways - breakdown complex molecules into energy release.

Decreases intake by inhibiting hunger.

CRF, 5-HT

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11
Q

Name the two types of peripheral mechanisms in food intake.

A

Episodic Factors

Tonic Factors

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12
Q

Describe the role of episodic factors in food intake.

A

Episodic factors act in response to a meal and have a short term influence.
For example ghrelin is a hunger hormone that stimulates appetite by lowering leptin. Studies show that PPS eat 30% more when ghrelin is infused in the stomach.

Another example is CCK which is the satiety signal, released by stretch receptors in the stomach and received by the hypothalamus.
Implicated in BN as blunted CCK release when given a test meal (no satiety boundary)

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13
Q

Describe the role of tonic factors in food intake.

A

Monitor energy levels and storage in the long term (weeks).
How much fat you have can be a marker of energy stores so related to adipose tissue & immune system.

For example Leptin is a satiety hormone produced in adipose tissue thought to regulate genes involved in basal metabolism.

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14
Q

Outline the 3 components of energy expenditure.

A
Basal Metabolism (60-75%)
Thermogenesis (10%)
Physical Activity (15-30%)
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15
Q

Define Thermogenesis

A

Burning food by act of digestion e.g. celery

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16
Q

Define basal metabolism

A

basic or least amount of wenger required to survive when resting.

Energy is used to support life sustaining functions:
Liver - 26%
Muscle - 26%
Brain - 18%
Heart - 9%
Kidney - 7%

BMR = weight x 21 (F) 24 (M)

17
Q

Outline the 4 macronutrients and their associated contents.

A

Fat - 9kcal/g
Carb - 4kcal/g
Protein - 4kcal/g
Alcohol - 7kcal/g

Fat is more energy dense and less satiating than carb and protein (also highly palatable)

18
Q

How does volume affect satiation?

A

How much is in our stomach e.g. same calories but different volume (choc vs pasta) learn to like fattening foods as feel nicer at post-ingestive level. Full up for longer on fattening foods (choc) despite volume.

19
Q

Outline the ways to measure body fat.

A

Skinfold - pinch amount of fat.
Bioelectrical Impedance - scales send pulse around the body. How easy it travels is a measure of how much fat. Hard to travel through muscle. Based on water content.

20
Q

What is the problem with using BMI as an indicator of obesity?

A

Muscle weighs more than fat so may not be carrying excess adiposity but still numerically be obese.

21
Q

Outline the epidemiology surrounding obesity.

A

WHO, 2000 suggests obesity is a global public health crisis.
In 2016, WHO recorded 39% women & 39% men as being overweight.

Foresight 2007 estimated that by 2050, 60% men, 50% women and 25% children will be obese.

22
Q

Outline the complications of childhood obesity.

A

Obesity is not just a physiological problem as there are many psychosocial and medical factors involved such as poor self-esteem, depression, ED, endocrine and cardiac issues.

Reduced life expectancy but is not linear.

23
Q

What are the risk factors for childhood obesity?

A
SES
Cultural Differences
Permissive PArenting
Types of Food
Generational Effects
24
Q

Outline how SES is a risk factor for childhood obesity according to Cecil et al 2005, drawing on cultural differences.

A

Low SES may include; easy foods, deprivation, lack of education and single-parent abilities. Cecil et al found that children are shorter in dperived areas with high BMIs.

Cultural Differences - US Hispanic & Black - sit below the poverty line, where healthy food is less accessible and high crime means some children may lead sedentary lives due to it being unsafe to go out.

25
Q

Explain how environmental and behavioural factors contribute to obesity.

A

Modern day is now an obeseigenic environment as individuals have a positive energy balance (more in than out).

Portion sizes have also increased over time along with availability, price of food and convenience.

Jebb & Prentice 1995 suggest inactivity is as important as foods and portion size for obesity.

26
Q

Explain how there may be a genetic predisposition to obesity.

A

For many illnesses, 50% variation between individuals can be explained by genetic polymorphisms - how different people express genes.
Cecil et al 2007 found that the gene PPARg Pro12Ala protects but is not associated with ST energy compensation (compensating for previous intake). This suggests that overconsumption is not just a learned behaviour.

No single gene found for obesity.

27
Q

Outline the biological factors contributing to obesity.

A

Metabolic rate is higher in obese people due to the need to burn more energy in thermogenesis.

Fat Cell Theory - number and size of fat cells determines quantity of fat stored - Av = 25bill, Obese= 100bill+.

Diseases: obesity is a comorbid factor - Prada-Willi syndrome, Down’s Syndrme, PCOS.

28
Q

Explain how obesity genetics (hereditary) may play a role in obesity.

A

With obese parents, a child has 80% chance of being obese, compared to a child with no obese parents at 7% chance.

Twin studies, Stunkard et al 1990- 70% variance accounted for in indentical twins compared to non-identical twins reared together. Suggests the genetic material is shared as opposed to shared environment.

Biological Vs Adoptive mothers - stronger relationship with biological.

Leptin high in obese people as produced by fat cells.

29
Q

What problems are there with the study of biological factors in obesity?

A

Research in the area is not robust as there are many contradicting studies, all of which have many confounding variables.

30
Q

Explain how studies using mice provide insights into the role of Leptin.

A

Mice who are reared to have a missing leptin gene get fat as the satiety hormone is absent.
When injected with leptin, or grafted with a mouse with leptin, dramatic weight loss is seen.
However there s no evidence of this in humans as mutations of leptin gene are rare.

31
Q

According to Brownell & Wadden 1992, what approach should be taken to provide multi-dimensional treatment?

A

Reasonable weight goals should be made for each individual to ensure positive impact on lives.
Each individual will have different medical, biological, behavioural and pro-social consequences of intervention, suggesting it is much more than a case of energy balance (EI,EE).

32
Q

Name and describe the 3 methods of studying food intake.

A

Behavioural Assays - ratings of hunger, appetite and satiety following test meals to identify responses to deprivation, preloads, distractions, stress etc. Compliments physiological data.

Food intake in Lab - preload & test meal, controlled by repeating and balancing over time.

Microstructure - Universal Eating Monitor - measures continuous FI during meal by weighing table. Can plot against appetite ratings etc.

33
Q

What are the problems with obesity research?

A

Lab & Observational studies change what people actually eat (SDB).
Self-report open to under-reporting, forgetting & SDB.
Comparing intake amongst individuals ignores variability in energy requirements, body shape, portion size etc.
Data is correlational with third variables occuring making it a multi-faceted phenomenon.
Ecological fallacy = Population level Vs individual level. Population data can hide many IDs - say something different at each level.
Values of Researcher - overeating assumed to be wrong, only in cultures where food is freely available and weight gain is regarded as unacceptable.

34
Q

Explain Cannon & Washburn’s 1912 experiment regarding the physiological-psychological dichotomy, and identify the advantages and disadvantages of this method.

A

Gastric Balloon - subjective hunger alongside gastric contractions seen by balloon inflating.

Adv - broken down into different levels of analysis, systemic to molecular, and allows to test theory in hypothetic-deductive manner.

Disadv- invasive, ecological validity, demand characteristics.

35
Q

Why is the physiological- psychological dichotomy a false one?

A

They reflect different entities of the same system.

36
Q

What are the factors associated with consumption in a lab?

A

Previous meal - what and when.
Adult/Child, Gender
Choice of test meal - buffet or large portion
Portion size
Alone or in group, familiar or strangers.