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Nutrition week 10

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winniesmith2's version from 2018-01-18 13:16

Section 1

Question Answer
Malnutrition definition deficiencies, excesses of imbalances in intake of energy, protein and/or other nutrients.
Over-nutrition defintiona chronic condition where intake of food is in excess of dietary energy requirements.
Global prevalence of obesity (Lancet)Looked at trends in adult BMI in 200 countries from 1975-2014, pooled analysis of 198 population measurement studies with 19.2 million ppts. Found that 'if these trends continue, by 2050, global obesity prevalence will reach 18% in men and surpass 21% in women.
Childhood obesity prevalence according to the annual UK national child measurement programme 2012-13– 18.9% of 10-11 year olds were obese – 14% were overweight
Childhood obesity prevalence NHANES showed – Among 6-11-year-olds obesity prevalence increased from 7 to 18% – For 12–19-year-olds, the increase was from 5 to 21%
International prevalence of obesity in children (<15 yrs)may countries have an obesity rate of 25% such as Greece and the USA, meaning 1/4 children are obese
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Section 2

Question Answer
How is obesity measured body mass index
What is BMI surrogate measure of body fatness -measures excess weight (not fat). Defined as the individuals body mass (kilograms) divided by the square of the height (metres)
underweight>18.5
normal range18.5 - 24.9
overweight>/= 25
preobese25-29.9
obese>/=30
obese class 130-34.9
obese class 235-39.9
obese class 3>/=40
BMI classification for childrenDefinitions of obesity (BMI) for adults generally unacceptable because of dynamic process of growth & development – Appropriateness of BMI depends upon age, timing of adiposity rebound and degree of sexual maturity
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Section 3

Question Answer
What is adiposity rebound • The point of maximal leanness or minimal BMI • An early AR is associated with an increased risk of adult obesity • Early adiposity rebound (AR) recorded in obese children (2 years) as compared with 6 years in average
US; CDC BMI-for-age growth charts; >/=95th percentileobese
US; CDC BMI-for-age growth charts; 85th - <95th percentileoverweight
US; CDC BMI-for-age growth charts 5th-<85th percentilenormal weight
US; CDC BMI-for-age growth charts; <5th percentileunderweight
WHO BMI-for-age cut-offs different charts for girls and boys. from 5-19 years of age. Used in conjunction with the WHO child growth standards from 0-5 years.
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Section 4

Question Answer
BMI has its limitations Two people with the same BMI can have very different patterns of body fat distribution. And different risk of cardiovascular disease and risk of developing type 2 diabetes.
What is a DEXA scannera way at looking at body composition, bone density and body fat.
BMI vs Body Fatthat BMI and body fat are highly positively correlated. Good agreement between the 2 measurements.
BMI has low sensitivity; what does this mean that it was unable to detect more than half of individuals with %BF defined obesity.
why use BMI?• Simple, inexpensive and non-invasive tool • High BMI is an important risk factor for CVD, T2D etc. • Good tool for tracking and identifying population trends- comparisons across time, regions and population subgroups e.g. NCD-RisC network:
Issues with BMI?• Surrogate measure of body fatness • Age, sex, ethnicity and muscle mass can influence interpretation of BMI • Does not distinguish between excess fat, muscle or bone mass • Does not provide indication of body fat distribution
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Section 5

Question Answer
What other methods can be used to assess obesity DEXA scanner, MRI scan (but very expensive) skin fold test etc
How do you measure abdominal obesity and whyby waist circumference - more indicative of the metabolic syndrome than increased BMI. Gives indication of intra-abdominal (visceral) fat - lines internal organs.
What kind of adipose tissue is found in the obese statedysfunctional adipose tissue. linked with increased risk of CVD.
What does dysfunctional adipose tissue do releases pro-inflammatory adipokine signaling. which leads too insulin resistance. Both of these then lead to stroke, myocardial infarction and peripheral artery disease.
What is affected by the pro-inflammatory adipokine signaling due to/causing insulin resistanceVasculature (defective insulin signaling). Skeletal muscle (impaired glucose uptake). Liver (dyslipidemia gluconeogenesis).
What is metabolic syndrome causing its driving the twin global epidemics of type 2 diabetes and CVD.
According to the international diabetes federation; for a person to be defined as having metabolic syndrome they must have; Central obesity (defined as waist circumference with ethnicity specific values) plus any two of the following 4 factors; Raised triglycerides, reduced HDL cholesterol, raised blood pressure, raised fasting plasma glucose.
Europids waist circumference cut off points male; >94cm and female >80cm. (some Asian countries are slightly lower).
Research at Loughborough; adipose tissue biopsy procedure; uses whatlocal anaesthetic (1% lidocaine hydrochloride), Scalpel blade, 14 gauge suction catheter and 60mL syringe (suction device) and 6mm barnstorm needle.
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Section 6

Question Answer
What is energy balance state in which energy intake, in the form of food and/or drinks, matches the energy expended.
Positive energy balanceEnergy in> energy out -results in weight gain
Negative energy balance Energy in
Obesity basic definition causewhen your energy intake is more than your energy expenditure over a long period of time.
Aetiology of obesity; main components social influences, food production, food consumption, individual psychology, biology, individual activity, activity environment,
Health consequences of obesity; diagram page 11metabolic syndrome, sleep apniaee, depression and anxiety.
Who- global risks for mortality top 5 cause. due to increase risk of chronic diseases. e.g. cancer and heart disease.
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Section 7

Question Answer
Foetal programming-barker hypothesis, evidence shows that that obesity starts in the womb, both over and under eating in pregnancy can increase risk of obesity of infant.
What is the barker hypothesis/ foetal origins of adult disease hypothesis/ foetal programming hypothesis'adverse environments in foetal life and early childhood establish increased risk of disease in adult life'
Foetal programming hypothesis processInadequate maternal nutrition/disturbances in maternal ability to transport nutrients-> Foetal undernutrition -> Foetus adapts by altering the structure and metabolism of its organs and tissues -> Adaptations result in permanent changes which ‘programme’ the development of risk factors for non-communicable diseases in later life
Birth to twenty cohort study- south africa. what did they do;Looked at babies over lower birth weight and normal birth weight - longitudinal study. -Babies of low(er) birth weight exhibit rapid growth during infancy • Rapid growth sometimes called “catch-up” growth • Rapid weight gain: Catch-up growth >0.67 Z-scores from 0 – 2 years
Birth to twenty cohort study- found that looked at 9 years of age, they looked at children of normal weight and children of rapid weight gain. found that children with rapid weight gain had significally higher BMI, Wasit circ, hip circ, sum skinfolds, bone mineral composition, fat weight and %fat.
What do the findings of the birth to twenty study show (page 14)That lower birthweight, causes rapid or catch up growth during infancy/childhood, which causes increase in measures such as central fat, insulin resistance, increased glucose intolerance and these can all lead to metabolic syndrome, obesity, type 2 diabetes and CVD.
Maternal obesity and foetal metabolic programming• Maternal obesity + pregnancy = ↑ maternal circulating lipids with advancing gestation • ↑ foetal lipid exposure may impact the liver, skeletal muscle, adipose tissue, brain, and pancreas to increase the risk for metabolic disease in childhood
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Section 8

Question Answer
Genetics component of obesity - how can we tell thisby looking at • Familial aggregation – Familial clustering of obesity in families and • Twin studies – Greater concordance among monozygote compared with dizygote twins
Genetic factors of obesity • The full range of genes that promote obesity is largely unknown • Single gene defects explain a small proportion of childhood obesity – Melanocortin receptor defects (MC4R)- 5% – Leptin receptor defects- up to 3% • Most of obesity risk will be the result of having obesity promoting variants of multiple genes. – Harder to identify
Recently discovered factors that may play a major role in risk ; FTO geneFTO gene – Explains 1% of variance in whole population BMI – 16% have an obesity-promoting variant of FTO. – FTO plays a role in controlling food intake • Obesity-promoting variant prolongs intake and promotes eating between meals.
Heritability of obesity estimated at 40-60%
Over how many genes may influence adiposity 300
Genetic factors may influencebody size and shape, body fat distribution, metabolic rate, brain chemistry.
What is the thrifty metabolism gene (summary)allows for increased fat storage to protect against famine.
Thrify metabolism gene cause • Cycle of feast and famine • Those that were better at fuel storage or utilization more likely to survive during famine • Over generations, we developed genetically to be exceptionally efficient at the intake and utilization of fuel
Brown study on thifty gene of Samoan obesity • 35% higher of being obese vs. those who do not have the CREBRF gene variant but the rapid rise in obesity cannot be explained by genetics only… • Stephen McGarvey- Brown University School of Public Health “Samoans weren’t obese 200 years ago. The gene hasn’t changed that rapidly — it’s the nutritional environment that changed that rapidly.”
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Section 9

Question Answer
Obesity is due to what both the environment and genetics. The current environment potently facilitates the development of obesity. Genetics has an effects but its the energy intake v energy expenditure due to environment that is the deciding factor for variation in body weight
Change in food portions over the last 20 years food portion sizes have grown, especially for junk food such as pizza, crisps etc.
TV watching and obesity risk, study of children aged 7 TVs in bedroom linked to childhood obesity. • Impact most likely due to changes in food intake rather than reduced physical activity – More exposure to adverts for energy dense food – Greater consumption of sugar sweetened beverages and energy dense snacks .
Sugar case study (no recording)page 19 onwards. go over
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