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HL22015 physiology > Nutrition health and exercise > Flashcards

Nutrition health and exercise Flashcards

1
Q

What is known about the causal effect of diet on hard outcomes?

A

Little

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2
Q

Issues with non-randomised data?

A

It can be biased

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3
Q

What is revesed causality?

A

Smthn ab a disease might cause someone to change their diet

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4
Q

Example of reverse causality?

A

Obese people drink diet soft drinks–> diet soft drinks dont cause obesity its just that obese people drink them bc they want to lose weight

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5
Q

What are confounding factors?

A

One factor directly causing the disease, and another cause

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6
Q

Example of confounding factors?

A

Smoking–> causes cardiovascular disease, and changes in diet which in turn also cause cardiovascular disease

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7
Q

How does randomisation minimise systemic bias?

A

It can minimise the effect of known and unknown confounding factors

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8
Q

Example of long term study on diet effect on outcomes?

A

Mediterranean diet (oil, fish, vegetables and no red and processed meats) vs low fat diet (low fat dairy products, bread, potatoes, pasta) for 5 yrs

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9
Q

Observations of Mediterranean diet vs low fat diet?

A

Mediterranean diet has a lower risk of getting a cardiovascular event compared to low fat diet

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10
Q

What is metabolic health?

A

The ability to maintain metabolic control

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11
Q

Maximal eating study?

A

Ate dominoes pizza until comfortably full vs eating until they physically couldnt eat anymore

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12
Q

Results of maximal eating study?

A

1500kcal for normal, 3000 for maximal. 57g fat vs 113g. 187g Cho vs 367g

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13
Q

What happens when double the amount of fat is eaten?

A

Fat levels in the blood don’t increase by 2* (triglyceride conc in blood increase was buffered)

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14
Q

Why do fat levels in blood not increase by 2* when 2* the amount of fat is consumed?

A

Metabolite conc in the blood is buffered

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15
Q

What is observed regarding insulin secretion in maximal eating group?

A

It is secreted more

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16
Q

What is the oral glucose tolerance test?

A

drink w/ 75g of glucose

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17
Q

What is an oral fat tolerance test?

A

Give people x amount of fat and observe the metabolism

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18
Q

What is measured in oral glucose tolerance test?

A

Blood glucose response

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19
Q

Association between metabolic control and cardiovascular mortality?

A

Better metabolic control = lower CVD mortality

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20
Q

Healthy blood glucose cond 2 hrs post OGTT?

A

<7.8 mmol/L

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21
Q

Prediabetic blood glucose cond 2 hrs post OGTT?

A

7.8-11 mmol/L

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22
Q

Diabetic blood glucose cond 2 hrs post OGTT?

A

> 11 mmol/L

23
Q

Average triglyceride conc difference between sexes?

A

Women have a lower average triglyceride conc than men

24
Q

Issue with measuring conc of glucose?

A

Metabolism is dynamic so conc might be 5mmol/L, but there could be 130mg per min going in and out

25
Q

Where does glucose come from if we haven’t eaten a meal?

A

Liver–> breakdown of glycogen, and gluconeogenesis

26
Q

What is the main glucose consumer from the bood when resting?

A

Brain

27
Q

Causes of an abnormally high BGC?

A

Defective liver glycogen metabolism (too much) or defective glucose uptake in muscles (too little)

28
Q

Glycemia?

A

Blood glucose cond

29
Q

Effect of eating in blood?

A

Rise in BCG and lactate conc that reduces over time, and a suppression of circulating FAs

30
Q

Why does blood lactate conc increase after eating?

A

Glycolysis stimulated by insulin

31
Q

Why are circulated FAs suppressed after eating?

A

If FA conc remained high there would be competition for the muscle fuel uptake–> want muscle to take up glucose instead to buffer BGC

32
Q

Effect of insulin on FFAs?

A

Suppresses their availability-> inhibits adipose tissue lipolysis

33
Q

Effect of insulin on liver?

A

Suppresses liver glucose output

34
Q

Postprandial meaning?

A

After a meal

35
Q

What is glycaemic index?

A

A way to classify carbs

36
Q

How is glycaemic index calculated?

A

Give people 50g of available carbs, measure blood glucose conc over 2 hrs and calculate area under curve and compare this to a refernce

37
Q

What is the reference for a glycaemic index?

A

Pure glucose, white bread

38
Q

What if the area under the curve of a food is the same as glucose?

A

GI=100

39
Q

What if the area under the curve of a food is half that of glucose?

A

GI=50

40
Q

What are high GI foods?

A

> 55

41
Q

What are low GI foods?

A

<55

42
Q

What GI is spaghetti regardless of wholemeal or white?

A

Low GI

43
Q

What GI is bread regardless of wholemeal or white?

A

High GI

44
Q

Monosaccharides example?

A

Glucose, fructose, galactose

45
Q

Difference between sucrose and isomaltulose?

A

Bond between glucose and fructose is stronger isomaltulose

46
Q

Oligosaccharide example?

A

Maltodextrin

47
Q

Polysaccharides?

A

Amylopectin (starch) and amylose (starch)

48
Q

Benefits of isomaltulose over sucrose?

A

Lower GI (more slowly digested) and better for teeth as it isnt fermented in the mouth

49
Q

What is maltodextrin used ?

A

Sports nutrition products

49
Q

What is maltodextrin made up of?

A

8-12 glucose molecules

50
Q

Differences between amylopectin and amylose?

A

Amylopectin is branched, amylose is straight & Amylose has a lower GI as it takes longer to digest–> enzymes can only work on ends and in branch there is more ends

51
Q

How is area under curve counted for BGC?

A

Look at resting BGC, only count area that goes above it (incremental area under curve)

52
Q
A

HL22015 physiology (17 decks)

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