symposium Flashcards

1
Q

how much of our diet is fat

A

diet and exercise modify risk of arterial disease (endothelium dysfunction)
95% dietary fat is triacylglycerol
Fatty acids (saturated, monounsaturated or polyunsaturated) and glycerol
Dietary fat and formation of lipid profile
Consists of a range of fatty acids

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2
Q

how does fat interact with the liver

A

liver>VLDL>LPL>IDL(back to liver)or>LPL>LDL>LIVER

Adipose tissue and muscle>FFA>LPL(SI>Chylomicron>LPL)>Chylomicron remnant>LIVER

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3
Q

what is saturated fatty acid intake associated with

A

with increased CHD risk
Dietary fats and fatty acids are complex – not one answer as to their CHD risk
Meta analysis reaffirms guidance to reduce

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4
Q

how do fatty acids vary

A

Different individual fatty acids, such as odd or even saturated or short, medium, long saturated fatty acids have different metabolic pathways.
Eg Extra virgin coconut oil promoted to healthy oil, main saturated fatty acid is lauric acid
Butter, palm oil and animal fat, main saturated fatty acids are palmitic acid

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5
Q

what are polyunsaturated fatty acids

A

omega 3
ALA-EPA-DHA>minimally inflammatory and inflammation resolving
omega 6
LA-AA>pro inflammatory

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6
Q

what is omega 3

A

Long chain PUFA, EPA and DHA acid derived from oily fish
Shorter chain PUFA can act as a EPA precursor
Health benefits of omega 3 are associated with anti inflammatory responses ans decreased expression of genes involved in inflammatory and atherogenesis related pathways
Recent review = increasing DHA/EPA had little effect on cardiovascular death, coronary death or events, stroke or heart irregularities.

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7
Q

what is omega 6

A

Linoleic acid
Main dietary sources include corn oil, intakes of omega 6 have exceeded saturated fats in recent years
Metabolised to form AA which is considered pro inflammatory
LA in adipose tissue, but also in platelets, is positively associated with CAD

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8
Q

what is the CVD risk of LA

A
Opposing views 
Arguments for reduction 
Reduced TC and LDL
Argument for increased risk 
Increases susceptibility of LDL and other lipoproteins to oxidation 
Increases small dense LDL
Reduce HDL
Increase TGs
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9
Q

what are dietary carbs

A

Dietary carbs include non starch polysaccharides, starch polysaccharides, disaccharides and monosaccharides
From these only three sugars are absorbed glucose, galactose and fructose

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10
Q

how do carbs link to lipid profile

A

Low carb fashionable – type 2 diabetes remissions
Short term impact on reducing wight, insulin resistance, HbA1c and TG profile
But long term, heterogenous in nature with no definition for low carbs

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11
Q

how do carbs affect diet

A

Reduction in dietary intake of fat = inc intake of carbs,
decreases total LDL (but increases small dense LDL so greater atherogenesis)
A down reg of insulin response due to continued stimulation from higher carbs = lipolysis
Increases a greater delivery of fatty acids and an increase in hepatic esterification over production of VLDL, particularly TG-rich VLDL1
Carbs hepatic synthesis of VLDL and reduction in HDL

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12
Q

how do fruits and veg affect diet

A

Diets higher in vegetables and fruits commonly associated with a reduction in CVD risk
Soluble fibre in plants shown to decrease serum cholesterol by inhibiting reabsorption in GI tract
Consumption improves antioxidant status by improving plasma total antioxidant capacity and glutathione peroxidase activity in healthy young adults
Primary emphasis on improving lipid profile
Increase low calorie fruit and vegetable intake to at least 5 portions a day

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13
Q

what are dietary patterns

A

Increased interest in pattern as opposed to single nutrients of food groups
Study on Mediterranean diet without energy restriction on CVD risk
USA DASH eating plan with no special foods just nutritional goals (fruit, veg, whole grains including fat-free/low fat dairy, fish, poultry, beans, nuts and veg oils and limiting food in high saturated fat like meats, full fat dairy and tropical oils, also limiting sugar)

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14
Q

what did the PREDIMED and DASH studies find about diet

A

PREDIMED (Mediterranean)
1 year randomised control trial of those at high CVD risk
Reduced ambulatory bp, fasting blood glucose and total cholesterol

DASH
Compared to control diet
Lowered BP, total cholesterol (LDL and HDL)

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15
Q

what is obesity

A

Weight gain associated with energy intake being greater than energy expenditure
Excess energy intake leads to obesity
Reducing energy intake and increasing exercise can lessen
Fat tissue provides a source of FFA in circulation providing fatty acids for metabolism
Visceral adipose tissue is less responsive to insulin and delivers FFA to circulation (inc ROS, inhibit NO, activate RAS, induce adiposis)

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16
Q

how does visceral obesity affect lipoproteins

A

High lipolytic activity of visceral fat contributes to deliver an increased load of FFA to liver
FFA converted to TG and stored in cytosol
Via cholesteryl ester transfer protein and hepatic lipase activity, TG enriched low density lipoprotein become small and denser
High atherogenic and easily transformed into oxidised LDL

17
Q

how does fat and exercise link

A

Psychological and physiological benefits of exercise are well documented
Up regulates lipoprotein lipase activity in skeletal muscle, increasing TB clearance
Decreases hepatic VLDL synthesis
Decreases total cholesterol, TG and LDL-C
Aim to be active daily, 150 mins of moderate activity (bouts of >10 mins)

18
Q

what studies show the effects of exercise

A

STRIDE-1 – target risk reduction intervention through defined exercise
Independent of diet exercise
Reduced LDL cholesterol particle number, increases LDL-C size
Increased HDL-C particle number and size
Clinical trials showing sig effect of diet or exercise
DASH
DART – 29% REDUCTION IN DEATH
GISSI – SIG REDUCTION OF ONE OF TWO COMBINED END POINTS
PREDIMED

19
Q

what are the stages of change

A
pre-contemplation
contemplation
preparation 
action
maintenance
relapse
20
Q

what is motivational interviewing

A

A collaborative conversation to strengthen a person’s own motivation for and commitment to change

21
Q

how should an MI be delivered

A
Collaboration, evoking and autonomy. Not confrontation, imposing and authority 
Express empathy
Support self-efficacy
Roll with resistance
Develop discrepancy
22
Q

what are MI core skills

A

Open questions
Affirmations
Reflections
Summaries

23
Q

what are open questions

A

Cannot be answered in one word, usually begin with what or how
Encourages talking expression
Helps establish an atmosphere of trust and acceptance

24
Q

what are affirmations

A

Noticing what is right about someone
Recognition and acknowledgement of strengths, values, effort, achievement
More than simple praise or compliment

25
Q

what is reflective listening

A

Repeating back to the speaker something of what they said but not word for word (repeating, mirroring) – rather, rephrasing in own words
Serves to
Help person feel listened to and understood them correctly
Encourage other person to keep talking
Sometimes help the other person understand themselves better

26
Q

what are summaries

A

Capturing elements of what a person has said
Saying back without giving advice or judgement
Useful at start, when stuck and definitely at end
A way to interrupt politely

27
Q

what is ambivalence

A

Ambivalence normal
Listen for change talk
Differentially reflect change talk