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Metabolism 2 > Diet and CHD > Flashcards

Diet and CHD Flashcards

1
Q

What is atherosclerosis

A
  • A focal disease of large and medium sized arteries characterised by fatty deposition and intimal thickening
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2
Q

What is bad and good cholesterol

A

HDL is a good cholesterol – high density lipoprotein

LDL – low density lipoprotein – bad cholesterol

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3
Q

triglyceride is not as bad as…

A

LDL

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4
Q

what are the modifiable major risk factors of cardiovascular disease

A

Hyperlipoproteinaemia - LDL, HDL, triglycerides
hypertension
smoking
diabetes

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5
Q

what are some more modifiable risk factors for cardiovascular disease

A 
Obesity 
dietary pattern 
physical inactivity 
ethanol intake 
psychosocial
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6
Q

How much does modifiable factors account for MI risk

A

90% risk factors of MI

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7
Q

What are the non modifiable risk factors for developing cardiovascular disease

A 
Increasing age  (development of atherosclerosis is a life-long process)
	Male gender (females before menopause protected – female sex hromoens stops the cholesterol and lipoproteins getting into the wall )
	Family history/ genetic – heritability  0.57 / 0.38 ♂/♀. Ethnic:- increased in South Asians
	1.7 million genetic loci identified [polygenic +++!] – total makes only a modest 	contribution to total risk, roughly = any one standard risk factor
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8
Q

as blood pressure and cholesterol increases…

A
  • As blood pressure increases death rate increases

- As cholesterol increases death increases

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9
Q

what is the NHS cholesterol range normally

A
  • cholesterol ranges normally below 5mm/L
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10
Q

what does obesity predispose you to

A
  • type 2 diabetes
  • hypertension
  • And MI
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11
Q

women have a …

A
  • Women have a 90 times risk of getting type 2 diabetes if they are obese
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12
Q

What is metabolic syndrome

A
  • A syndrome including an increased risk of cardiovascular disease consisting of:-
  • Insulin resistance/ Type II diabetes
  • Abdominal obesity
  • Dyslipidaemia (particularly hypertriglyceridaemia)
  • Hypertension
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13
Q

How does the metabolic syndrome work

A
  • cells take up fatty aids
  • lipoproteins takes the fatty acids of blood lipids
  • CD36 then carries the fatty acids into the cells
  • these fatty acids are normally metabolised in the mitochondria
  • but if there are too much fatty acid production this can make toxic byproducts such as ceramide
  • the toxic by products block signalling from the insulin receptor
  • this means that the cells cannot take up glucose from the GLUT4 transporter as it cannot go to the surface
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14
Q

any source of calories can be metabolised too…

A

cholestrol and therefore lead to CVD so instead of reducing intake of saturated fat and cholesterol we should control the total amount of calories that we intake

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15
Q

what can be cardioprotective

A
  • polysaccharide carbohydrate (starch) as whole grain

- dietary fibre

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16
Q

what are the classes of fatty acids

A

saturated
monounsaturated
polyunsaturated

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17
Q

describe saturated fatty acids

A
  • No double bond

- come with a different number of carbons

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18
Q

what is a monounsaturated fatty acid

A
  • single double bonds
  • less harmful forms of fat
  • has a Cis double bond
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19
Q

describe polyunsaturated fatty acids and some examples

A
    • Contain multiple double bonds

- 2 categories omega 3 (alpha-linolenic acid) and omega 6 (alpha Linoleic acid)

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20
Q

where are trans double bonds made

A
  • they are only made in industry these are very harmful so there is a reduction in the number we have produced (only 0.7% intake in the uK)
  • they are atherogenic so damage blood vessels
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21
Q

what are the difference names for omega 3 and omega 6

A 
omega 3 (alpha-linolenic acid) 
omega 6 (alpha Linoleic acid)
22
Q

what type of omega acid is arachidonic acid

A

Omega 6 fatty acids (Linoleic acid)

23
Q

what is the proper name for arachidonic acid

A

eicosa tetra enoic acid

24
Q

describe the structure of arachidonic acid

A
  • Has 4 double bonds
25
Q

describe what arachidonic acid is used for

A
  • Found in membranes phospholipid
  • It is released from the membrane by phospholipase A2
  • Metabolised to leukotrienes and prostaglandins - therefore gives rise to pro-inflammatory mediators
26
Q

what is a difference between omega 6 and omega 3

A

Omega 3 - gives rise to anti-inflammatory mediators which inhibit inflammation therefore better in the diet than omega 6, (e/g. resolvins, protectins & maresins)
omega 6 - sometimes gives pro inflammatory mediators

27
Q

omega 3 fatty acids are…

A

are relatively anti-inflammatory and anti-atherogenic

28
Q

what do aspirins and statin do in regards to omega 3 and omega 6

A

enhance anti-inflammatory mediators from 3 & 6 FAs

29
Q

What effect does egg have on cardiovascular disease

A

Choelstorl
• Egg consumption  1/day (major source of cholesterol -200mg/egg) shows no correlation with CVD, except possibly in diabetes patients
• Currently reported that egg consumption reduces stroke incidence

30
Q

what is most cholesterol synthesised from and why is this important

A
  • More cholesterol is synthesised in the body from saturated fatty acids each day (about 1g), than is ingested (about 0.3g).
  • Conclusion: Dietary cholesterol has little importance in regulating serum cholesterol or risk of CVD
31
Q

What are flavonoids

A

Pigmented polyphenol (flavone-like) plant compounds involved in photosynthesis and protection from UV light.

32
Q

Where are flavonoids found

A

Found in fruit, vegetables, tea, chocolate/ cocoa, wine, olive oil.

33
Q

What do flavonoids have beneficial effects on and why

A

Have beneficial effects on MI & stroke in epidemiological studies, particularly flavone & flavonol groups.
- Are inhibitors of inflammatory enzymes, including NADPH oxidase that generates damaging reactive oxygen intermediates.

34
Q

Name some examples of flavonoids

A

quercetin (flavonol) - apples, onions, citrus fruits

epicatechin (flavon-3-ol) - tea, chocolate

35
Q

what is the best diet to act as secondary protection for an MI

A

Mediterranean diet

36
Q

What does the Mediterranean diet consist of

A

Fish, pasta, salads laced with olive oil, vegetables++, cereals, pulses, fresh fruit, nuts, red wine

37
Q

how are nitrates protective

A

Nitrates: from beetroot & green leafy vegetables  nitric oxide production

38
Q

How are sulforaphane protected

A

Sulforaphane: protective organosulfur molecule in brassica vegetables e.g. Cabbages

39
Q

why can wine be cardioprotective

A
  • Protective effects of alcohol through improving blood lipid profile and inhibiting thrombosis
  • Wine contains multiple flavonoids and flavonoid like compound resveratrol with anti-CVD and possible life prolonging effects
40
Q

how can a deficiency in B12 and folate cause cardiovascular risk to increase

A
  • causes low level of methionine and high blood homocysteine level
  • homocysteine spontaneously converts to thiolactone which can damage to the endothelial cells
41
Q

how does exercise reduce cardiovascular risk

A
  • Exercise stimulates blood flow through arteries which increases production of nitric oxide which can cause dilatation and is anti-atherosclerotic
  • This reduces hypertension through the dilatation and reduction of peripheral resistance in the blood vessels
42
Q

What should blood cholesterol be lower than if you are normal and if you are at high risk of CVD

A
  • Total cholesterol should be less than 5 mmol/L in healthy
  • If you are high risk of CVD then below 4 mmol/L
  • The lower cholesterol can be kept the better
43
Q

what are the things that regulate atherosclerosis forming

A

endothelial dysfunction

  • pro-infllammtory
  • pro-atherosclerosis

normal

  • anti-inflammatory
  • init atherosclerosis
44
Q

what factors are endothelial dysfunction, pro inflammatory and pro atherosclerosis

A
  • hyperlipideamiea and LDL
  • smoking
  • hyperglycaemia (diabetes)
  • homocysteinaemia
  • oxidised LDL and atherosclerosis itself as it creates a positive feedback loop
45
Q

what factors are anti-inflammatory and anti-atherosclerosis

A
  • HDL
  • increased blood flow due to exercise
  • nitrites from nitrates
  • nitric oxide
  • flavonoids in fruit, veg and wine
  • anti inflammatory mediators from omega 3 fatty acids
  • statins
46
Q

why things during birth and pregnancy can predispose the feotus to cardiovascular disease

A
  • Low birth weight increases risk
  • this is because eating during pregnancy - starved fetus reprogrammed neuro-homronal pathways for lipid metabolism and therefore increases cardiovascular risk later in life
47
Q

Wha happens if you increase your fat intake and total saturated fat intake

A
  • Obesity
  • Increase hepatic cholesterol synthesis – increases hypercholestrolaemia
  • Increase LDL
48
Q

what happens if you increase refined carbohydrate

A
  • Obesity
  • Metabolic syndrome
  • Type 2 diabetes
  • Hypertriglyceridaemia
49
Q

what happens if you increase salt intake

A
  • Hypertension
50
Q

what happens if you decrease folate/B6/B12

A
  • Homocysteinaemia
51
Q

what happens if you decrease physical activity

A
  • Decrease HDL

- Decrease nitrix oxide in arterial wall

52
Q

What does the NHS recommend for diet

A
  • Eat a balanced diet, not to excess.
  • Plenty of potatoes, bread, rice, pasta or other starchy foods (polysaccharides with a low glycaemic index)
  • Plenty of fruit & vegetables:- 5 portions (of 80g) a day
  • Moderate amounts of low fat milk and dairy foods
  • Moderate amounts of meat, fish, eggs & beans (sources of protein)
  • Restrict food & drink with a high fat, sugar or salt content (e.g.chips, fizzy drinks, crisps)

Metabolism 2 (40 decks)

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