SSEH3301 Lecture Notes - Lecture 3: Phospholipid, Blood Lipids, Trans Fat

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29 May 2018
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Lecture 3: SSEH3301: Risk Factor Modiļ¬cation
-RF needs to: in a population, when present,
increases risk of CVD!
-must have underlying association as to why it
causes the disease (must be able to explain
pathophysiologically)!
!
-modiļ¬able: have control over this!
-non-modiļ¬able: inherited!
- BIG 6! Together they are modiļ¬able !
!
-if modify RF, can alter risk of CVD!
- changes in physical activity, high cholesterol, BP = massive
aļ¬€ect!
!
-especially for CVD!
-Age: as we get older, other RF
worsen (BP, weight, physical inactive),
our arteries naturally harden !
-gender: up until women reaches
menopause (risk of CVD between M and W tend to even up when
menopause = most likely because oestrogen was protective)!
-1st order relative: one line between you and that person on family
tree (parents, children, siblings)!
-With premature CVD, increases 30%!
-Premature = CVD that occurs early in life!
-can be environmental (same diet, same PA and patterns,
genetics)!
-Not necessary, just increased likelihood only, so be cautious!
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Modiļ¬able: HBL, smoking and HT!
-Blood lipids (blood cholesterol):!
- cholesterol made in body/consumed in diet!
- important roles in body: for transporting fats around
bloodstream!
- important in being part of CSM!
- Prod VD, steroid hormones (oestrogen/testosterone), bile
salts (digestion of fat)!
- when too much of it = problems (when body makes too
much/consume too much from animal product. Even if
donā€™t consume animal product, high fat diet can aļ¬€ect it
too)!
-3 types of cholesterol !
-these LP: phospholipid
structure, inside have cholesterol
and TG (fat carriers)!
-TG (free fats ļ¬‚oating around bloodstream) -> fat not soluble in blood so have to be carried
around!
Right diagram:!
-when consume meal that has fat/cholesterol, broken down in digestive tract, then absorbed
into GI, then transported around body by LP!
-Once fat/cholesterol absorbed by GI tract, goes through bloodstream to:!
-Adipose tissue = body fat!
-Muscle = stored as TG!
-Go via liver, continue to be transported around bloodstream and dropped oļ¬€ as body fat/
muscle!
-As fat/cholesterol travel, make up of LP changes to VLDL and as it drops oļ¬€, becomes LDL
cholesterol!
-LDL cholesterol that can potentially be oxidised, increasing chance of depositing fat/cholesterol
on artery wall = atherosclerosis, can damage endothelial layer!
-LDL is the bad guy, dropping fat/cholesterol under endothelial layer !
-HDL: comes along and pick up fat/cholesterol from circulation, bring back to liver, broken down
there and can be excreted of body (HDL reverses what LDL does)!
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!
-more LDL, increase chance of damage to endothelial
layer, increase chance of it being oxidised = plaque
formation !
- deposits fat/cholesterol under endothelial layer!!
!
-HDL = good guy!
-Decrease risk of CVD!
-Reverse cholesterol trpt, HDL pick up fat/cholesterol transport
back to liver -> some can be excreted from body!
-= plaque regression!
-decreases adhesion of monocytes sticking to endothelial layer
= monocytes are WBC that enter endothelial layer following fat/
cholesterol to clean it up. Less monocytes sticking to
endothelial, less likely for foam cell process to occur!
-keeps endothelial functioning well!
VLDL is precursor to LDL = bad guy also!
!
= high blood lips proļ¬le levels shown here!
- total: all 3 types, although VLDL not
usually shown on the sheet!
-exercise not huge eļ¬€ect on cholesterol
levels!
-Exercise does increase HDL (good) with
aerobic (intensity not as important, its the
overall energy expenditure = higher, more
HDL) = eļ¬€ect is slow and over time!
-DIET: if have high fat diet (animal/not),
can aļ¬€ect internal body cholesterol level!
-ļ¬bre (oats - high in beta gluten, source of
ļ¬bre help reduce LDL cholesterol)!
-drug therapy: if just above cut oļ¬€, use
diet and exercise to see if can alter to
break it back down, if after 3-6 months
and diet and exercise doesnā€™t really alter
it, USE MEDICATION!
-Problem is: donā€™t compensate for
unhealthy lifestyle!
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Document Summary

Rf needs to: in a population, when present, increases risk of cvd. Must have underlying association as to why it causes the disease (must be able to explain pathophysiologically) If modify rf, can alter risk of cvd. Changes in physical activity, high cholesterol, bp = massive a ect. Age: as we get older, other rf worsen (bp, weight, physical inactive), our arteries naturally harden. Gender: up until women reaches menopause (risk of cvd between m and w tend to even up when menopause = most likely because oestrogen was protective) 1st order relative: one line between you and that person on family tree (parents, children, siblings) Premature = cvd that occurs early in life. Can be environmental (same diet, same pa and patterns, genetics) Not necessary, just increased likelihood only, so be cautious. Important roles in body: for transporting fats around bloodstream. Prod vd, steroid hormones (oestrogen/testosterone), bile salts (digestion of fat)

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