Unit Test 2 Flashcards
(162 cards)
1
Q
what are the 3 major causes of death in the Canada?
A
- cancer
- CAD
- stroke
stroke and CAD together amount to more than cancer
2
Q
stress test
A
ECG measured on a treadmill at different intensities and used as a diagnostic tool for CVD
3
Q
CHD
A
Coronary Heart Disease
- coronary heart damage, the largest portion of deaths attributed to this part of CVD (42%)
- artery damage, not being able to deliver enough O2 to heart muscle
4
Q
mortality from heart disease in the US patterns
A
it has decreased to 59% since the 1960s
- primarily due to smoking awareness/prevention, better technology and medicine for treatment and diagnosis
- awareness of risk factors and people are surviving heart attacks more
5
Q
CHD is the #_ cause of death in the US? in Canada?
A
1 in both
accounts for about 20% of deaths annually
also costs a lot of money
6
Q
AMI
A
acute myocardial infarction
heart attack
7
Q
what proportion of heart attacks are sudden?
A
half; no signs or symptoms; people die
8
Q
male vs female risk for CVD
A
males have greater risk up to age 74
females have greater risk than men after age 50 (post menopause, atherosclerosis takes time to develop but is speed up by lack of estrogen present)
9
Q
ischemic heart disease
A
anything that causes a decrease in blood flow
10
Q
how is all cause mortality described?
A
as death rates in the population
11
Q
male vs female life expectancy
A
- females live longer than males on avg
12
Q
life expectancy
A
the number of years you’re expected to live from the year you’re born
- on average, half lives to be above this and half dies before then
- can also be measured from different points in life
- max is 122 years
13
Q
Health Adjusted Life Expectancy (HALE)
A
the number of healthy years you’re living
- PA can improve this
- canada’s is 10th in the world: we drive everywhere and it;s killing us
- in Canada it’s about 72
14
Q
physical inactivity as a risk factor for all cause mortality
A
wasn’t a problem before because people had to be active as a part of their daily lives at work, they had non processed food
- they also died of infectious disease around age 40 before chronic disease was an issue
15
Q
disturbing trends in PA and the impact it has on overall health/all cause mortality
A
with these large amounts of screen time, the resulting physical inactivity leads to increased levels of obesity, which is linked to CVD
16
Q
trends for countries with longer life expectancies
A
mostly European countries with more active transportation
- they also have lower obesity rates due to their being more physically active
17
Q
what is the relationship between obesity prevalence and active transportation?
A
an inversely proportional relationship
- when people are more physically active, they are less obese
18
Q
what proportion of deaths do chronic diseases contribute?
A
63%
(only developed nations really deal with chronic disease because undeveloped nations are dying from infectious disease as they have inadequate healthcare)
- almost half of these are due to CVD
19
Q
PA and harvard alumni study
A
- death rates were 25-30% lower in alumni expending 2000kcal or more per week
- active men gained 1-2 years of life for every hour of PA they did per week
20
Q
person years
A
the number of people in your study times the number of years they were in your study
21
Q
where is the greatest reduction in overall death risk seen?
A
- from people going from sedentary to lightly active lifestyles
- generally a drop and plateau
22
Q
moderately fit men and women have __ reduction in risk of all cause mortality compared to unfit
A
moderately fit people have a 50% reduction in risk
23
Q
what is a common relative risk in studies on PA and mortalitu
A
a RR of 0.5 is common; it means that you half the risk or reduce it by 50%
24
Q
risk is reduced another __% in highly fit compared to moderately fit individuals
A
10-15% lower in highly fit
25
with regards to when you're physically active during your life, how does risk look in terms of all cause mortality?
- the risk b/w people who were active their whole lives and those who became active later in life was about the same
26
dose-response relationship b/w PA and mortality?
yes, reduction in risk seen largest by people who meet PA guidelines and are most active
27
what percentage of Canadians are meeting the PA guidelines?
15%
28
how does age influence our PA rates? why?
as we get older, our PA rates decrease
- because physiological changes make this more difficult
- possibly bc of biological reasons as this trend is also seen in monkeys
29
coronary risk factors def'n
characteristics that tend to increase the chances of developing coronary artery disease
- usually general narrowing/ blocking of arteries
30
major modifiable risk factors for CHD
1. tobacco use
2. hypertension
3. high blood cholesterol (LDL)/ lipids
4. physical inactivity
5. overweight/obesity
6. diabetes
7. unhealthy diet (incl alc abuse)
31
major non-modifiable risk factors for CHD
- age: older more risk
- sex: male early in life, females later in life
- race
- genetic predisposition
32
host susceptibility
can be measured by the number of non-modifiable risk factors that someone has
33
widow maker artery
anterior interventricular branch
aka the left anterior descending
- because ventricles need to pump blood to body and it can't if it has no blood supply itself
34
pathology
the anatomical changes underlying the condition
- structure change and result in condition
- use to come up with diagnosis
35
etiology
the development of the condition and how the disease progresses
36
symptoms reflect ___ and result from ___
pathology; etiology
37
symptoms of MI
- often unrecognized and are confused w heartburn
- 21% of heart attacks can be silent and thus left untreated
diff for men than women:
men- classic signs usually after physical activity
women- usually after emotional stress, usually don't go to doctor in time or have higher pain tolerance
38
atherosclerosis
often etiology for heart disease
- the build up of calcium and fats inside the inner walls of an artery causing it to become narrowed
- an intimal disease in intima layer
39
arteriosclerosis
- stiffening of arteries
| - happens in CT layers of artery
40
stenosis
narrowing of a structure
41
where in vessels is atherosclerosis usually found?
often in vessels that bifurcate or bend
42
intravascular ultrasound (IVUS)
- putting ultrasound probe through blood vessel and it sends a radio signal from the middle of the tube
- allows us to see plaque and how thick it us
43
cardiac catheterization
could insert catheter into brachial or femoral artery (pref. femoral since it's larger and can still allow blood flow around the catheter)
44
coronary angiogram
- cheaper and quicker than catheterization, hits lots of vessels at once
- radio-opaque dye injected into the coronary arteries and gives picture of obstruction where you don't see the black and an artery should be there (X-ray)
- you can only see black areas of reduced blood flow, but can't see the stenosis itself
45
methods of screening for atherosclerosis
cardiac catheterization
coronary angiogram
intraventricular ultrasound (IVUS)
46
using a stent to treat atherosclerosis
inflating a balloon on the end of a catheter in an area where stenosis is and balloon pushes fat out of the way and inflates the stent which holds lumen open
47
coronary artery bypass graft (CABG)
if there are multiple stenosed regions, they can do bypass surgery which often uses a subclavian branch of an artery and attach it to the area the artery is blocking flow to using a vein from the leg
48
there are 2 types of stenosis of arteries:
fixed obstructions
OR
dynamic blockages
49
fixed obstructionof a coronary artery
ex. atherosclerotic plaque that blocks blood flow through artery, most likely to result in heart attack if clot ruptures and blocks off vessels (the results from an inflammatory response)
50
dynamic obstruction of a coronary artery
caused by coronary arterial spasm that decreases blood flow to heart tissue
- typically transient, not lasting long enough to cause heart attack
- smoking, stimulant drugs, and diabetes can cause spasms
51
thrombus (clot) formation
at a bifurcation, vessel diameter gets smaller and endothelial wall deals with more stress at the bifurcation
- when plaque has ruptured, a clot forms, blocking blood flow so it can't move through the vessel
52
turbulent flow theory of artery injury
at a bifurcation, the fastest moving cells are in the centre of the blood vessel and so they hit the area where the vessel splits, causing more damage due to the sheer stress put on endothelial cells
53
vasomotor tone
- signals changes that cause blood vessels to change diameter
- cytosolic calcium stimulated release of NO caused by sheer stress on endothelium, triggers smooth muscle in media layer to dilate
54
nitric oxide (NO)
- a potent vasodilator, inhibits platelet adhesion and activation therefore also inhibits clotting
- antiflammatory agent: inhibits adhesion of leukocytes to endothelial surface when there's damage to endothelium
- has short half life so doesn't stay in circulation long
55
atherogenesis
- the building up of plaque
- begins w endothelial disruption caused by intimal injury
- platelets adhere to collagen at site activating fibrinogen
- fibrinogen increases platelet aggregation and releases platelet derived growth factor (PDGF)
- macrophages eat damaged cells, debris and oxidized LDL to make fatty streaks
- smooth muscle cells and fibroblasts migrate to intima to make fibrosis (cap)
- lipid deposits accumulate to increase stenosis
56
factors that cause endothelium injury
- LDL
- tobacco
- homocysteine
- oxidized LDL stimulates monocyte secretion
- high blood glucose
57
homocysteine
an intermediate AA
- present in people who eat a lot of protein, males, older people, sedentary, environmental toxins
- high levels increase risk, starting to breakdown an AA
- decreased by folic acid, exercise, vitamins B6 and B12
58
why is high blood glucose a problem
cells keep trying to take up the glucose, then it gets added to proteins which make them sharp and dysfunctional and causes endothelial damage
59
when do symptoms of atherosclerosis appear?
when the blockage reduces blood flow by about 80%
60
myocardial ischemia
inadequate oxygen supply to part of the heart caused by impaired blood flow
- results in angina
61
ischemia
a reduction in blood flow to anywhere in your body leading to insufficient O2 delivery to tissues
62
angina
symptoms of heart attacks without actually causing tissue damage
63
symptoms of ischemia
chest, arm neck and jaw pain, indigestion type pain
| - people take nitroglycerin which stimulates release of NO and increases blood flow again
64
secondary prevention vs primary prevention
primary: trying to keep from getting the disease
secondary: trying to keep the symptoms from getting worse
65
does primary prevention of atherosclerosis exist?
| risk factors of atherosclerosis?
not really, 1 in 6 teenagers has coronary plaques; we can't really stop it but we can slow it down
risk factors: smoking high BL, diet high in saturated fat and cholesterol
66
what types of stenoses cause most infarctions?
low grade ones, most people who have heart attacks have less than 50% stenosis and are therefore asymptomatic ; when more stenosed, the plaque has a strong fibrous cap and risk of rupture is lessened
67
what percentage of first heart attacks are fatal?
30-50%
- a lot of people don't know anything is wrong until they die from a heart attack; people don't usually get cardiac checkups
68
characteristics of plaque prone to rupture
- thin fibrous cap
- lipid, macrophage rich
- smooth muscle poor
69
how do we know about the relationship between PA and CHD?
evidence from:
- occupational studies
- leisure time PA studies
- studies of fitness
70
london bus study
- showed effects of occupational PA on CHD
- bus drivers had high BP, were obese and once there were factored out, there was still reduced risk for conductors compared for drivers
- when conductors had heart attacks, they were less severe
71
problems with PA studies
- might not measure every variable
- can't determine cause and effect w cross sectional or retrospective
- confounders
- inaccuracy of medical/autopsy records/ recall of habits by family members
72
physical fitness and its relationship to CVD mortality
more strongly related to reduce CHD than other estimates of PA
proof: greatest reduction in risk for those who are more physically fit
73
nurses health study
a large scale population study on nurses and PA rates
- when family history of CDV isn't a factor, risk goes down, thus deeming physical inactivity a risk factor
- supports that PA works in both women and men to prevent CVD
74
CVD risk in women and men and PA
- there was originally thought to be no relationship b/w PA and CVD in women
- however, PA reduces the risk of CVD to a similar extent in women as in men
75
PA and its influence on other CAD risk factors
it can reduce independent risk factors for CHD but also other risk factors like high BP, weight, lipids
76
PA and risk of recurrent heart attack
although there is a reduction in CAD mortality with exercise rehab, there is no reduction in risk of having another non-fatal MI
77
Mill's Canons for CVD
| temporal sequence, strength of assoc, consistency
temporal sequence: yes
strength of association: risk is 2x higher if inactive; also note 2000kcal/week protection against CVD
consistency of results: yes
78
fibrinolytic factors
break down clots
79
biological plausibility for PA to have an effect on CVD risk
exercise:
increases HDL cholesterol and fibrinolytic factors
reduces BP, TG, body fat, blood coagulability and MVO2 (heart is getting more efficient and so needs less O2 during PA)
80
MVO2
myocardiac VO2: the amt of oxygen needed for heart to survive to do work
- decreases with exercise training because heart is getting to be more efficient and requires less O2
81
functional adaptation
we get healthier endothelium and the release of things like NO contribute to better vasodilation
82
structural adaptation
over time, remodelling by significantly increasing the size of your arteries (diameter, thickening)
83
the relationship between functional adaptation and structural adaptation
starting by relying more on functional adaptation. then, as structural adaptation increases, then we rely less and less on functional adaptation
84
cerebrovascular disease and stroke definition
a stroke is the loss or impairment of bodily function resulting from injury or death of brain cells after insufficient blood supply
- results from hypoxia (inadequate oxygen delivery) caused by ischemia
85
hypoxia
inadequate oxygen supply
86
warning signs of stroke
1. weakness
2. trouble speaking
3. vision problems
4. headache
5. dizziness
87
what is the mnemonic for the public to recognize the stroke?
```
FAST
face drooping
arm weakness
speech difficulty
time to call 911
```
88
types of stroke
```
ischemic
- thrombotic or embolic
- also TIAs
hemorrhagic
- subarachnoid or intracerebral
```
89
ischemic stroke
- interruption of blood flow to the brain due to a blood clot or possibly swelling of the brain
- 80% of strokes are ischemic
- atherosclerosis usually involved
- either thrombotic or embolic
90
thrombotic stroke
category of ischemic stroke
- a blood clot that forms in an artery directly leading to the brain
- more typical
91
embolic stroke
category of ischemic stroke
- clot develops somewhere else in the body and travels through the blood stream to the brain
- usually in older people if someone falls and gets injured, the clot forming might move to the brain and cause a stoke
- also can be caused by irregular heart rhythm (AFib) where blood spends too much time in ventricles and clots
92
TIA
transient ischemic attack
- similar to angina in the heart, called a mini stroke where O2 delivery to brain is interrupted temporarily but no cells die so it's not really a stroke
- symptoms similar to ischemic stroke except they go away w/in a few hours
1/3 of people who have a TIA have a stroke within 5 years therefore it puts you significantly at risk
93
hemorrhagic stroke
caused by uncontrolled bleeding in the brain when a blood vessel bursts
- bleeding interrupts normal blood flow and by flooding the brain (also lots of pressure), kills brain cell because they damage the brain cell env't
- 20% of strokes
2 types: subarachnoid or intracerebral hemorrhage
94
subarachnoid hemorrhage
a category of hemorrhagic stroke
| - uncontrolled bleeding on the surface of the brain in the area between the brain and skull
95
intracerebral hemorrhage
a category of hemorrhagic stroke
| - occurs when an artery deep within the brain ruptures
96
types of hemorrhage
both types of hemorrhage can cause hemorrhagic stroke
- therefore if you take aspirin, it thins your blood and you'll bleed out
- aneurysm
- AVM (atriovenous malformation)
97
aneurysm
a weakened area in the blood vessel wall of he blood vessel that fills with blood and bulges
- turbulent flow is here now and puts blood at a greater risk of clotting
98
AVM
atriovenous malformation
- a malformation of the brain's blood vessels usually present at birth, causing the artery walls to be weak and could break over time
99
how much of a problem is cerebrovascular disease and stroke?
3rd leading COD is US
| 5th leading in Canada (5%)
100
incidence of stroke
10-15% higher in women than in men
| - maybe bc of hormones released during pregnancy or bc of loss of protective estrogen bc of menopause
101
why does someone usually do PA after having a stroke?
rehab probably, rather than prevention
102
non modifiable risk factors for stroke
- age: greater than 65 and increases exponentially after this
- gender: before menopause women have decreased risk but after, their risk is greater than that of men
- family history: if someone has a stroke before a certain age, it's likely a result of genetics
- ethnicity: First Nations and South Africans have higher incidence
- PRIOR STROKE or TIA puts you at greatest risk of having another
103
modifiable risk factors for stroke
- high BP, blood cholesterol (LDL)
- heart disease, atrial fibrillation (causes 50% of strokes)
- diabetes, being overweight
- excessive alc consuption
- physical inactivity
- smoking, stress
104
what is the #1 modifiable risk factor for stroke
hypertension
| - an estimated 45% of people have high BP
105
how does age influence someone's risk of having a stroke?
after age 55, risk doubles with each decade
106
classifications of blood pressure
normal
prehypertension
stage 1 hypertension
stage 2 hypertension
107
normal blood pressure
<120/
| <80
108
prehypertension
systolic: 120-139
disatolic: 80-89
109
stage 1 hypertension
systolic: 140-159
diastolic: 90-99
110
stage 2 hypertension
systolic: >160
diastolic: >100
- pretty dangerous
111
systolic pressure
the peak pressure in arteries during ventricular ejection
112
diastolic pressure
the pressure in the arteries during ventricular relaxation
113
what happens when someone's systolic blood pressure is less than 100mmHg
they have almost no risk of CVD
| - they also faint a lot if they don't have sufficient oxygen delivery to body tissues
114
how does high blood pressure work?
- when arterioles constrict, the heart has to work harder to force the blood through and often becomes enlarged which is not good
- when we have lots of resistance in the system, it's harder to move blood through, arteries stiffen and increases resistance more
115
framingham results re: BP and stroke risk
systolic BP over 150 doubles stroke risk
| which is 4x that of risk of heart disease
116
physiological effects of cigarette smoking
- heart rate increases: NE release causes increasing resting heart rate but heart isn't getting any more O2 supplied bc body is at rest
- blood O2 carriage decreases: Hgb has a higher affinity for carbon monoxide than O2
- blood clots form: nicotine causes coagulation of blood which can cause coronary thrombosis or stroke
117
effects of nicotine
- increases BP
- causes heart to work doubly hard (increases contraction force and stroke volume)
- dysrhythmias by stimulation of ectopic pacemakers
- increase in both plasma FFAs and platelet adhesiveness, predisposing someone to atherosclerosis
118
smoking and how it increases stroke
- in general, smoking more than a pack a day has twice the risk of a heart attack and increases risk of stroke 5x over someone who doesn't smoke
- when combined with high blood cholesterol and hypertension, smoking increases risk of stroke by 7x (double that of MI)
119
physical activity and risk of stroke trends
no trends,
| there is no clear associations that show PA as a preventative for stroke, but there probably is some protective effect
120
what do case control studies show in terms of the association between stroke and PA?
- when comparing people who've had a stroke to those who haven't, a lifelong reduction in risk is present for those who have been physically active throughout their lifespan (50% more)
- also the greatest reduction in risk is seen in those who are active more recently as well
121
study results re: PA exercise frequency, intensity and amount on stroke
Harvard alumni study shows that:
- lowest amount of PA has greatest reduction in risk regardless of other factors
- in terms of PA frequency and intensity, PA acts as an effect modifier on stroke where it improves certain risk factors that decrease the likelihood of having a stroke
122
Nurses' health study results on stroke
- all women study looking at if doing a little PA would reduce risk
- found that the more PA and at greater intensity had the greatest reduction in risk
123
Mill's canons for stroke and PA
- temporal sequence: yes, PA later in life was still effective
- **strength of association: risk reduction 30-60%
- consistency of results: yes most studies show reduction in risk, consistent w diff pop also
- does response: not as clear; extra benefit of vigorous controversial opinion
- biological plausibility: yes. PA reduces risk factors, blood clotting, etc
124
how are people categorized into levels of blood pressure if systolic and diastolic BPs are part of different classifications
have to put them in whichever is higher because you don't want to underestimate someone's hypertensiveness
125
Korotkoff sounds
- first heard when brachial artery is partially open: pressure at this point is systolic
- when sound stops, brachial artery is mostly open, the pressure at this point is diastolic
126
cause of hypertension
cause is unknown in 95% of cases
127
prevalence of hypertension
NHANES III study says that prevalence is 20%, most people don't know they have it though so it's estimated to be about 50% of Canadians
128
methods for primary prevention of hypertension
- normal body weight
- reduce dietary sodium intake so that you can expel water
- regular aerobic PA
- limit alcohol consumption
- maintain adequate dietary K+
- consume diet that would prevent atherosclerosis
129
drugs for treatment of hypertension
generally either decrease HR or help eliminate fluids from body
- diuretics
- SNS receptor blockers
- ACE inhibitors
- calcium channel blockers
- also a combo of some of the above
130
fundamental regulatory equation of the circulatory system:
flow/cardiac output (Q) = change is pressure / resistance (or total peripheral resistance- TPR)
- anything that affects cardiac output or TPR will effect arterial pressure
131
contributing factors to arterial pressure
- total blood volume (more vol=more pressure)
- rate of blood flow (CO)
- blood vessel diameter (bc flow= length of tube X viscosity of blood/radius^4)
- -- arteriolar resistance is important because of total cross-sectional area in the body
132
SNS impact on BP
sympathetic nervous system (SNS) increases BP
- SNS nerves release NE, adrenal glands release epinephrine
- both bind w adrenergic receptors which act to increase HR and force of contraction
- this causes vasoconstriction to increase TPR and BP increases
133
PNS impact on BP
parasympathetic nervous system (PNS) decreases BP
- Ach released from vagus nerve of PNS binds with cholinergic receptors
- this causes vasodilation and BP decreases
134
risk factors for hypertension
age - stiffening and changes in CNS increase resistance
ethnicity - african americans have greater resistance and less flow
obesity - more flow because of expanded plasma volume and increased SNS activity
135
PA and hypertension risk
epidemiological and clinical experiments both provide evidence that moderate intensity PA is assoc with prevention and treatment of MILD hypertension
- it doesn't work well for severe hypertension (greater than stage 1)
- heavy activity doesn't have huge reductions in risk
136
PA and treatment of hypertension
- works for mild, not for severe hypertension
- seems to benefit women more than men (greater BP drop)
- doesn't work as well for overweight individuals (systolic drops less) BUT drops are independent of weight change++
- most benefit is from moderate PA, not much more for high
- diastolic changes seen most in longer durations of PA
137
Mill's Canons for hypertension
- temporal sequence: yes. also can do experimental studies to show this
- strength of association: risk reduction 30-50% active
- consistency of results: most studies show reduced risk w PA and this is across diff pop.s also
- does response: unclear bc less seems to be more
- biological plausibility: yes, PA can reduce BP by decreasing Q and/or TPR
138
hyperlipidemia
having high blood cholesterol/TG levels
139
4 types of lipids
cholesterol
triglycerides
phospholipids
fatty acids
140
cholesterol
a modified steroid, made in the liver
- used to make steroid hormones (testosterone, estrogen)
- involved in keeping cell membrane fluid, skin waterproofing
141
triglycerides
how we store energy in the body
- a glycerol and 3 FAs
- an efficient storage method
142
phospholipids
make up cell membranes
- hydrophilic head (phosphate/diglyceride)
- hydrophobic tail (2 FA chains)
143
fatty acids
long hydrocarbon chains with carboxyl groups on the ends
| - how we store large amounts of energy
144
lipoproteins
transport fats through blood since they aren’t dissolvable in fluid
145
classes of lipoproteins
```
least dense to most dense, also largest to smallest:
chylomicron
VLDL
LDL
HDL
```
146
chylomicron
least dense lipoprotein, largest in size
| - carries fats from food in SI to liver to be processed via the blood
147
VLDL
second least dense, second largest in size
| - carry from liver to cells of body
148
LDL
second most dense, second smallest in size
- carry primarily cholesterol to body tissues
- most dangerous bc gets oxidized and can lead to atherosclerosis in our blood vessels
149
HDL
most dense, smallest in
size
- carry cholesterol from body tissues and drops off at liver
150
endogenous fats
made in the body, not found in our food
151
triglyceride
a fatty substance found in the body and our food
- manufactured by body from excess alcohol, sugar and fats
- FA chains vary dramatically in length, chains can be saturated or unsaturated (good bc keeps from packing too tightly): the fats we consume have an impact on the type of FA in TG
152
main TG sources
adipocytes
| intramuscular
153
intramuscular TG
- TG interspersed in muscle fibers
- when mobilized from adipose tissue during exercise are hydrolyzed into FFAs and glycerol which body can use for energy
- transported in plasma by albumin to where needed
154
total blood cholesterol and heart disease
- greater levels of overall cholesterol increase risk for CHD
- higher or equal levels of HDL to LDL cholesterol reduces your risk of CHD
- --- its most important to know how much good to how much bad you have; having more LDL increases your risk the most
155
amount of HDL cholesterol needed to reduce risk of CHD
in men: 40-50 mg/dl
| in women: 50-60 mg/dl
156
Apo B
a protein present on the outside of cell membranes in lipoprotein molecules caring cholesterol
- is a better indicator of CHD risk than LDL cholesterol levels are
157
cholesterol levels, CHD risk and treatment of cholesterol
only treat high levels of LDL-C when risk for CHD is also high, otherwise, cholesterol isn't as big of a problem as we thought it might be
158
risk factors for high hyperlipidemia
- sex (postmenopausal women)
- age (HDL decreases w age)
- % body fat causes HDL to be lower and LDL greater
- diet, alcohol overuse, diabetes all bad for HDL, increase LDL and TG
- smoking and steroids decrease HDL
- exercise increases HDL :)
159
prevalence of high blood cholesterol in Canada
40% of Canadians have it
160
Mediterranean diet and cardiac events
people who eat lots of fish, fruits and veg, olive oils, nuts, seeds, minimal red meat: have a LOT less cardiac events than those consuming the traditional Western diet
161
dietary recommendations by canadian cardiovascular society
- keep fat intake to less than 30%
- less than 200mg cholesterol
- v. little saturated fat
- limit alcohol intake to 1-2 drinks/day
162
PA and training on hyperlipidemia
- most improvement with aerobic exercise (decreases TG)
- resistance exercise equivocal
- dose response equivocal
- also range in amount of aerobic exercise
-- exercise needs to be coupled with either diet changes or medication if looking to reduce hypercholesterolemia
