Week 7 & 8: Met Syndrome Flashcards
What is Metabolic Syndrome?
Is a cluster of the most dangerous heart attack risk factors
- Twice as likely to die and 3 times as likely to have a heart attack or stroke.
- 5 times greater risk of developing T2D
Slide 8 of Week 7
How do you Define Metabolic Syndrome?
The IDF definition
Person MUST HAVE Central Obesity (based on waist circumference with ethnicity specific values)
Plus any TWO of the following
1. Raised Triglycerides: <1.7mmol/L
2. Reduced HDL: < 1.03 males, <1.29 females
3. Raised Blood Pressure
4. Raised fasting plasma Glucose
Why do we care? Remember –> they have 5x risk of developing diabetes
Slide 10 in Week 7
What are the Ethnic Waist Circumference Values?
Europids
Male: ≥ 94cm
Female: ≥ 80cm
Non European
Male: ≥ 90cm
Female: ≥ 80cm
What is the best way to measure insulin resistance?
OGTT
This test looks overtime, what is the insulin doing to get the BGL below the cutoff
If the Insulin levels are getting really high to maintain the BGL –> is a sign of insulin resistance
Fasting glucose shouldnt be used to measure insulin levels
Slide 10 of Week 6 (Lizz explains it verbally)
What is Atherogenic Dislipidemia?
Is the lipid profile that leads to atherosclerosis
Combination of:
- Raised TG
- Low HDL
- Elevated Apolipoprotiein B
- Small Dense LDL
- Small HDL particles
All of which are independently atherogenic
Slide 14 of Week 7
Prevalence & Incidence of Metabolic Syndrome
Nearly 1/3 of populations have Met Syndrome in 2011-2012
almost 1/4 of Aus has been diagnosed with Met Syn
As we age these rates increase (particularly around 55-65 Years old)
rates higher in men
Waist circumference is higher –> greater risk of developing met syndrome
Slide 16 - 19 of Week 7
Why do we care about metabolic syndrome?
very very important
If we know people are going to have disability, cognitive impairment OR depression
→ all of which are likely to lead to parkinsons or dementia
→ this will have an impact or burden on the society at a greater scale
increased components of Met Syn = increased risd of CV mortality rate
before blood glucose levels are high enough for a diabetes diagnosis, hyperglycaesmia and increased triglycerides, decreased HDLc, all increase risk of CVD
Slide 20 and 24 in Week 7
Can a patient be diagnosed with Met syndrome if they dont have insulin resistance?
Fran expressed belief on 2/06/2024
VERY VERY IMPORTANT
Yes; a patient does NOT have to have insulin resistance to be diagnosed with met syn, according to the International Diabetes Federation (IDF) definition
insulin resistance is a causative factor that can lead to met syn
Relate how physical inactivity and Excess energy intake can lead to metabolic Syndrome
NOTE: ITS COMPLEX!!!!
Sarcopenia
As you begin to lose muscle there is a subsequent increase in insulin resistance (No GLUT4 Translocation to the membrane)
Visceral Obesity (VO)
Ageing can cause increase in VO –> increase in VO can drive an inflammatory state (refer week 6 lecture) which contributes to insulin resistance
Insulin resistance means the tissues are subsequently impacted causing:
1. Impaired muslce glucose uptake
2. No inhibition of hepatic Gluconeogenesis
3. Impaired smooth muscle relaxation
4. Increase plasma Triglycerides
~**All this leads to Metabolic Syndrome!!**~
Refer slide 27 of Week 7
What are the 3 ways our body’s cholesterol can be changed?
Think of relation to dyslipidemia
HDL (scavanger molecule) [diet]
- Picks up cholesterol sitting in tissues and redelivers to places that need it
- Is important for maintaining cell membrane in ALL CELLS
- Exercise increases HDL activity and therefore reduces poor cholesterol
Endogenous Pathway [internal to body]
- Excess LDL –> the body says we have too much and breaks it down
- Causes the foaming up and resulting in plaque
- Genetic can result in less reuptake of LDL in the liver and go down a destorying pathway and putting more in the blood stream and contribute to plaque build up
Exogenous [diet]
- Food is consumed and absorped into the bowl and taken up by chylomicrons
- This then allows for reuptake into the liver
HOWEVER!
- in genetic disorders the chylomicrons are not reuptaken into the liver
- meaning its floating around in the blood and sticks to things (e.g. blood vessel wall)
Slide 44 of Week 7
What is the primary treatment intervention for Metabolic Syndrome?
IDF Guidelines
Primary intervention
Moderate Calorie restriction - To achieve 5-10% body weight loss in first year
- (500 cal reduction per day to produce half kilo weight loss/wk)
Moderate increase in PA
Change in dietary composition
e.g. processed foods, reduce sugar intake, saturated fats (due to immediately being in the body as cholesterol
Slide 48 of Week 7
What is the Secondary Treatment for Metabolic Syndrome?
IDF guidelines
If lifestyle changes (PRIMARY) arnt enough –> move to secondary interventions
While there is no medication to prevent met syndrome directly, treat each individual component that are symptoms for the client
these individual components are …
- elevated BP
- atherogenic dyslipidemia
- insulin resistance and hyperglycaemia
For those considered high risk of CVD
- Drug therapy to treat hypertension or cholesterol
Slide 50 of Week 7
What is the categorical level for hypertension?
Blood pressure
≥ 140 / ≥ 90 mmHG
In patients with diabetes
≥ 130 / ≥ 80
(JNC7)
Lower cut off if they have diabetes due to the increased risk factors
Medications for Hypertension
Thiazides - reduce blood volume
- Reduce water reabsorption in kidney
ACE inhibitor - Vasodilator
- Blocks action of ACE
- Drug end in ‘Pril’
ARB - Vasodilator
- Blocks action of Angtiotensin II by blocking the receptor
Calcium Channel Blocker
- Vasodilator & Reduces contractility of the Heart
Beta Blocker - Reduces HR
- be mindful during exercise because it changes the contractility of the heart
- Drugs end in ‘OLOL’
52 - 53 of Week 7
Medications for Dyslipidemia
Statins
- Focuses on decreases LDL
Fibrates
Focus on increasing HDL and reducing TG (doesnt do much for LDL
Bilce Acid Sequestrants
Focus on decreasing LDL
Niacin / Nicotinic Acid
Focus on increasing HDL and reducing TG
May cause decreased HR
Most have no effect on HR, BP or ECG –> main side effet is Myalgia
57 of Week 7
Goal levels of TG & Cholesterol for people with no CVD, Diabetes or Kidney Disease
Total Cholesterol
Below 4.5
LDL
Below 2.5
HDL
Above 1
TG
Below 2
What is the role of exercise in the management of metabolic syndrome?
Combination of increase in PA and dietary modifications are the most optimal for to achieve weight loss of 5-10%
We dont want the client coming off medication and relying solely on lifestyle modifications (e.g. diet) –> causing CVD risk profile to still be high as the lifestyle modification only isnt enough
What did the Diabetes Prevention Program Results indicate?
Adults that were randomly assigned to the lifestyle group had:
- 39% reduction in T2D compared to metformin group
- 58% reduction in T2D compared to placebogroup
TLDR
Reduction in likelihood of developing T2D if you are physically active
Slide 24 of Week 8
What is the rationale for Progressive Resistance training for Metabolic Syndrome?
PRT leads to improved metabolic fitness aswell as increased Anabolic activity (AA)
AA
- Leads to an increase in body compositional change driven by an increase in muscle mass and fat loss
- Client may have an increased weight gain –> but this would be as a result from increased muscle mass NOT fat
Slide 25 of Week 8
Summary of Exercise in management of Metabolic Syndrome
- Exercise is effective at managing hypertension
- Inclusion of aerobic, dynamic RT and isometric RT leads to a greater reduction in SBP than other interventions
- Exercise has minimal effect on lipoproteins but small evidence for increasing HDL and reducing LDL
- Exercise with or without dietary co-intervention can reduce risk of developing T2D by 51% (more effective than meds)
Slide 31 - 32 in Week 8
Considerations for Exercise and Hypertension
Absolute Contraindications
Resting SBP ≥ 180 OR DBP ≥110
Beta Blockers
Blunten the exercise HR –> HR not a good predictor of intensity
Diuretics
Can impair exercise tolerance / performance but normalises after afew weeks
Abrupt termination of exercise
Sudden termination can cause venus pooling –> large drop in BP
Greater risk with medications
Greater risk with aerobic exercise
Slide 40 - 41 of Week 8
consequence of no inhibition of hepatic Gluconeogenesis
- insulin and glucagon work together in a feedback loop
insulin resistance –> gluconeogensis not turned off –> abudance of glucose pumped out endogenously into the blood –> long term hyperglycaemia
slide 27 week 7 lecture 42:07 what lizzie said
what are the consequences of impaired fibrinolysis? (factor that leads to accelerated atherosclerosis)
impaired fibrinolysis = lack of breakdown of connecting parts of blood –> increased likelihood of blood clots –> more viscous, thicker, stickier blood –> increased BP
refer to slide 28 of week 7 lecture
what do studies say about the consequences of metabolic syndrome?
riskof chronic kidney disease increases with every additional MetS component
3x more likely to develop T2D and 1.7x more likely to develop CVD (Ford, 2005 )
those with Met Syn 2.71 hazard ratio for CVD morality
those with met syn AND T2D 3.63 hazard ratio for CVD morality
CVD + T2D 7.88 hazard ratio for CVD mortality
patients with both met syn and depression had 6.6x higher risk for diabetes –> interaction of the comorbidities magnifies the risk (molecular psychiatry, 2016)
refer to slides 30, 31,32, 33, 35 of week 7 lecture
