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Institute for Functional Medicine exam > Cardiometabolic > Flashcards

Cardiometabolic Flashcards

1
Q

PFCMVPs associated with cardiometabolic disease (4)

A

Fe, Mg, CoQ10, MUFA/olive oil

from Cardiometabolic decision tree

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2
Q

Treatment considerations for insulin resistance

A

Cr, Vn (caution re: high dose long term), Mg; berberine, n3-fatty acids, MCT/MCFA, MUFA/olive oil; ALA for peripheral neuropathy, cinnamon

(from Cardiometabolic decision tree)

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3
Q

Treatment considerations for dyslipidemia

A

C:12 Lauric acid (increases TC & HDL, decreases TC/HDL), B3/B5, EPA/DHA +GLA, berberine, bergamot, garlic, red yeast rice

(from Cardiometabolic decision tree)

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4
Q

Treatment considerations for vascular disease

A

Mg/K; Arg, BH4, B2; taurine; pomegranate: lycopene, garlic; D3, K2-MK7

(from Cardiometabolic decision tree)

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5
Q

Treatment considerations for autonomic dysfunction

A

Meditation, breath Rx, biofeedback, HRV, adrenal support

from Cardiometabolic decision tree

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6
Q

Treatment considerations for coagulation disorders

A

ASA; B6, B12, FA; bromelain; nattokinase; vitamin E

from Cardiometabolic decision tree

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7
Q

Treatment considerations for immune & detox dysregulation

A

Probiotics, curcumin, quercetin, caloric restriction, vitamins C/E/A, ALA, NAC, resveratrol

(from Cardiometabolic decision tree)

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8
Q

What are some of the physiological interconnections between insulin, inflammation and adipocytes?

A

Think Gluco- and Lipotoxicity

  1. Excess nutrition/obesity increases adipocyte mass & death, which in turn increases release of inflammatory adipocytokines (TNF-alpha, IL-6, etc) & drives recruitment of macrophages from bone marrow into fat cells–> inflammation (paracrine response)
  2. High sugar & fat diet activates also TLR -> activates NF-kB and JNK pathways in adipocytes, hepatocytes and macrophages -> inflammation -> local & systemic insulin resistance
  3. Insulin resistance leads to fatty and inflamed liver and eventually insulin resistant muscle –> more inflammation
  4. Microbiome changes also increase leaky gut -> LPS and endotoxemia –> inflammation, inadequate SCFA, and further metabolic dysfunction

(from Dr. Saxena’s “Fire in the Hole” lecture)

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9
Q

What is the paracrine response to obesity, that drives insulin resistance in the adipocytes?

A

Increased resistin and decreased adiponectin (adipokines), release of pro inflammatory cytokines (TNF-alpha, IL-6, etc), and increased FFA -> leads to insulin resistance & inflammation within adipocyte

(from Dr. Saxena’s “Fire in the Hole” lecture)

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10
Q

What are some causes of insulin resistance?

A

Poor lifestyle, environmental toxins, mitochondrial dysfunction (b/c decreases insulin production), dysbiosis, altered body composition (increased BMI, WHR, WC, & body fat %), genetic predisposition

(from Dr. Saxena’s “Fire in the Hole” lecture)

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11
Q

What are the conventional “Should know” cardiometabolic lab tests & assessments?

A

BMI, WC, fasting BG & insulin, A1C, cholesterol or lipoprotein profile, hsCRP, CBC w/differential, homocysteine, GGT, vitamin B12, Mg, vit D25OH, CMP (esp AST, ALT), microalbumin creatinine ratio

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12
Q

What are some components of an expanded lipid panel?

A

LDL-P size and number, LDL pattern A vs B, HDL 2 vs 3, VLDL size
Modified (oxidized or glycated LDL),
ApoB (protein core of LDL/VLDL -bad), ApoA1 (protein core of HDL - good), ApoB:ApoA1 (target<0.8)
Lp-PLA2 (assoc w/oxLDL, inflammation & progression of atherosclerosis)
TGs, IDL (genetically determined and an independent risk factor), Lp(a)

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13
Q

What are some emerging cardiometabolic risk markers?

A

Oxidative stress (myeloperoxidase, F2I), CIMT, coronary artery calcium/CAC scoring, trimethylamine-N-oxide (TMAO;gut measure), omega-3 index, ASA resistance, aldosterone:renin ratio (ARR; 40+ suggests low renin HTN, <10 suggests high renin HTN)

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14
Q

How does TMAO respond with increasing CV risk?

A

Increases (via lipid dysregulation & macrophage function)

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15
Q

What is the relationship of TG level with insulin response?

A

Increased TG with excess insulin; precedes impaired fasting glucose.

TG/HDL ratio <3=normal; if >/=3 suggests insulin resistance

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16
Q

Which LDL particle pattern is preferred (A vs. B)

A

A; pattern B occurs with smaller and more dense LDL; increased LDL apo-B

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17
Q

What is the difference between HDL 2 & HDL 3?

A

HDL 2=large and buoyant (preferred), HDL 3= small & less protective

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18
Q

Which type of VLDL is associated with most risk?

A

VLDL 3 - most dense (compared to 1&2)

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19
Q

What are some conditions related to cardiometabolic dysfunction outside of CVD?

A

Obesity, sarcopenia, NAFLD, Type 2 & 3 DM, MetSx; Hormonal - E2 dominance/cancers (breast CA), PCOS, osteoporosis, men - decreased testosterone

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20
Q

How does insulin relate to increased risk of breast CA?

A

Increased insulin & IGF, decreased adiponectin -> inflammation; also increases estradiol & testosterone, decreases SHBG by increasing aromatase activity (testosterone binds SHBG preferentially)

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21
Q

What anthropometrics can be predictive for breast CA prognosis pre- and post-menopause?

A

BMI - post-menopausal
WHR - pre-menopause

Can focus on these for prevention

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22
Q

How does insulin relate to hormone changes in PCOS?

A

Increased insulin in ovaries -> increases testosterone, which binds to SHBG

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23
Q

In the natural history of Type 2 DM, what happens to: insulin resistance & secretion?
post-prandial and fasting glucose?

A

Insulin resistance increases before diagnosis and levels off
Insulin secretion increases until diagnosis and then decreases
Post-prandial glucose increases gradually then speeds up around diagnosis and beyond
Fasting glucose gradually increases toward diagnosis and beyond (increase is slower that post-prandial)

Note: incretin and B-cell function both declines over time

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24
Q

What are the differences between android obesity & gynoid obesity?

A

Android - apple shape; over fat, over VAT (visceral adipose tissue); assess w/WC & WHR
Gynoid - pear shape; over fat, over SAT (subcutaneous adipose tissue); assess with BIA (high %body fat, but normal WHR)

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25
Q

What are the risk levels associated with ApoE?

A

Apo E3 - least risk (prevalence 3/3 = 62%, 3/4 - 2%; most common)
Apo E2 - intermediate risk (2/3 - 1%, 2/3 - 10%; lower risk of elevated LDL, but higher TGs; associated with type III hyperlipoproteinemia)
Apo E4 - highest risk (3/4 - 20%, 4/4 - 5%)

ApoE is important for catabolism of TG-rich lipoproteins

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26
Q

What are some bacteria associated with CVD?

A

Brucella, Chlamydia pneumoniae, H pylori, P. gingivitis, hepatitis C

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27
Q

What type of fat is olive oil and what are some of its benefits on lipids?

A

n9 (oleic acid) MUFA; less LDL oxidation (compared to saturated fats), protects against LDL oxidation with high PUFA & SFA intake

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28
Q 
What is the MOA or impact on lipids &/or CVD  for each of the following nutraceuticals:
trans-resveratrol
Niacin
Red Yeast Rice
Turmeric
ECGC
Plant sterols
Pomegranate
Pantethine
Probiotics
Berberine
Omega-3 FAs
NAC
Aged Garlic
A

t-resveratrol: blocks LDL uptake - decreases TC, TG & LDL
Niacin: decreases TC, LDL, apo-B & TGs; shifts type B-> type A
RYR: decreases LDL (HMGCoA inhibitor), decreases TG, but no significant change to TC or HDL
Turmeric: increases HDL, decreases TG & atherosclerosis
ECGC: HMGCoA inhibitor, decreases oxLDL & ap0B, increases LDL-receptors
Plant sterols: reduces TC & LDL, anti-inflammatory
Pomegranate: improves HDL function, platelet inhibitor
Pantethine: decreases TC, LDL, apoB & TGs; increases HDL and Apo-A1
Probiotics: reduces TC, LDL & TGs
Berberine: decreases PCSK9 activity & blood glucose; anti-inflammatory
Omega-3: decreases TG, COX-2 inhibition
NAC: blocks LDL uptake
Aged garlic: decreases CAC, plaque progression & hsCRP

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29
Q

What nutraceuticals increase HDL?

A

Curcumin, pomegranate, pantethine, omega-3, niacin

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30
Q

What are some precautions for niacin?

A

May increase blood glucose, homocysteine, uric acid & gout; S/E - rash, flushing, hyperpigmentation, gastritis, SVT & palpitations

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31
Q

What are the diagnostic criteria for metabolic syndrome?

A

3 of: increased waist circumference (M>40”, F>35”), BP >130/85 or on meds, FBG >/=100mg/dL, TG >/= 150, decreased HDL (M<40, F<50)

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32
Q

What are the ethno-specific criteria for waist circumference?
(USA, Asian/Hispanic, Euro/SS Africa/Middle East/Med)

A

USA: M >40”, F>35”
Asian/Hisp: M>35”, F>31”
Euro/SS Africa/Middle East/Med: M>37, F>31

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33
Q

What are the consequences of enhanced sympathetic response and reduced parasympathetic tone on CV indices?

A

HPA-dysfunction & SNS hyperactivity increases cortisol

Leads to; Enhanced coagulation, high RAAS, weight increase, insulin resistance, abnormal lipids, tachycardia, high BP, trophic effects, decreased HRV

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34
Q

How does nitric oxide benefit endothelial health?

A

Dilatation, growth inhibition, antithrombotic, anti-inflammatory, antioxidant

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35
Q

How is Angiotensin II detrimental to endothelial health?

A

Vasoconstriction, growth promotion, pro-thrombotic, pro-inflammatory, pro-oxidant

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36
Q

What factors can worsen endothelial function?

A

Sleep apnea, PCOS, Type 1 DM, malaria (improves with Arg), pre-eclampsia, high fat meals

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37
Q

What interventions can improve endothelial function?

A

Sildenafil (in men with T2DM), flavonoids improve endothelial dysfunction from high fat meals, cocoa flavanols (increase NO), Herbst Mandibular splint

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38
Q

What’s the difference between waking BP and sleeping BP? (systems involved)

A

Waking BP: controlled by sympathetic nervous system

Sleeping BP: controlled by RAAS (thus RAAS meds better at night and for nocturnal hypertension)

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39
Q

What are features of the Cardiometabolic food plan?

A

Modified Mediterranean diet, Low glycemic impact, targeted calories, balances blood sugar, high in fiber, low in simple sugars, balanced quality fats, condition-specific phytonutrients

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40
Q

What are the roles for Apolipoprotein E?

A

Required for clearance of chylomicrons and IDLs
Mediates cholesterol metabolism
Principal cholesterol carrier in the brain
(produced in the liver, macrophages & astrocytes)

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41
Q

Which ApoE profiles have increased risk of MCI & Alzheimer’s?

A

ApoE 3/4 and 4/4
Also increases risk of hyperlipidemia, Type 2 DM & CHD
Worse outcomes w/alcohol & smoking

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42
Q

What MTHFR SNPs are clinically relevant for CVD?

A

MTHFR A1298C, C677T

Heterozygous < homozygous

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43
Q

What are the mental benefits of Exercise?

A

Improves memory, increases hippocampus size, increases BDNF

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44
Q

What are the 4 parts of an Exercise Rx?

A

Frequency
Intensity
Time
Type

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45
Q

What are recommended FITT for cardiorespiratory, resistance, flexibility & neuromotor fitness?

A

CR: 150min/week, 30-60min moderate intensity 5x/wk or 20-60min vigorous 3x/wk
Resistance: train each muscle group 2-3x/wk
Flexibility: accumulate 60s/stretch per muscle group 2-3d/wk
Neuromotor: exercises for agility, balance, gait & coordination 20-30min, 2-3d/wk

46
Q

What inhibits desaturase enzyme (in omega FA conversion)

A

Insulin, glucose, alcohol, glucocorticoids, hydrogenated & trans fats

47
Q

What is the dosing for DHA for ApoE4 SNP?

A

Larger doses of omega-3 FAs (>1g) needed to increase brain BA in patients with ApoE4 (due to increased catabolism).
Also early supplementation needed to prevent Alzheimers

48
Q

What are some of the comorbidities associated with insulin dysfunction?

A

Obesity, sarcopenia, Type 2 DM, NAFLD, Type 3 DM, CV disease, hormonal issues (E2 dominance/cancers, PCOS, osteoporosis)

49
Q

What is the natural history of incretin, B-cell function, insulin secretion, insulin resistance, post-prandial and fasting glucose in Type 2 DM?

A

Incretin & B-cell function declines with time
Insulin secretion increases and then declines starting around diagnosis
Insulin resistance increases and plateaus around diagnosis and thereafter
Postprandial glucose steadily increases (normal w/prediabetes)
Fasting glucose gradually increases over time (less steep slope than post-prandial glucose)

50
Q

What are causes of insulin dysfunction?

A

Poor lifestyle
Environmental burden (including endocrine disruptors)
Mitochondrial dysfunction
Microbiome imbalances (endotoxemia, inflammation)
Altered body composition (central adiposity)
Genetic predisposition

51
Q

What are common ATMs in cardiometabolic disease?

A

A: age, smoking, gender, APOE status, family hx
T: stress, injury, infection/dysbiosis, toxins
M: hyperinsulinemia, VAT, oxidative stress/inflammation, chronic stress, nutrient depletions

52
Q

What is the key differences between conventional and functional treatment of early/prediabetes?

A

Conventional - reactive; FBG, A1C, etc are already elevated
Functional - Proactive: address root causes before markers become abnormal (mitochondrial health, microbiome, body composition, environmental burden)

53
Q

How dose insulin resistance relate to osteoporosis?

A

Sustained hyperglycemia and insulin resistance reduces osteoblast function and increases osteoclast bone resorption –> osteoporosis

54
Q

What are micronutrient recommendations for insulin resistance?

A

Chromium 1000mcg daily
Vitamin D
Magnesium 200-400mg daily
CoQ10 100-200mg daily (give if also hypertensive)
ALA 600mg if diabetic + peripheral neuropathy
EPA/DHA 1g daily (3g daily if high TG)
Vanadium 1-2mg (caution re: high dose long term)
Biotin 4-8mg
Antioxidants (C,E,Se)

55
Q

What medications can reduce CoQ10?

A

Statins, beta-blockers, sulfonylureas

56
Q

What micronutrients can statins reduce?

A

Se, omega-3s, fat soluble vitamins, carnitine, free T3

57
Q

What micronutrients can diuretics reduce?

A

Potassium, Mg, folate, B6, B12, thiamine, iodide, Se

58
Q

What micronutrients can digoxin reduce?

A

Mg, Ca, phosphorus

59
Q

What vitamins can metformin reduce?

A

Folate, B12

60
Q

What minerals are decreased with ACEI and ARBs?

A

Zinc, sodium

61
Q

What is the significance of over-VAT?

A

People with low BMI can still have high abdominal visceral fat (metabolically obese)
OverVat tends to be android obesity

62
Q

What anthropometric may be a better discriminator for CV risk than BMI?

A

Waist to Height Ratio - 0.5 ideal

63
Q

How many times more likely does familial hypercholesterolemia increase the risk of premature heart disease?

A

20 times, if untreated

50% of untreated men will have MI by age 50
30% of untreated women will have MI by age 60

64
Q

What are the manifestations of familial hypercholesterolemia?

A

Extremely high LDL, cholesterol deposits under skin, tendons, corneas

Heterozygous: premature CVD at age 30-40 (most common type - 1/250ppl)
Homozygous: severe CVD in childhood

65
Q

What SNP does 95% of patients with familial hypercholesterolemia have?

A

LDLR

Also ApoB and PCSK9 SNPs

66
Q

How is familial hypercholesterolemia diagnosed? (AHA criteria)

A

LDL >190 + first-degree relative with LDL>190 or known premature CHD

67
Q

What are examples of methylation reactions?

A

Methylation of homocysteine to SAMe
Methylation of tyrosine to dopamine and norepinephrine
Methylation of Trp to serotonin and melatonin
Breakdown of histamine

68
Q

What are symptoms of undermethylation?

A

Fatigue, depression, OCD, HA, histamine overload, high libido

69
Q

What are symptoms of overmethylation?

A

Anxiety, depression, paranoia, nervousness, sleep problems, low libido

70
Q

What is MTHFR?

A

Last enzyme in metabolism of folate (from 5,10-methyleneTH4folate -> 5-methylTH4folate); needs B6 and B2

71
Q

What are the most relevant MTHFR SNPs? And what interventions are recommended?

A

A1298C and C677T
Keep homocysteine levels low (optimal 7?)
- Increase dietary sources of folate, bypass MTHFR by supplement w/methyl forms of folate, B2 & B6 supplementation

72
Q

What is the relationship between 5-MTHF (active form of folate) and BH4?

A

BH2 –> BH4 requires 5-MTHF

BH4 is then needed for metabolism of Trp to 5-HT, Phe–>Tyr–> L-dopa, arginine –> NO + citrulline

73
Q

What is the role of methionine synthase?

A

Conversion of homocysteine to methionine (and eventually to SAMe)
Requires B12 & MTHF; Zn (carrier for homocysteine)

Note - blocked by alcohol

74
Q

What is clue of methionine synthase dysfunction?

A

Elevated MCV

75
Q

What is methionine synthase reductase? (MTRR)

A

Enzyme required for regeneration of methionine synthase
(note: MS is inactivated by oxidation w/B12)

SNPs: MTRR A66G, MTRRC524T

76
Q

What interventions are recommended for MS & MTRR SNPs?

A 
Lower homocysteine levels
Monitor MCV
Avoid alcohol and candida overgrowth
Support Zn, B12 & MTHF
Note: if homocysteine isn't budging, support betaine
77
Q

What is the role of COMT?

A

Catechol-O-methyl-transferase
Breaks down catecholamines (E & NE -> VMA); requires SAMe and Mg
Part of estrogen metabolism (2- and 4-hydroxyestrone -> 2- and 4-methoxyestrone)

78
Q

What is the relevant SNP for COMT? Whats the significance of hetero, vs homozygous Val/Met

A

COMT V158M

Val/Val - upregulated COMT; can be blocked using quercetin & EGCG; increased CV risk w/ASA & vitamin E
Val/Met - normal
Met/Met - downregulated: avoid caffeine, stress and consider supplementation with SAMe, Mg, reduced CV risk with ASA and vitamin E, support methionine synthase, creatine supplement (to avoid using SAMe for this), optimize estrogen levels (DIM, sulforophane)

79
Q

What if a patient has a MTHFR SNP + down regulated COMT (Met/Met)?

A

Can lead to excessive catecholamine production.
In this case, lower methylated Bs, consider Mg & SAMe support (+creatine), consider GSH or NAC; slowly added methylated folate later and use hydroxycobalamin

80
Q

What interventions should be considered for familial hypercholesterolemia?

A

High intensity statin (rosuvastatin, atorvastatin)
CoQ10
Vitamin D
+ screen all 1st degree relatives

81
Q

How does the Mediterranean diet benefit signs of metabolic syndrome?

A

Improvements in: waist circumference, HDL, TGs, BP, and glucose; lower inflammatory markers (IL-6, TNF);
Decreased oxidative stress and enhanced glutathione levels

82
Q

How does sulforophane benefit CVD?

A

Antioxidant and anti-inflammatory, Nrf2 activation, lowers serum total cholesterol, leptin & liver triglyceride levels

83
Q

What is the PFC ratio for the cardiometabolic food plan?

A

30 protein, 30 fat, 40% CHO

84
Q

What are some therapeutic foods in the cardiometabolic food plan?

A

EVOO - 2-6Tbsp daily
Tree nuts - 1-2 oz/day, ideally 1oz, 5x/wk (most potent are walnuts, peanuts, pistachios, almonds, pecans & macadamia nuts)
Green tea (weight loss, GHS, antioxidant)
Kimchi (improves insulin sensitivity, BP) - 3oz TID

85
Q

Who are ideal candidates for ketogenic (Mito) food plan

A

Highly motivated
MetS patients with obesity, insulin resistance and/or neurological conditions like migraine, epilepsy
Able to keep track of ketosis

86
Q

What are some precautions for ketogenic (Mito) plan?

A

Hx of gallbladder dysfunction, insulin dependent, hypercholesterolemia, long QT

87
Q

What are neurotransmitter, ROS and leptin benefits w/ketosis?

A

Decreased glutamate when ketones used for energy instead of glucose
Decreased ROS and mitochondrial damage
Increased leptin (satiety), leading to reduced appetite, increased lipolysis, greater metabolic efficiency for fat consumption

88
Q

For what conditions is there strong or emerging evidence of benefit for ketogenic diet?

A

Strong: epilepsy, diabetes, weight reduction, hypercholesterolemia
Emerging evidence: Cancer, PCOS, acne, neurological disease

89
Q

What indices should be monitered with every visit for patient following keto diet?

A

Caloric intake, height & weight, medications, ketone measurements, bowel habits

90
Q

What dietary interventions could be considered for hypertension?

A 
DASH diet (salt 1500-2300mg/day)
Limit: Na to 2000mg/day, processed foods, soft drinks, sweeteners, alcohol, caffeine, oils + high heat

Add: fermented soy, hydrolyzed whey (supports GSH and is ACEI), legumes, cold water fish, foods high in L-arginine (lentils, hazelnuts, walnuts, peanuts), unsalted mixed nuts, cocoa (30g dark chocolate/day), dried bonito, sardines (natural ACEI - 2/day)
Taurine (diuretic, vasodilator, insulin sensitizer) - 6g/day
Fruits & Veg - especially those high in K, leafy greens high in nitrates, lycopene, pomegranate, mushrooms, blueberries, celery, garlic, seaweed/wakame
Olive, flax, and sesame oils
High fiber whole grains

CoQ10 supplementation

91
Q

What dietary interventions could be considered for hyperlipidemia? (reduce inflammation, immune dysregulation)

A

Avoid: processed foods, sucrose, refined carbs, trans fats, high saturated fats, margarine

Include: fish, leafy greens, low GI fruits, EVOO, tomatoes, green tea, soy beans, dark chocolate, pomegranate, seeds and nuts (esp sesame), red wine, garlic, rice bran oil, beans & legumes

Fish & crucifers - lower TGs (sulforaphanes, omega-3)

92
Q

What is the significance of high TMAO?

A

Trimethylamine N-oxide - made in liver from TMA made by gut bacteria from metabolism of choline, lecithin & carnitine
High TMAO has been associated with CVD

BUT - fish is high in TMA

Suggest - if high TMAO, switch to plant-based or Mediterranean diet; limit high saturated fat, eggs and eat more veggies

93
Q

What are the 3 key stress hormones?

A

Adrenaline
Aldosterone
Cortisol

94
Q

What is the stress response on the SNS & PNS?

A

Increased SNS, Decrease PNS - leading to:
High renin/angiotensin, weight increase, insulin resistance, abnormal lipids, tacchycardia & arrhythmias, HTN, trophic effects, enhanced coagulation, decreased HRV; HPA-axis dysfunction

Also increases homocysteine, CRP, fibrinogen, coronary vasoconstriction and deep abdominal fat deposits, “broken heart syndrome”;
Decreases resistance to infection

95
Q

What are some nutraceuticals to help with depression?

A 
SAMe (antidepressant)
SJW - caution with drug interactions (reduces OCP, cyclosporin, digoxin, warfarin, HIV & theophylline potency; increases MAOi, SSRI, alcohol, triptans, and narcotic potency)
Vitamin D
EPA (1g or more)
B complex - B6 50mg and folate 1mg

Also - exercise, protein, inner work, light therapy; check thyroid . Vitamin D & ferritin

96
Q

What patterns of night BP are associated with higher risk?

A

Non-dipping (ie BP doesn’t drop >10mmHg overnight), reverse dipping and nocturnal hypertension

97
Q

How can plasma renin activity and aldosterone be used as BP/CV biomarkers?

A

random serum PRA and aldosterone
High PRA is associated with higher risk of MI, CVA, CHF, CKD, mortality

Drug choice
Low renin HTN = PRA <0.65 + increased intravascular volume (volume dependent) -> use volume drugs, CCBs, spironolactone, alpha-blockers (more common in African American)

High renin HTN = PRA >0.65 + decreased intravascular volume -> use RAAS drugs ACE, ARBs, beta blockers
Very high renin = PRA >6.5 + volume depleted

98
Q

What is elevated asymmetric dimethylarginine (ADMA)? And what can increase it?

A

ADMA inhibits NO production (by NO synthase) and impairs endothelial function

Increased by: PPIs, LDL, diets poor in arginine and folate, methionine & homocysteine

99
Q

What genetic SNPs can increase oxidative stress?

A 
NADPH oxidase
Xanthine oxidase
SOD-3
Catalase
GPx1
Thioredoxin
100
Q

What tests can be used to evaluate oxidative stress?

A 
8OHdG
Lipid peroxides, oxidized LDL, isoprostane F2
A1C, AGEs (damaged sugars)
3-nitrotyrosine (damaged proteins)
Total Antioxidant Capacity
Micronutrient deficiencies
GSH, glutathione peroxidase, SOD
101
Q

What tests can be used to evaluate endothelial health?

A

Vascular Reactivity Index
Digital pulse amplitude/Reactive Hyperemia (pre- and post occlusion ratio index)
Carotid intima media thickness

102
Q

What are other emerging CV risk markers?

A 
hsCRP
ADMA (asymmetric dimethylarginine)
Uric acid
Lead, Cadmium, arsenic
TMAO
Nutrient deficiencies
103
Q

What is the benefit of weight loss on BP?

A

Each pound of weight loss = 1mmHg drop in SBP and DBP

Body fat reduction is more important than weight loss

104
Q

What are some natural CCBs?

A

ALA, vitamin C, Hawthorne, magnesium, NAC, B6, celery, garlic, taurine

105
Q

What are some natural ACEIs?

A

Garlic, sardines, bonito flakes, dried salty fish, zinc, hydrolyzed casein, Hawthorne, seaweed, tuna, fish sauce, pycnogenol, whey protein, omega-3, pomegranate, sour milk

106
Q

How to calculate maximum heart rate?

A

220-age
High intensity exercise is 77-93% max heart rate
Low intensity is 50-63% of max heart rate

107
Q

What nutraceuticals/herbs do NOT decrease TG?

A

NAC, aged garlic, bergamot

108
Q

Which nutraceuticals/herbs improve Pattern B lipids?

A

Niacin, green tea, pantethine, probiotics, berberine, omega-3

109
Q

Which nutraceuticals/herbs do NOT decrease LDL?

A

NAC, aged garlic, curcumin, pomegranate, omega-3s

110
Q

How does abdominal obesity/adipose tissue contribute to NAFLD?

A

Increases TNF-alpha and decreases adiponectin which drives increased glucose, insulin, free FAs and TGs in the liver

111
Q

How does abdominal obesity/adipose tissue contribute to higher risk of CVD?

A

Drives increase in IL-6 which in turn increases inflammation & CRP = higher risk of CVD

Institute for Functional Medicine exam (7 decks)

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