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NUTRITIONAL ASSESSMENTS
NUTRITIONAL ASSESSMENTS
sample type:
sample type:
BLOOD
BLOOD
CV Health Plus Genomics analyzes blood for state-of-the-art lipid markers and independent risk factors that
illuminate the clinical complexity of cardiovascular disease (CVD) as well as a patient’s genomic predisposition
to cardiovascular diseases. Together, these markers provide a thorough assessment of cardiovascular health
status, revealing the biochemical environment and cardiogenomic risk associated with inflammation, lipid
deposits, endothelial dysfunction, and clotting factors underlying cardiovascular disease.
The CV Health Plus Genomics is a comprehensive evaluation featuring an advanced lipid profile that
utilizes NMR fractionation technology, inflammatory markers and a novel Insulin Resistance Score.
It also includes an assessment of single nucleotide polymorphisms (SNPs) in 4 cardiovascular genes.
These markers provide insight to clinically modify the expression of these genes.
• Analytes:
LDL-C
HDL-C
Triglycerides
Total Cholesterol
LDL-P
HDL-P
LDL-Size
Lipoprotein (a)
hs C-Reactive Protein
Lp-PLA2
Homocysteine
Fibrinogen
Insulin Resistance Score
• HDLL-P
• LDLS-P
• VLDL-P
• HDL-Size
• LDL-Size
• VLDL-Size
• Genomic Analytes:
ApoE
MTHFR
Factor II
Factor V (Leiden)
• Optional Add-On Analytes:
Vitamin D
• Specimen Requirements:
- Two 4 ml serum,
- 3 ml plasma,
- 5 ml Z-serum separator and
- 3 ml whole blood
• Before Patient Takes this Test:
- Fast overnight (at least 12 hours)
Nearly 50% of all heart attack victims have normal levels of typical risk markers for CVD, including
total cholesterol. This unique combination of advanced markers for cardiovascular disease helps
physicians to identify up to 85% of individuals at risk for cardiovascular disease. In addition, the
markers for cardiogenomic risk provide an understanding of genetic concerns related to cholesterol
metabolism, methylation and clotting activity.
The CV Health Plus Genomics includes:
Markers for Cardiogenomic Risk
• Apolipoprotein E (APO-E) plays a key role in the metabolism of cholesterol and triglycerides.
The genomic variations of ApoE influence disease risk and treatment response. APOE4 is associated
with hyperlipidemia and increased risk of coronary heart disease, myocardial infarction, and stroke.
APOE genotypes determine effective dietary and pharmaceutical therapies for dyslipidemia.
• Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme in folate metabolism. Two variants
of the MTHFR polymorphisms result in reduced enzyme activity, impaired methylation, and
increased risk of cardiovascular disease, stroke, abdominal aortic aneurysm, hypertension, and
venous thrombosis.
• Factor II is also known as prothrombin. Polymorphisms of Factor II result in increased coagulability –
and increased risk of venous thrombosis. Factor II SNP is also associated with increased risk of CVD,
carotid atherosclerosis, atrial fibrillation, and MI (when other cardiovascular risk factors are present).
• Factor V (Leiden) is the name given to the variation of the gene that affects the conversion of
prothrombin to thrombin. Individuals with this polymorphism have increased risk for coagulation
and coronary artery disease, worsened by coexisting SNPs in Factor II or MTHFR.
Advanced Markers for Cardiovascular Disease
• LDL-Particle Number (LDL-P) is independent of the LDL cholesterol concentration. A person
with normal LDL-C concentration and high LDL-P, is still at high-risk for plaque build-up.
• HDL-Particle Number (HDL-P) indicates increased risk of coronary events for individuals with
a low HDL-P number, even in individuals with optimal levels of LDL-P.
• LDL-Size is highly associated with triglycerides and insulin resistance.
• Lipoprotein(a) or Lp(a) is influenced by heredity and has a strong association with coronary
and peripheral cardiac events.
• hs C-reactive protein (hs-CRP) is an independent marker for systemic inflammation.
High levels are linked to coagulation and vascular endothelium damage.
• Lipoprotein-associated phospholipase (Lp-PLA2), aka PLAC, is produced in the intima,
promoting inflammation and plaque instability. It is specific for vascular inflammation.
• Homocysteine is an amino acid that has been linked to damaged endothelium, increased platelet
aggregation, and the formation of atherosclerotic lesions.
• Fibrinogen plays a key role in arterial occlusion by promoting thrombus formation,
endothelial injury and hyper-viscosity.
• Insulin Resistance Score determined by lipid sub-fractionation.
ONE-PAGE TEST DESCRIPTION
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Apo E
Apolipoprotein E : CHOLESTEROL REGULATION
051
Apolipoprotein E (Apo E) plays a key role in lipid metabolism by helping to remove dietary cholesterol
Location:
Chromosome 19
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APOE
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APO E2: cys
APO E3: cys
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APO E4: arg / arg
Your Genotype:
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The two SNPs lead to 3 possible
variants for each chromosome,
known as ApoE2, E3, & E4.
Health Implications
· The APO E3/4 genotype is the second most prevalent after E3/3 and accounts for >25% in most populations
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· APO E4 confers a tendency toward higher total- and LDL-cholesterol and lower HDL-C
as well as toxicity
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stroke,
for atherosclerosis, myocardial infarction,
osteoporosis,
· Risk is also increased
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by heavy metals such as lead and mercury
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Treatment Options
· Restriction of saturated fat and cholesterol lowers total- and LDL cholesterol the most effectively in E4
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individuals
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· Avoid smoking and minimize high-glycemic index foods, both of which augment E4-associated risk of
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coronary heart disease
· Reduce excess weight, which synergizes with effects of E4 on insulin and lipids
· Fish oils and exercise should improve the lipid profile, dietary fiber only moderately so
· Alcohol may raise LDL-C in men (neutral effect
in women)
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· Cholesterol responds only slightly to statin drugs in E4 carriers (especially in men)
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· Estrogen therapy is particularly efficacious for both cholesterol and bone in postmenopausal E4 carriers
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(chylomicrons and VLDL) from the bloodstream.
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Page 2
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· Consider
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vitamin K supplementation for bone protection
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MTHFR
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Location:
Chromosome 1
C677T
Your Genotype:
5,10-methyltetrahydrofolate
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reductase : METHYLATION
is a key enzyme in folate metabolism, facilitating the
5,10-methylenetetrahydrofolate reductase (MTHFR)
formation of methyltetrahydrofolate, a required cofactor in the remethylation of homocysteine (Hcy) to methionine.
Health Implications
· Homozygosity for 677 (+/+) results in 60-70% reduction in MTHFR
+'/ enzyme
/'/activity 9/'/
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6L]H
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· Increased risk of high homocysteine, esp. if low levels of B2,
B6, B12, or6L]H
folate
impairment, including disrupted neurotransmitter metabolism and synthesis of DNA,
,56FRUH· Possible methylation
carnitine and coenzyme Q10
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!
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congenital heart
! depression,
bipolar disorder,
· Increased risk of autism,
schizophrenia,
neural
tube defects,
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Your Genotype:
defects, cardiovascular disease, essential hypertension, atherosclerosis, diabetic retinopathy, osteoporosis
· Increased risk of cancers of the breast (esp. if prolonged estrogen exposure and/or low folic acid intake),
stomach, pancreas (esp. if smoke or drink)
· Possibly decreased risk of colorectal cancer and lung cancer only when high folate status; otherwise
3HUFHQWLOHV$SSO\WR%LRPDUNHUVLQGLFDWHGZLWKDQGDUHSHUIRUPHGXVLQJ105WHFKQRORJ\
increased risk
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· Low levels
of vitamins B2, B6, B12, and/or folate often determines the risk of these associated disorders
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Treatment
Options
· Ensure adequate intake of folate-rich green vegetables; folate levels tend to be lower
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· Consider supplementation with folic acid (or folinic acid or 5-methyltetrahydrofolate),
riboflavin, B6 (pyridoxal
5-phosphate), B12 (or methylcobalamin), and betaine (trimethylglycine); individuals with this genotype show
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the best homocysteine response to B-vitamin supplementation
· Easier toxicity and less clinical efficacy with methotrexate chemotherapy
‹ *HQRYD 'LDJQRVWLFV à &/,$ /LF ' à 0HGLFDUH /LF For test kits, clinical support, or more information contact:
Know Your
Patient’s CVD
Risk:
• Know the
Cardiogenomic Risk.
The four genes
evaluated – Apo-E,
MTHFR, and Factor II
and V Leiden – provide
information related to
cholesterol
metabolism,
methylation and
clotting activity. While
variations in these
genes have been
associated with
increased
cardiovascular risk,
their phenotypic
expression is clinically
modifiable.
• Know the Lipid
Particle Number.
Recent data indicates
that LDL-P is a more
accurate assessment
of LDL-related risk
than LDL-C
concentration, and
that HDL-P is strongly
associated with
atherosclerosis, even in
individuals with normal
LDL-P numbers.
• Know the level of
Inflammation. hs-CRP
is an independent risk
for adverse coronary
events in individuals
without overt
hyperlipidemia, and
Lp-PLA2 is a specific
marker for vascular
inflammation.
Increased activity of
this intimal-based
enzyme promotes
plaque instability.
• Know the Insulin
Resistance Score.
Insulin resistance
promotes the
inflammation and
oxidative stress that
drives atherogenesis,
and is the ultimate
catalyst for glucose
intolerance,
dyslipidemia, and
hypertensive damage.
Client Services
Genova Diagnostics
63 Zillicoa St.
Asheville, NC 28801-1074
800-522-4762 • Fax: 828-252-9303
More detailed publications with references are also available: www.GDX.net
© 2012 Genova Diagnostics
g,td,cvhealth+genomics,021312