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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 &9+HDOWK3OXV*HQRPLFV 3DWLHQW 6$03/( 3$7,(17 &RPSOHWHG 2FWREHU Patient: SAMPLE PATIENT ID: '2%1RYHPEHU 5HFHLYHG 2FWREHU 2FWREHU &ROOHFWHG 6H[) Apo E Apolipoprotein E : CHOLESTEROL REGULATION 051 Apolipoprotein E (Apo E) plays a key role in lipid metabolism by helping to remove dietary cholesterol Location: Chromosome 19 5HVXOW APOE / cys APO E2: cys APO E3: cys / arg / APO E4: arg / arg Your Genotype: &KROHVWHURO /'/&KROHVWHURO +'/&KROHVWHURO 7ULJO\FHULGHV 7RWDO&KROHVWHURO The two SNPs lead to 3 possible variants for each chromosome, known as ApoE2, E3, & E4. Health Implications · The APO E3/4 genotype is the second most prevalent after E3/3 and accounts for >25% in most populations QPRO/ PJG/ /'/3DUWLFOH/'/3 + · APO E4 confers a tendency toward higher total- and LDL-cholesterol and lower HDL-C as well as toxicity !PJG/ +'/3DUWLFOH+'/3 / and!MPRO/ stroke, for atherosclerosis, myocardial infarction, osteoporosis, · Risk is also increased 3DUWLFOH&RQFHQWUDWLRQ6L]HE\105 5HIHUHQFH5DQJH 5HVXOW 5HIHUHQFH5DQJH by heavy metals such as lead and mercury PJG/ /DUJH3DWWHUQ$ 6PDOO3DWWHUQ% Treatment Options · Restriction of saturated fat and cholesterol lowers total- and LDL cholesterol the most effectively in E4 PJG/ individuals /'/6L]H · Avoid smoking and minimize high-glycemic index foods, both of which augment E4-associated risk of PJG/ /SD 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) 5HODWLYH5LVNIRU&DUGLRYDVFXODU'LVHDVH · Cholesterol responds only slightly to statin drugs in E4 carriers (especially in men) PJ/ KV&53 · Estrogen therapy is particularly efficacious for both cholesterol and bone in postmenopausal E4 carriers 5HVXOW /S3/$3/$& (chylomicrons and VLDL) from the bloodstream. 5HIHUHQFH5DQJH 5HVXOW KV&53 Page 2 + · Consider 5HIHUHQFH5DQJH vitamin K supplementation for bone protection QJP/ /S3/$ )LEULQRJHQ 5HVXOW 5HIHUHQFH5DQJH PJG/ MTHFR 5HVXOW +RPRF\VWHLQH ,QVXOLQ5HVLVWDQFH6FRUH )LEULQRJHQ 5HIHUHQFH5DQJH MPRO/ Location: Chromosome 1 C677T Your Genotype: 5,10-methyltetrahydrofolate +RPRF\VWHLQH 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/'/ +'/ / /'/ 6 9/'/ / 6L]H 6L]H · 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 7KH,QVXOLQ5HVLVWDQFH6FRUHFRPELQHV6PDOO/'/3DUWLFOH/'/6L]H/DUJH ! ! congenital heart ! depression, bipolar disorder, · Increased risk of autism, schizophrenia, neural tube defects, QPRO/ QP QP QP MPRO/ QPRO/ A1298C 9/'/3DUWLFOH9/'/6L]H/DUJH+'/3DUWLFOHDQG+'/6L]HWRDVVHVVLQVXOLQ UHVLVWDQFHDQGGLDEHWHVULVN 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 2SWLPDO (LWKHUWKRUWKSHUFHQWLOHEDVHGRQUHIHUHQFHSRSXODWLRQ %RUGHUOLQH WK3HUFHQWLOH · Low levels of vitamins B2, B6, B12, and/or folate often determines the risk of these associated disorders $EQRUPDO ,QYHUVHRI2SWLPDOWKRUWK SHUFHQWLOHGLVWULEXWLRQ Treatment Options · Ensure adequate intake of folate-rich green vegetables; folate levels tend to be lower 7KH/3DKV&53+RPRF\VWHLQHDQG)LEULQRJHQDQDO\WHVKDYHEHHQDSSURYHGE\WKH86)RRGDQG'UXJ$GPLQLVWUDWLRQDQGDUHSHUIRUPHGE\*HQRYD'LDJQRVWLFV,QF · 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 $OORWKHUDVVD\VDUHSHUIRUPHGE\/LSR6FLHQFH,QF6XPQHU%OYG5DOHLJK1& *HQRYD'LDJQRVWLFVÃ&/,$/LF'Ã0HGLFDUH/LF the best homocysteine response to B-vitamin supplementation · Easier toxicity and less clinical efficacy with methotrexate chemotherapy *HQRYD 'LDJQRVWLFV Ã &/,$ /LF ' Ã 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