article_assessing_genes_lifemap_system

12 HEALTH & WEALTH MANUAL “Nourishing Human Potential”

A Quick Genetics Tutorial

Within every human cell is an individual’s blueprint for life —

their DNA. DNA contains the master information that is needed

to construct and maintain the human body.

DNA is long. About six feet long, to be exact, if you took the DNA contained within one cell and stretched it end to end.

There are several different ways that these long strands of DNA can be divided into smaller pieces.

1. Chromosomes The largest unit of DNA is a chromosome. There are 23 pairs of chromosomes

inside of our cells: one set from each parent. These 23 pairs contain all of our

genetic information.

2. Genes The next unit down is a gene, which is simply a sequence of DNA that

corresponds to a particular inheritable trait. There is a gene for hair color, for

example, and a gene for height. We get one gene from each parent for each

inheritable trait. These are called alleles.

The main job of each gene is to encode — or tell the body how to build —

different proteins. While that may seem like a small job, proteins serve many

critical functions in the body. Enzymes, for example, are proteins.

3. Nucleotides The smallest unit is a nucleotide, which is the “building block” of DNA.

Nucleotides are tiny: less than one millionth of a millimeter!

Small Changes in DNA that Impact Our Physiology

On a strictly DNA basis, humans are surprisingly alike. Despite our apparent differences,

the DNA between any two people is 99.1% identical. That 0.9% variation in DNA,

however, is hugely important, accounting for all of our genetic differences.

Small variations in DNA are called polymorphisms. Blood type is a common human

polymorphism. Depending on the order in which the nucleotides in your DNA line up,

you could have blood type A, B, A/B, or O. Some polymorphisms are so small, they

affect the order of just one pair of nucleotides. These are called single nucleotide

polymorphisms or SNPs (pronounced “snips”).

COMPANY ANd PeOPle

SCieNCe ANdPROdUCT

BUSiNeSSBUildiNg

HEALTH & WEALTH MANUAL “Nourishing Human Potential” 13

A Quick Genetics Tutorial

There are about 10 million SNPs in the human genome.

Most of these SNPs occur in the DNA between genes and

account for non-consequential differences.

However, some SNPs occur in the DNA within genes.

These SNPs can have a dramatic impact on human health.

They can predict how you will react to certain drugs. They

can determine how susceptible you will

be to environmental toxins. And they can cause you

to produce faulty proteins that have a negative impact

on the functioning of the body, and may lead to

diminished health and wellness.

Our Genes are not Our Destiny

Without a doubt, SNPs can have a strong influence on our health and well-being.

However, our genes are not our destiny.

With the mapping of the human genome completed in 2003, scientists now have the ability

to identify small variations in the genetic code that can lead to diminished health and wellness.

By identifying which of these variations (vulnerabilities) you have, it is possible for the first time

to customize a targeted nutritional supplement regimen for your specific genotype.

“Each of us has a unique chemical makeup that induces various responses to foods, drugs and the environment. The reason we are different is that our genes are different.”

“For optimal function we each have unique nutritional needs and specific environmental requirements.”

Biochemical Individuality: Roger J. Williams, Ph.D.

BUSiNeSSBUildiNg

SCieNCe ANdPROdUCT

COMPANY ANd PeOPle

SNP VArIATIONS


Why Testing Our Genes Is So Important

“Science is organized knowledge. Wisdom is organized life.”

Immanuel Kant, German philosopher (1724 - 1804)

Aging is the Challenge – Nourishing Your Cells is the Solution

Before we tell you more about the genetic test we need to give you some information as to why it is so important to

know what’s going on inside our bodies.

The moment we are born we begin the aging process. We have the weapon to fight

disease and aging with something called superoxide dismutase. We get half of it from our

mother and half from our father. It’s our natural antioxidant that fights and

neutralizes free-radicals.

In our population, 60% of us have only one functional superoxided dismutase gene and

20% have no functional gene. That is why introducing antioxidant formulas into our daily

regimens are vitally important.

Antioxidants could be considered a sort of life insurance policy against aging and

its visible effects. It’s a weapon in our arsenal to fight those pesky free radicals that

rob us of a longer life expectancy. Antioxidants are our protectors and lower our risk of

developing many diseases and illnesses.

Again, free radicals are basically little marauders bouncing through our cells causing

damage everywhere they go. You might wonder why and how they are formed in the first

place. In our bodies we have a process called oxidation. It creates free radicals and it goes

on every day through our normal metabolic processes and through exposure to

our environment and the damage it can cause.

This may sound very scary and perhaps that’s a good thing. It’s time to arm yourself with

the information you’ll need to improve the health and wellness of yourself and your family.

Everything we do, from each breath we take, the food we eat and even the sun causes

oxidation within our bodies and with it free radical formation.

Let’s compare our bodies to an automobile. Say you buy a beautiful, brand new car and with no thought to the

consequences you leave it outside with the hood, trunk and doors open. Imagine you allow it to sit outside like that

through every kind of weather imaginable. Eventually the car would begin to rust and one day it would be too late to

repair. You’d be looking at a rusted heap of metal.

Our bodies are like that that car in many ways. We too are a machine that needs to be well-cared for. If we allow free

radicals to run rampant through our bodies and do nothing about it we will have deterioration of our bones, joints and

connective tissue; our organs will wear out and our immune system will break down and become unable to fight off

disease and all the visible effects of the aging process. You could say we can “rust” just like an automobile.

COMPANY ANd PeOPle

SCieNCe ANdPROdUCT

BUSiNeSSBUildiNg


Every day two processes are going on in our bodies. On one hand our cells are being

damaged. On the other hand we’re repairing our cells. If there is no balance

between the two processes going on we’re in trouble. Unfortunately in most cases

we have more damage than we can repair.

The more the cumulative damage piles up we get to the point of critical mass and

cell damage occurs. This can cause the cells to spin out of control and we get a

disease like cancer.

Every day we lose more and more cells. As we lose those cells that produce

collagen, elastin and more skin we then begin to see our skin wrinkle, sag and

become thin. Now we have a much harder task to bring our bodies back from the

ravages of time and the damage we’ve allowed to happen.

In a perfect world our repair system would remain healthy or could increase its ability

to repair our cells on its own. Unfortunately that isn’t the case.

Human beings have a love/hate relationship with oxygen. As we evolved we needed

oxygen to increase our energy supply. As our cells became more complex through our

movement and intelligence, our body required more energy. Through the Krebs cycle,

oxygen became a way of producing this much-needed energy.

As we breathe in oxygen it combines with the sugar in our cells and tiny energy

pellets are produced in the cell’s mitochondria. (Mitochondria are the cells’ power

sources) The more energy pellets we have (They are called ATP molecules) the

younger, healthier and longer we live. Producing lots of ATP is wonderful. It let’s us live

energetic lives. The downside is that every action has a reaction.

We can now give you nourishing solutions. By using the right nutritional building blocks in their proper amounts to

neutralize free radicals we can minimize daily damage to our cells.

Our repair system is now better able to prepare for the days when we are flooded with free radical damage. By boosting

and enhancing our repair system, more damage can be fixed. Now we can keep up and have a reserve for those

unforeseen ‘free radical bursts,’ like viral and bacterial infections.

You may not like to hear this, but inside you right now are cancer cells, virus, bacteria and other nasty invaders just

waiting to attack. When our blood cells detect a threat by these hostile little devils they release free radicals. It makes

sense because we want to destroy these bad cells and demolish their DNA. So not all free radicals are bad.

Life as we know it really is a balancing act.

Why Testing Our Genes Is So Important

BUSiNeSSBUildiNg

SCieNCe ANdPROdUCT

COMPANY ANd PeOPle


Genes serve as the building block in our bodies and every gene is present in the body in two copies:

one from Mom and one from Dad.

Genewize Life Science utilizes a simple color-coded system on your Healthy Aging DNA Assessment that is easy to

follow. GrEEN simply means you have no disadvantaged Gene-SNPs in this nutritional health area. (Geneticists call

this homozygous negative). YELLOW means you have one disadvantaged Gene-SNP from one of your parents, in this

nutritional health area (Geneticists call this heterozygous negative). rED simply means you have two disadvantaged

SNPs in this nutritional health area. (Geneticists call this homozygous positive).

Most important! No matter what mix of colors you have on your assessment, it simply means you now have the

information you need to have a nutritional supplement regimen customized to your personal needs. For the RED

and YELLOW coded areas, GeneWize will add specific SNPboost™ nutrients to your formula to help keep your

body functioning optimally.

GrEEN = Only Basic support nutrients added to your formula for this specific healthy aging area

YELLOW = Additional support nutrients added to your formula for this specific healthy aging area

rED = Maximum support nutrients added to your formula for this specific healthy aging area

Sample assessment for illustration purposes.

Understanding Your LifeMap™ Healthy Aging DNA Assessment

COMPANY ANd PeOPle

SCieNCe ANdPROdUCT

BUSiNeSSBUildiNg


The LifeMap Healthy Aging Assessment measures SNPs. What are SNPs and why are they important?

SNPs are small variations in DNA, called single nucleotide polymorphisms (pronounced “snips”), that account for all human genetic differences, including how efficient the body performs key biological processes. There are about 10 million SNPs in the human genome. Some of these SNPs account for nonconsequential differences. But, some SNPs result in the production of faulty proteins that have a negative impact on the functioning of the body. The GeneLink Scientific and Medical Advisory Board has developed the GeneWize LifeMap™ Healthy Aging DNA Assessment which specifically evaluates a total of 12 key SNPs that regulate critical functions an measure risks for diminished health and wellness. These include:

SNP 1: VDr (Vitamin D receptor)

The strength of our bones is influenced by the VDR gene. In fact, among healthy people, this one gene accounts for 75% of the entire genetic influence on bone density.1 People with SNPs in the VDR gene tend to have lower bone min-eral density than those without these variations. 2,3,4 SNPs in this gene may also influence young adult growth5, parathyroid hormone production6, normal cell division6, and blood sugar regulation.7

SNP 2: EPHX (Microsomal Epoxide Hydrolase)

Epoxides are toxic, highly reactive foreign chemicals present in cigarette smoke, car exhaust, charcoal-grilled meat, smoke from burning wood, pesticides, and alcohol. The body’s way of dealing with epoxides is through the enzyme microsomal EPHX, which detoxifies these foreign compounds. Due to a SNP in the EPHX gene, people with lowered EPHX activity will have difficulty detoxifying harmful substances and thus be particularly vulnerable to their effects.8

SNP 3: NQO1 (Coenzyme Q10 reductase)

Free radicals are considered by many scientists to be the primary cause of aging. The coenzyme Q10 reductase (NQO1) enzyme converts coenzyme Q10 (ubiquinone) to its reduced form, ubiquinol, which scavenges free radicals in the mitochondria and lipid membranes.9 Some individuals have a SNP in the NQO1 gene that slows the reduction of ubiquinone to ubiquinol, resulting in very low blood levels of this key antioxidant. Consequently, people with this SNP are at high risk of free radical attack.10 Because NQO1 is also involved in the detoxification of compounds foreign to the body, a SNP in the NQO1 gene may cause aberrant cellular changes.

SNP 4: SOD2 (Manganese Superoxide Dismutase)

The SOD2 enzyme is also involved in scavenging free radicals. However, SOD2 is focused on one particularly toxic type of free radical: superoxide. 11 Since the superoxide radical is produced in abundance in all cells, it is the starting point for the free radical chain of production. SOD2 has the distinction of being the only enzyme in the mitochondria that can neutralize superoxide. 12 Individuals with a SNP in this gene therefore have a weak first line of defense against free radicals.

SNP 5: GPX1 (Glutathione Peroxidase 1)

The GPX1 antioxidant enzyme specifically scavenges hydrogen peroxide, a reactive oxygen species. GPX1 is a selenoprotein, meaning it incorporates selenium into its protein structure. 13 Therefore, how much GPX1 a person produces is dependent on their selenium level.13 A SNP in the GPX1 gene can reduce a person’s ability to utilize selenium. 14. 15 That means higher-than-normal selenium intake is needed to afford protection to hydrogen peroxide-sensitive tissues, particularly lung and breast tissues.14, 16, 17

Understanding Your Healthy Aging DNA Assessment

BUSiNeSSBUildiNg

SCieNCe ANdPROdUCT

COMPANY ANd PeOPle


SNP 6: MMP1 (Matrix Metalloproteinase)

Collagen is the main component of cartilage, ligaments, tendons, and bone. It is constantly synthesized and broken down in an on-going cycle. MMP1, also known as collagenase, is an enzyme that degrades collagen. People with a SNP in the MMP1 gene produce collagenase at an increased rate, which means their bodies may break down collagen faster than they can rebuild it.18, 19 These individuals will likely benefit from added support for collagen-rich structures such as the bones and joints.

SNP 7: MTrr (Methionine Synthase reductase)

Homocysteine is a metabolite of the amino acid methionine. Research has shown it is important to control homocysteine levels in order to preserve cardiovascular health.20, 21, 22 One of the body’s methods for keeping homocysteine levels in check is the MTRR enzyme, which transforms homocysteine back to either methionine or cysteine. When an individual has a SNP in the MTRR gene, their ability to clear homocysteine from the blood may be hindered. However, only certain population groups appear to be negatively affected by this SNP.23, 24, 25

SNP 8: TNF (Tumor Necrosis Factor)

Inflammation is a response of the immune system to a perceived attack. While it is a helpful response in the short-term, if inflammation continues on-going, it can negatively affect the cells, tissues, and ultimately, the organs. TNF- is a cytokine (a chemical messenger of the immune system) that plays a role in inflammatory processes. Individuals with a SNP on the TNF-_ gene may have an over-reactive inflammation mechanism, which can negatively affect the joints,26

brain,27 lungs,28 and heart. 29

SNP 9: MTHFr (Methylene Tetrahydrofolate reductase)

Like the MTRR enzyme, the MTHFR enzyme is responsible for reducing blood levels of homocysteine. People with a SNP in the MTHFR gene manufacture defective enzymes that can’t clear homocysteine from the blood efficiently. Research has shown there is a direct association between a SNP in the MRHFR gene and elevated levels of homocysteine,30 particularly in those with low levels of folate.31

SNP 10: PON1 (Paraxonase 1)

While it used to be thought that high cholesterol posed a health issue in and of itself, it is now believed that cholesterol only becomes a problem once the cholesterol carrier, low-density lipoprotein (LDL), becomes oxidized (attacked by free radicals). The PON1 enzyme attaches itself to high-density lipoprotein (HDL), which protects both HDL and LDL from oxidation. 32 Due to common SNPs in the PON1 gene, blood levels of PON1 can vary by a factor of 10 to 40-fold among different individuals. 33, 34 Those with low levels of PON1 have higher levels of oxidized LDL, which can lead to diminished cardiovascular health. 35, 36

SNP 11: CYP11B2 (Aldosterone Synthase)

Maintaining blood pressure within the normal range is essential to a healthy heart. The CYP11B2 gene encodes an enzyme called aldosterone synthase, which plays a role in regulating blood pressure. A SNP in the CYP11B2 gene can decrease the ability of blood vessels to relax and constrict in response to changing demands for blood flow. (For example, extra blood flow is needed during exercise.) That inability of the vessels to respond properly can set the stage for cardiovascular issues down the road.38


COMPANY ANd PeOPle

SCieNCe ANdPROdUCT

BUSiNeSSBUildiNg


SNP 12: APOB (Apolipoprotein B)

Cholesterol is carried through the bloodstream on various lipoproteins: low-density lipoprotein (LDL), high-density lipoprotein (HDL), and very low-density lipoprotein (VLDL). Apolipoproteins make up the protein part of lipoproteins. One of the more researched apolipoproteins is apolipoprotein B (ApoB); it constitutes the protein component of LDL, the “bad” kind of cholesterol carrier. In fact, without ApoB, LDL cannot form. Because people with SNPs on the ApoB gene have higher ApoB levels, they experience moderate increases in total cholesterol, LDL cholesterol, and triglycer-ides,39, 40, 41, 42 as well as impaired glucose tolerance43 and increased blood lipid response after meals.44

references

1Morrison NA et al. Prediction of bone density from vitamin D receptor alleles. Nature. 1994;367(6460):284-7.2Thakkinstan A et al. Haplotype analysis of VDR gene polymorphisms: a meta-analysis. Osteoporos Int. 2004;15(9):729-34.3Thakkinstan A et al. Meta-analysis of molecular association studies: vitamin D receptor gene polymorphisms and BMD as a case study. J Bone Miner Res. 2004;19(3):419-28.4Valdivielso JM, Fernandez E. Vitamin D receptor polymorphisms and diseases. Clin Chim Acta. 2006 Sep;371(1-2):1-12.5D’Alesio A et al. Two single-nucleotide polymorphisms in the human vitamin D receptor promoter change protein-DNA complex formation and are associated with height and vitamin D status in adolescent girls. Hum Mol Genet. 2005;14(22):3539-48. 6Marco MP et al. Influence of vitamin D receptor gene polymorphisms on mortality risk in hemodialysis patients. Am J Kidney Dis. 2001;38(5):965-74.7Dawson-Hughes B et al. Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. N Engl J Med. 1997;337(10):670-6.8Morisseau C and BD Hammock. Epoxide hydrolases: mechanisms, inhibitor designs, and biological roles. Annu Rev Pharmacol Toxicol. 2005;45:311-339Hosoe K et al. Study on safety and bioavailability of ubiquinol (Kaneka QH) after single and 4-week multiple oral administration to healthy volunteers. Regul Toxicol Pharmacol. 2007;47(1):19-28.10Ross D et al. NAD(P)H:quinone oxidoreductase 1 (NQO1): chemoprotection, bioactivation, gene regulation and genetic polymor-phisms. Chem Biol Interact. 2000 Dec 1;129(1-2):77-97.11Robinson BH. The role of manganese superoxide dismutase in health and disease. J Inherit Metab Dis 1998;21:598–603.12Bandy B and AJ Davison. Mitochondrial mutations may increase oxidative stress: implications for carcinogenesis and aging? Free Radic Biol Med 1990;8:523–39.13Rayman MP. Selenium in cancer prevention: a review of the evidence and mechanism of action. Proc Nutr Soc 2005 Nov;64(4):527-42.14Hu YJ and AM Diamond. Role of glutathione peroxidase 1 in breast cancer: loss of heterozygosity and allelic differences in the re-sponse to selenium. Cancer Res 2003;63(12):3347-51.15Hu Y et al. Allelic loss of the gene for the GPX1 selenium-containing protein is a common event in cancer. J Nutr 2005;135(12 Suppl):3021S-3024S.16Ratnasinghe D et al. Glutathione peroxidase codon 198 polymorphism variant increases lung cancer risk. Cancer Res 2000 Nov 15;60(22):6381-3.17Moscow J. A., Schmidt L., Ingram D. T., Gnarra J., Johnson B., Cowan K. H. Loss of heterozygosity of the human cytosolic glutathione peroxidase I gene in lung cancer. Carcinogenesis (Lond.), 15: 2769-2773, 1994.18Cunnane G et al. Early joint erosions and serum levels of matrix metalloproteinase 1, matrix metalloproteinase 3, and tissue inhibi-tor of metalloproteinases 1 in rheumatoid arthritis. Arthritis Rheum 2001;44:2263–2274.19Dörr S et al. Association of a specific haplotype across the genes MMP1 and MMP3 with radiographic joint destruction in rheuma-toid arthritis. Arthritis Res Ther 2004;6(3):R199-207.20Refsum H et al. Homocysteine and Cardiovascular Disease. Ann Rev Med 1998;49:31-62.


BUSiNeSSBUildiNg

SCieNCe ANdPROdUCT

COMPANY ANd PeOPle


references (continued)

21Eikelboom J et al. Homocyst(e)ine and Cardiovascular Disease: A Critical Review of the Epidemiological Evidence. Ann Intern Med 1999;131:363-375.22Hankey G et al. Homocysteine and Vascular Disease. Lancet 1999;354 (9176): 407-413.23Gaughan DJ et al. The methionine synthase reductase (MTRR) A66G polymorphism is a novel genetic determinant of plasma ho-mocysteine concentrations. Atherosclerosis. 2001;157(2):451-6.24Guéant-Rodriguez RM et al. Association of MTRRA66G polymorphism (but not of MTHFR C677T and A1298C, MTRA2756G, TCN C776G) with homocysteine and coronary artery disease in the French population. Thromb Haemost. 2005;94(3):510-5.25Barbosa PR et al. Association between decreased vitamin levels and MTHFR, MTR and MTRR gene polymorphisms as determinants for elevated total homocysteine concentrations in pregnant women. Eur J Clin Nutr. 2007, in press.26Lee et al. Tumor necrosis factor-alpha promoter -308 A/G polymorphism and rheumatoid arthritis susceptibility: a metaanalysis. J Rheumatol. 2007;34(1):43-9.27Alvarez V et al. Association between the TNFalpha-308 A/G polymorphism and the onset-age of Alzheimer disease. Am J Med Genet. 2002;114(5):574-7.28Witte JS et al. Relation between tumour necrosis factor polymorphism TNFalpha-308 and risk of asthma. Eur J Hum Genet. 2002;10(1):82-5.29Elahi MM et al. A variant of position -308 of the Tumour necrosis factor alpha gene promoter and the risk of coronary heart disease. Heart Lung Circ. 2007 Jun 18; [Epub ahead of print]30Frosst P et al. A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase. Nat Genet 1995; 10:111–113.31Jacques PF et al. Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homo-cysteine concentrations. Circulation 1996;93: 7–9.32Aviram M et al. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions: a possible peroxidative role for paraoxonase. J Clin Invest. 1998;101:1581-1590. 33Garin et al. Paraoxonase polymorphism Met-Leu54 is associated with modified serum concentrations of the enzyme. A possible link between the paraoxonase gene and increased risk of cardiovascular disease in diabetes. J Clin Invest. 1997;99(1):62-6.34Humbert R et al. The molecular basis of the human serum paraoxonase activity polymorphism. Nat Genet. 1993;3:73-76.35Robertson KS et al. Human paraoxonase gene cluster polymorphisms as predictors of coronary heart disease risk in the prospective Northwick Park Heart Study II. Biochim Biophys Acta 2003;1639(3):203-12.36Voetsch B et al. The Combined Effect of Paraoxonase Promoter and Coding Region Polymorphisms on the Risk of Arterial Ischemic Stroke Among Young Adults. Arch Neurol. 2004;61(3):351-356.37Ylitalo et al. Baroreflex sensitivity and variants of the renin-angiotensin system genes. J Am Coll Cardiol. 2000;35(1):194-200.38Hautanen A et al. Joint Effects of an Aldosterone Synthase (CYP11B2) Gene Polymorphism and Classic Risk Factors on Risk of Myo-cardial Infarction. Circulation 1999;100:2213. 39Benn M et al. Polymorphism in APOB Associated with Increased Low-Density Lipoprotein Levels in Both Genders in the General Population. J Clin Endocrinol Met 2005;90(10):5797-5803.40Talmud PJ et al. Apolipoprotein B gene variants are involved in the determination of serum cholesterol levels: a study in normo- and hyperlipidaemic individuals. Atherosclerosis 1987;67:81–89.41Law A et al. Common DNA polymorphism within coding sequence of apolipoprotein B gene associated with altered lipid levels. Lancet 1986;1:1301–1303.42Hegele RA et al. Apolipoprotein B-gene DNA polymorphisms associated with myocardial infarction. N Engl J Med 1986;315:1509–1515.43Bentzen J et al. Further studies of the influence of apolipoprotein B alleles on glucose and lipid metabolism. Hum Biol 2003;75(5):687-703.44Moreno-Luna R et al. Two independent apolipoprotein A5 haplotypes modulate postprandial lipoprotein metabolism in a healthy Caucasian population. J Clin Endocrinol Metab 2007;92(6):2280-5.


COMPANY ANd PeOPle

SCieNCe ANdPROdUCT

BUSiNeSSBUildiNg

Documents

article_assessing_genes_lifemap_system