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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”).
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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. SNP
The reason we are different is that VArIATIONS
our genes are different.”
“For optimal function we each have
unique nutritional needs and specific
environmental requirements.”
Biochemical Individuality: Roger J. Williams, Ph.D.
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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.
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Why Testing Our Genes Is So Important
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.
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Understanding Your LifeMap™
Healthy Aging DNA Assessment
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.
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Understanding Your Healthy Aging DNA Assessment
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
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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
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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
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Thakkinstan A et al. Meta-analysis of molecular association studies: vitamin D receptor gene polymorphisms and BMD as a case
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Hu 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
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Ratnasinghe D et al. Glutathione peroxidase codon 198 polymorphism variant increases lung cancer risk. Cancer Res 2000 Nov
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19
Dörr S et al. Association of a specific haplotype across the genes MMP1 and MMP3 with radiographic joint destruction in rheuma-
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Understanding Your Healthy Aging DNA Assessment
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Hankey G et al. Homocysteine and Vascular Disease. Lancet 1999;354 (9176): 407-413.
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Gaughan 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.
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Guéant-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.
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Barbosa PR et al. Association between decreased vitamin levels and MTHFR, MTR and MTRR gene polymorphisms as determinants
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Lee et al. Tumor necrosis factor-alpha promoter -308 A/G polymorphism and rheumatoid arthritis susceptibility: a metaanalysis.
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Humbert R et al. The molecular basis of the human serum paraoxonase activity polymorphism. Nat Genet. 1993;3:73-76.
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Voetsch B et al. The Combined Effect of Paraoxonase Promoter and Coding Region Polymorphisms on the Risk of Arterial Ischemic
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Ylitalo et al. Baroreflex sensitivity and variants of the renin-angiotensin system genes. J Am Coll Cardiol. 2000;35(1):194-200.
38
Hautanen A et al. Joint Effects of an Aldosterone Synthase (CYP11B2) Gene Polymorphism and Classic Risk Factors on Risk of Myo-
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39
Benn 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.
40
Talmud 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.
41
Law A et al. Common DNA polymorphism within coding sequence of apolipoprotein B gene associated with altered lipid levels.
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42
Hegele RA et al. Apolipoprotein B-gene DNA polymorphisms associated with myocardial infarction. N Engl J Med
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43
Bentzen J et al. Further studies of the influence of apolipoprotein B alleles on glucose and lipid metabolism. Hum Biol
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44
Moreno-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.
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