Could you be “programmed” to fail when it comes to detoxifying?
The human body is exposed to a wide array of toxins such as toxic substances and heavy metals in one’s lifetime, and normally complex enzymatic mechanisms are “genetically” available to detoxify these substances, but for large percentages of society many people are genetically programmed without this ability leaving them in big trouble when it comes to detoxification.
A variety of mechanisms support or impair the body’s natural ability to detoxify and scientific literature suggests an association between impaired detoxification and certain diseases. Missing or non-functioning enzyme systems impair bio-transformation systems, consequently increasing the need for genetic testing, lifestyle changes, including the avoidance of certain toxins.
An individual’s ability to tolerate toxins depends on how quickly the body can eliminate the toxic burden, and this important biological detoxification mechanism depends on enzyme functions. The human body contains multiple enzyme systems involved in the detoxification process, but when one or more important enzymes are missing or the enzymes function improperly, the body’s ability to eliminate toxins is affected. This means normal detoxification is impaired.
Symptoms of genetic detoxification problems
The reality is, almost any illness or disease can be the result of a genetic detoxification problem, for the most part symptoms can be anything from mild persistent illness to the development of disease, here are only some of the signs & symptoms:
Metabolic disorders
Persistent nutritional problems (need for supplements)
Feeling unwell for a long time
Low immunity
Heavy metal toxicity & symptoms of heavy metal toxicity
Not responding to diets, exercise and nutrition
Weight problems
Metabolism problems
Allergies & sensitivities
Inability to cope physically & or mentally
Mental health problems
Genetic related illnesses (Diseases inherited from family)
Inability to overcome or recover properly form illnesses
What this means…
If a person is genetically challenged and is missing one or more enzyme systems, even a moderate exposure to metals can overwhelm the body, because the elimination process does not function properly. Heavy metal testing can often confirm if a person may have toxic overloads that could be coming from gene related enzyme deficiency.
Who has broken enzymes?
In the United States, case-control studies have reported that an important detoxification enzyme is missing in many of the worlds societies, here are some examples that show the enormity of the problem:
- 23%-41% for individuals of African descent
- 32%-53% for those of Asian descent
- 40%-53% for those of Hispanic descent
- 35%-62% for those of European descent.
Several population studies have reported the enzyme deletion among U.S. Caucasians as ranging from 48%-57%. Other countries have reported varying frequencies of the deletion polymorphism, and an Iranian study showed that in 31% to 38% of the population the GSTM1 enzyme was missing.
Groups such as Pacific Islanders and Malaysians have a reported frequency of 62%-100%. Other Asian populations have high-reported frequencies of the deletion genotype ranging from 48%-50% for Japanese and 35%-63% for the Chinese.
A population-based study conducted among Chinese reported a frequency of 51% for the GSTM1 deletion genotype. Two Korean case-control studies found frequencies of 53% and 56% for the GSTM1 deletion genotype.
People with the MTHFR gene mutation represent over 50% of the population.
People with methylation problems belong to the majority of those with gene related detoxification problems.
So on average 61% of the population is likely to have at least one genetically altered detoxification enzyme causing serious health problems that can be treated.
The above statistics demonstrate that missing enzyme systems are playing a large role in most populations. Genetic testing is relatively inexpensive and in most cases, needs to be done only once in a lifetime.
Are your enzymes working? Why test for genetic enzyme and detoxification problems?
When you have a genetic disability in terms of detoxification, you need to know what it is and then you need to provide the correct support your body needs to properly detoxify, failure to identify a gene alteration in enzymes results in toxicity which leads to disease and these diseases are often those associated with chronic illness and even premature death.
By understanding which gene enzymes are “broken” we can customize the right individual support process that can aid our body’s natural detoxification processes. When we know our individual genetic ‘disabilities’, we are in a better position to protect and support our detoxification system.
We are also then more aware of what measures we can take to prevent toxic overexposure which gives you a significant advantage in disease prevention. We can strengthen our detoxification ability by supporting and strengthening other enzyme systems that are working to make up for those that may not be working.
Also we may find that enzymes may be present, but not functioning properly. We can test if nutritional deficiencies are the cause of the enzyme dysfunction, by checking copper, zinc and manganese levels. Zinc and manganese deficiencies are not uncommon. While blood tests reveal acute and immediate deficiencies, this is not good enough, hair detects if the body has been chronically under supplied. If hair analysis results indicate a need for supplementation, it would be logical to supplement for a few weeks before genetic testing is attempted.
When we know that stage 2 enzyme systems are missing or non-functional, we need to support the body’s detoxification potential. Nearly 50% of the world population misses the GSTM1 enzyme. These people accumulate toxins more readily, simply because their body cannot properly detoxify.
When we know specifics about our individual detoxification potential, we will know how much outside support in the form of natural chelation treatment is needed to prevent our body from accumulating toxins. The sooner you act the better.
How to test for genetic enzyme problems
Genetic testing for detoxification enzymes is simple and inexpensive. Depending on your symptoms a simple test can be prescribed, it’s best to contact one our heath practitioners here for more information about your specific symptoms.
Test for MTHFR Gene mutation here.
Test for GSTM1 Gene mutation here.
Test for GSTT1 Gene mutation here.
See below for further gene tests available…
About detoxification enzymes
Detoxification enzymes are designed to help your body detoxify properly, so its important to know how they work and be able to identify if you may have a problem with one or more of the important detoxification enzymes. Detoxification happens in stages, lets take a look at each one here…
Stage 1 Enzymes
While much is known about the role of stage 1 enzymes in the metabolism and activation of environmental toxins, the role of stage1 detoxification in clinical practice has received less consideration than the stage 2 enzyme systems. Enzymes involved in the stage1 metabolism are Cytochrome P450, and the SOD Enzymes.
Cytochrome P450
The Cytochrome P450, specifically the CYT 450 1A1, these enzymes are involved in the metabolism of drugs or exogenous toxins such as chemical solvents or drugs, including steroids. The amount of the CYP enzymes present in the liver reflects their importance in the detoxification process.
Superoxide Dismutase (SOD)
The Superoxide Dismutase (SOD) Enzymes are present in practically all cells and in extracellular fluids. The SODs are considered free radical scavengers, preventing oxidative damage and thus are considered important to delay the aging process. Genetic polymorphism (changes) in SOD enzymes and their altered expressions and activities are associated with oxidative DNA damage and an increased cancer risk.
SOD enzymes contain metal cofactors, and the trace elements involved may be copper, zinc, manganese or iron. While all people have an abundance of SOD enzymes, deficiency in any of these metals will lower certain SOD levels and function. In other words, a nutritional deficiency in any of these trace elements potentially impairs SOD enzyme function, leading to a disruption in the detoxification pathway.
Superoxide Dismutase 1 (SOD1)
SOD1 is also called the copper/zinc superoxide dismutase or CuZnSOD. It is present in the cytosol, the nucleus and the mitochondria. Its primary function is to act as an antioxidant enzyme, lowering the steady-state concentration of superoxide. High concentrations are found in the liver, brain and testes, but also in red blood cells, pancreas and the lung. Inactivity of the SOD enzyme disturbs the cell metabolism.
SOD1 and amyotrophic lateral sclerosis: mutation and oligomerization (Oligomerization is a chemical process that links monomeric compounds (e.g., amino acids, nucleotides, or monosaccharides) to form dimers, trimers, tetramers, or longer chain molecules (oligomers). Complete loss of post translational modifications triggers fibrillar aggregation of SOD1 in familial form of ALS.
A copper or zinc deficiency reduces the function and activity of the SOD1 enzyme.
Superoxide Dismutase 2 (SOD2)
This gene, also called MnSOD, is a member of the iron/manganese superoxide dismutase family. Mutations in this gene have been associated with idiopathic cardiomyopathy, premature aging, sporadic motor neuron disease, and cancer.
SOD-Gene defects have been associated with diseases such as Amyotrophic lateral sclerosis (ALS) and neuro genetic disorders that can be tested for here.
Stage 1 Enzymes Summary
A reduced stage 1 enzyme metabolism reduces the detoxification ability of a variety of toxins including the potentially toxic metals.
Stage 2 Enzymes
Stage 2 enzyme reactions follow stage 1 reactions. Also known as conjugation reactions (with glutathione or amino acids or sulfonates), the stage 2 system is an important defense mechanism against intake of toxins. The glutathione transferases and NAcetyltransferase 2 (NAT2) belong to the group of stage 2 Enzymes.
A reduced stage 2 detoxification leads to the accumulation of toxins. Gene variants in the glutathione S-transferases (GST) may lead to poor management of the extremely radical intermediates from the Phase 1 responses and thereby transmit a predisposition for diseases associated with oxidative stress.
Glutathione S-Transferases
The glutathione S-transferases (GSTM1, GSTT1, etc.) are one family of enzymes responsible for the detoxification process, particularly mercury and other toxic metal compounds. These enzymes are known to play a role in the detoxification of polycyclic aromatic hydrocarbons found in tobacco smoke.
Glutathione S-Transferase M1 (GSTM1) GSTM1 is produced in the liver. Through conjugation with glutathione, it functions in the detoxification of environmental toxins and products of oxidative stress, electrophilic compounds, including carcinogens and therapeutic drugs.
Individuals with the GSTM1 Genotype do not have this functioning enzymes and are at greater risk to develop carcinomas. Glutathione S-Transferase T1 or GSTT1 is found in lymphocytes and the liver, and is involved in the detoxification process of a variety of environmental chemicals such as the ones used in polymer productions. Like all GST enzymes, GSTT1 detoxifies cancer-causing chemicals as found in cigarette smoke.
Approximately 38% of Caucasians show a complete lack of GSTT1 activity. Individuals with the GSTT1 Genotype show a high risk for carcinoma of the lung, breast and larynx.
Click here to test for GSTM1 enzyme deficiency.
Click here to test for the GSTT1 enzyme deficiency.
Glutathione S-Transferase P1
Glutathione S-Transferase P1 (GSTP1) or GSTP1 is produced in blood lymphocytes and tissues such as prostate, lung, breast and brain. It plays an important role in detoxification by catalyzing the conjugation of many compounds with reduced glutathione. About 50% of the Caucasian population shows complete loss of function, which aids the accumulation of reactive products, increasing the risk of cancer and neurological diseases.
N-Acetyltransferase 2 (NAT2)
NAT2 functions to both activate and deactivate arylamine and hydrazine drugs and carcinogens. Polymorphisms in this gene are responsible for the N-acetylation process in which humans are segregated into rapid, intermediate or slow acetylator phenotypes. Lack of NAT2 function is associated with higher incidences of cancer and drug toxicity. Rapid acetylators have a higher risk for colorectal cancer.
Apolipoprotein E (Apo E)
Apolipoprotein E is essential for the metabolism of triglyceride-rich lipoprotein constituents, having been recognized for its importance in lipoprotein metabolism and cardiovascular disease as well as the removal of mercury, lead and other thiol-reactive toxins.
The relationship of Apolipoprotein E to the toxic effects of mercury to exacerbation of the medical condition classified as Alzheimer’s disease, lead exposure and neurobehavioral function.
Stage 2 Enzymes Summary
A reduced stage 2 enzyme metabolism reduces the detoxification ability of a variety of toxins including the potentially toxic metals and significant findings associated to common diseases found in society.
Have any questions about genetic testing? Ask one of our qualified health practitioners here.