DNA Adducts: Blood Test Results

Disclaimer & Warning

The information presented on this page is for educational and informational purposes only. It reflects findings from our sound research and independent laboratory analyses, but is not intended to provide medical advice, diagnosis, or treatment. The content should not be used as a substitute for professional healthcare guidance, nor do we recommend self-diagnosis or self-treatment based on this information.

If you are experiencing symptoms, have existing health concerns, are pregnant, or are in poor health, you should consult a qualified doctor or healthcare practitioner for appropriate evaluation and care. We expressly disclaim responsibility for any adverse effects, misuse, or misinterpretation of the information provided. 

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MyReset and DNA Adducts

The myReset sound method may support the body’s natural detoxification processes by reducing the burden of DNA adduct formation. DNA adducts occur when toxins bind directly to DNA, compromising its structure and repair capacity. By applying specific sound frequencies, it is possible to influence cellular resonance and energy balance, which can enhance the body’s ability to clear or repair adducts. The reductions observed in adduct levels suggest that sound may play a role in restoring DNA stability and genomic resilience, key foundations for long-term cellular health.

 

Results of DNA Adduct Analysis by Toxin

The following section summarises the DNA adducts detected in relation to specific toxins. Each toxin is listed with the gene or genomic region affected, followed by a more detailed discussion below on its biological impact, potential health consequences, and broader implications.

Toxins Identified:

• Lindane - PPARG (3p25 #2)
• Benzoquinone - Acyl-CoA dehydrogenase #2
• Nitrosamine - IL6 (7p21 #4)
• Hippuric Acid - Non-gene regions (q5, q8)
• Mercury - Glutathione synthetase (20q11 #5)

 

Lindane and Its Biological Impact

Lindane (γ-hexachlorocyclohexane, γ-HCH) is an organochlorine pesticide that was widely used in agriculture and in topical pharmaceuticals for lice and scabies before being banned or severely restricted in most countries due to its toxicity and persistence in the environment. It is lipophilic, meaning it accumulates in fatty tissues, and has a long half-life in the human body. Lindane exposure can occur through ingestion of contaminated food and water, inhalation of pesticide residues, or dermal absorption from past medical or agricultural use.

Once in the body, lindane acts as a neurotoxin by interfering with the normal function of GABA (gamma-aminobutyric acid) receptors in the brain, reducing inhibitory signalling and potentially leading to hyperexcitability, seizures, dizziness, headaches, and other neurological effects. It is also recognised as an endocrine disruptor, capable of interfering with hormone signalling pathways, particularly those involving steroid hormones. Chronic exposure has been linked to immune suppression, reproductive issues, and possible carcinogenic effects. The International Agency for Research on Cancer (IARC) classifies lindane as carcinogenic to humans (Group 1), based on evidence of increased risk of non-Hodgkin lymphoma in exposed populations.

DNA Adduct Formation and Gene Implications 

The detection of lindane as a DNA adduct indicates that the compound, or its reactive metabolites, has bound covalently to DNA, potentially altering the structure and function of specific genes. DNA adducts are recognised biomarkers of genotoxic exposure and may contribute to mutations if not properly repaired. The presence of a lindane adduct on the PPARG gene (which encodes the nuclear receptor protein PPARγ), located at chromosome 3p25 #2, carries important implications.

PPARγ, the protein product of PPARG, plays a central role in regulating glucose metabolism, lipid storage, adipocyte differentiation, and insulin sensitivity. It is also involved in inflammatory pathways and cell cycle regulation. A disruption of this gene through chemical adduction could compromise its ability to regulate metabolic balance, thereby contributing to insulin resistance, obesity, dyslipidaemia, and chronic low-grade inflammation. Since PPARγ also has protective roles in controlling oxidative stress and suppressing tumour growth in certain tissues, damage to the underlying PPARG gene raises concern about long-term metabolic dysfunction and increased oncogenic risk..

Broader Implications

The identification of Lindane adducts on PPARG underscores how persistent environmental toxins can intersect with genetic regulation, particularly at genes critical for metabolism and immune function. Such findings emphasise the importance of biomonitoring chemical exposures, supporting detoxification pathways, and implementing early interventions to mitigate downstream health consequences such as metabolic syndrome, immune dysregulation, and cancer risk.

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Benzoquinone and Its Biological Impact

Benzoquinone is a highly reactive aromatic compound that exists in several forms, the most common being para-benzoquinone (p-benzoquinone). It is a toxic metabolite produced during the breakdown of benzene, a well-known environmental and occupational pollutant. Benzoquinone is used industrially in the manufacture of dyes, fungicides, and photographic chemicals, but the main route of human exposure comes from benzene-containing products, including fuels, cigarette smoke, and industrial solvents.

Because of its high reactivity, benzoquinone can readily bind to cellular macromolecules such as proteins, lipids, and DNA. This binding leads to oxidative stress, disruption of mitochondrial function, and direct genotoxic effects. Occupational exposure is associated with bone marrow suppression, immune dysfunction, and increased risk of leukaemia. The International Agency for Research on Cancer (IARC) recognises benzene, and by extension its reactive metabolites such as benzoquinone, as carcinogenic to humans (Group 1).

DNA Adduct Formation and Gene Implications

The detection of benzoquinone as a DNA adduct demonstrates that the compound has formed a covalent bond with DNA, potentially impairing the integrity and function of critical genes. DNA adducts are well-established biomarkers of genotoxic stress, and if not adequately repaired, they can lead to mutations and disruption of normal cellular function. Of particular importance is the identification of a benzoquinone adduct on the Acyl-CoA dehydrogenase #2 gene, a gene essential for mitochondrial energy metabolism.

Acyl-CoA dehydrogenase #2 is a key enzyme in the β-oxidation of fatty acids, the pathway by which long-chain fatty acids are converted into acetyl-CoA to generate ATP. Damage to this gene through chemical adduction compromises fatty acid metabolism, reducing the cell’s ability to produce adequate energy. Clinically, this disruption may manifest as chronic fatigue, muscle weakness, reduced exercise tolerance, and metabolic instability. In children or developing individuals, insufficient energy supply can also contribute to growth delays, since anabolic processes rely heavily on energy availability.

Broader Implications

The presence of benzoquinone adducts on Acyl-CoA dehydrogenase #2 illustrates how environmental toxins can interfere directly with mitochondrial energy pathways at the genetic level. When fatty acid oxidation is impaired, the consequences extend beyond fatigue and developmental delays to include hypoglycaemia, accumulation of toxic fatty acid intermediates, and increased oxidative stress. These findings highlight the need for stringent control of benzene exposure, targeted biomonitoring of susceptible individuals, and interventions that support mitochondrial health and detoxification. By identifying and addressing such disruptions early, it may be possible to mitigate long-term metabolic consequences and reduce the burden of toxin-associated disease.

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Nitrosamines and Their Biological Impact

Nitrosamines are a family of highly reactive, carcinogenic compounds formed when amines (from proteins or preservatives) react with nitrites under acidic or high-heat conditions. They are most commonly encountered in tobacco smoke, processed meats (such as bacon, sausages, and cured products), contaminated water, and certain industrial processes. Nitrosamines can also form endogenously in the stomach when dietary nitrates and nitrites are present.

Once in the body, nitrosamines are metabolised to reactive intermediates capable of damaging DNA, proteins, and lipids. They are known to form DNA adducts, leading to mutations if not properly repaired, and have been strongly associated with cancers of the oesophagus, stomach, liver, and other organs. The International Agency for Research on Cancer (IARC) classifies many nitrosamines as carcinogenic to humans (Group 1).

DNA Adduct Formation and Gene Implications

The detection of nitrosamine as a DNA adduct indicates covalent binding to DNA bases, potentially altering the expression and regulation of affected genes. DNA adducts are considered reliable biomarkers of genotoxic exposure and play a direct role in carcinogenesis. Of particular significance is the identification of a nitrosamine adduct on the IL6 gene (Interleukin-6), located at chromosome 7p21 #4.

IL-6 is a multifunctional cytokine that plays critical roles in immune signalling, inflammation, and metabolic regulation. It influences glucose homeostasis, lipid metabolism, and muscle protein turnover. Persistent upregulation of IL-6 is linked to chronic inflammation, muscle wasting, fatigue, and impaired growth. Conversely, disruption or dysregulation of IL-6 signalling caused by DNA adduct formation may contribute to an imbalanced immune response, oxidative stress, and altered energy allocation. This can manifest clinically as persistent fatigue, reduced growth potential, and susceptibility to metabolic dysfunction.

Broader Implications

The presence of nitrosamine adducts on IL6 highlights how environmental and dietary toxins can interfere with genes at the crossroads of inflammation, metabolism, and development. Such interference may reduce energy availability for normal growth and repair, while promoting chronic fatigue through sustained inflammatory signalling. Over time, these disruptions may contribute to growth delays in children, impaired recovery in adults, and heightened risk of chronic disease.

This finding underscores the importance of minimising nitrosamine exposure through dietary choices, smoking avoidance, and water safety monitoring. It also suggests a need for strategies that reduce inflammation and support immune resilience in individuals with evidence of DNA adduct formation on immune-related genes such as IL6.

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Hippuric Acid and Its Biological Impact

Hippuric acid (benzoylglycine) is an endogenous compound formed in the liver when benzoic acid (derived from food additives, polyphenol-rich foods, or environmental exposures such as toluene) is conjugated with the amino acid glycine and subsequently excreted in urine. Under normal circumstances, hippuric acid is a benign detoxification product and is considered a marker of exposure rather than a direct toxin. Elevated levels, however, are often associated with environmental solvent exposure (notably toluene), heavy intake of processed foods, or increased microbial production in the gut.

While hippuric acid itself is less acutely toxic than compounds such as nitrosamines or benzoquinone, its persistence at high levels may reflect underlying toxic burden or metabolic stress. In occupational medicine, urinary hippuric acid is used as a biomarker of solvent exposure, but its role in DNA adduction is less well studied, making recent findings of particular interest.

DNA Adduct Formation and Non-Gene Implications

The identification of hippuric acid adducts in non-gene regions (q5 and q8) suggests that even compounds traditionally considered “detoxification byproducts” can interact covalently with DNA. Unlike adducts formed on coding genes, adducts in non-coding or intergenic regions may not directly alter protein expression. However, these regions are increasingly recognised as regulatory landscapes, containing enhancers, silencers, and structural DNA elements critical for gene expression control and chromatin organisation.

Adduct formation at q5 and q8 could therefore interfere with gene regulation, DNA replication timing, or chromatin stability, leading to subtle but significant downstream effects. Disruption in these areas may not cause immediate gene silencing or mutation but can contribute to epigenetic dysregulation, increasing the susceptibility of nearby genes to mis-expression or instability over time.

Broader Implications

The discovery of hippuric acid adducts in non-gene regions highlights an often-overlooked mechanism by which seemingly minor metabolites can influence health. While not directly mutagenic in the way carcinogenic adducts are, such findings suggest a background level of genomic “noise” caused by environmental or metabolic byproducts. Over time, this may contribute to fatigue, reduced cellular efficiency, and developmental delays, especially when combined with other toxic exposures.

These results stress the importance of not overlooking low-level metabolites in toxicology. Even compounds like hippuric acid, generally considered markers of exposure rather than active toxins, may play a subtle role in genomic instability and regulatory disruption when adducted to DNA. Monitoring these findings, alongside more classically toxic compounds, may offer a more complete picture of environmental and metabolic stress on the genome.

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Mercury and Its Biological Impact

Mercury is a heavy metal with no known beneficial role in human physiology and is well recognised for its toxicological effects. It exists in several forms - elemental, inorganic, and organic (such as methylmercury) - each with distinct exposure routes and health risks. Major sources of exposure include contaminated fish and seafood, dental amalgams, industrial emissions, artisanal gold mining, and certain medical or cosmetic products. Mercury is persistent in the environment and bioaccumulates in the food chain, particularly in predatory fish.

Once absorbed, mercury readily crosses biological membranes, including the blood–brain barrier and placenta, and accumulates in tissues such as the brain, kidneys, and liver. Its primary mechanisms of toxicity involve binding to thiol (-SH) groups, disrupting the structure and function of proteins and enzymes, and inducing oxidative stress. Mercury exposure has been associated with neurological impairment, immune dysfunction, cardiovascular risk, and developmental delays. The International Agency for Research on Cancer (IARC) has classified methylmercury compounds as possibly carcinogenic to humans (Group 2B).

DNA Adduct Formation and Gene Implications

The detection of mercury as a DNA adduct demonstrates that reactive mercury species can covalently bind to DNA, leading to structural modifications and potential disruption of gene function. DNA adducts are biomarkers of genotoxic exposure and, if not repaired, can contribute to mutations or impaired gene expression. The presence of a mercury adduct on the Glutathione synthetase (GSS) gene, located at chromosome 20q11 #5, is especially significant.

GSS encodes a key enzyme in the synthesis of glutathione (GSH), the body’s most abundant intracellular antioxidant and a critical detoxification molecule. Glutathione plays a central role in neutralising reactive oxygen species, maintaining redox balance, and facilitating the elimination of toxins, including mercury itself. If mercury adducts impair the integrity or expression of the GSS gene, the result may be reduced glutathione synthesis. This would diminish the body’s detoxification capacity, amplify oxidative stress, and exacerbate mercury’s toxic effects in a vicious cycle. Clinically, this could manifest as fatigue, impaired immune resilience, slowed recovery, and developmental delays due to reduced protection against oxidative and toxic insults.

Broader Implications

The identification of mercury adducts on GSS illustrates how toxic metals can directly undermine the very systems responsible for neutralising them. By compromising glutathione synthesis, mercury not only exerts direct toxicity but also weakens one of the body’s primary defence mechanisms, leaving cells vulnerable to ongoing oxidative stress and toxin accumulation. This dual impact helps explain the persistent fatigue, immune dysfunction, and growth or developmental challenges often observed in mercury-exposed individuals.

These findings emphasise the critical need for monitoring heavy metal exposure, supporting glutathione pathways through nutrition and supplementation, and implementing strategies for safe detoxification. Protecting the integrity of genes like GSS is essential for maintaining resilience against both mercury and other environmental toxicants.