Is It Really Genetic?

One of the most deeply entrenched medical/scientific beliefs, is that which suggests that your DNA is like a blueprint with your destiny written into it. As far as metabolic health goes however, there is a lot of good science showing that stress plays a more important role than many think.

When it comes to deciding what causes diseases like cancer, heart disease or diabetes, the experts seem to be caught somewhere between, ‘it’s your genes’, and ‘it’s something you did or ate, or didn’t do or didn’t eat’. And in case you aren’t confused enough, the gene mutations that they say drive disease, apparently occur, largely because of random copying errors. Just to add insult to injury, they can’t really say which genes are supposed to cause what.

“…since core genes are hugely outnumbered by peripheral genes, a large fraction of the total genetic contribution to disease comes from peripheral genes that do not play direct roles in disease…we propose that disease risk is largely driven by genes with no direct relevance to disease, and propagated through regulatory networks to a much smaller number of core genes with direct effects.”

Personally, I think blaming genes is very convenient. It allows doctors to be able to avoid taking responsibility for not being able to help patients figure out what to do, and in many cases, it gives them an excuse for bad treatment outcomes. It also gives government bodies and big industries, justification for the continued profit from ineffective and sometimes dangerous products.

What the medical world rarely seems to acknowledge however, is the large body of scientific evidence, showing the things that interfere with proper metabolic function, that are known to promote cellular dysfunction and disease, and that consistently cause damage to, mutate, or vary the expression of genes.

It’s one thing to say that genetics plays a role in the development and progression of disease states, but it’s an altogether different thing to ignore the factors that determine the influence genes might have, and that can promote or protect against illness, regardless of what is written in the blueprint. All of these things fall under the umbrella of metabolism and stress.

I’m not saying that genetics is irrelevant, but I think a better way to look at disease, is to see the ways that things that promote biological stress and interfere with metabolic function – things like chronic inflammation, sugar restriction, rising exposure to stress substances like estrogen, nitric oxide, endotoxin, and polyunsaturated fats (PUFAs) – have been shown to increase illness, and have a damaging impact upon genes.

The fact that genes are involved does not necessarily mean, that it’s the genes that are driving disease. For one thing, evidence has shown that the effects of stress can impact upon the health of future generations without a genetic change, people recover from illnesses in spite of genetic change, and many do not get sick, even in the face of genetic change.

But when you look at the things that interfere with metabolism and promote stress, you’ll find that there are good explanations for susceptibility to disease (irrespective of what the genes say), and things can really start to make practical sense. Take inflammation for example.

Chronic inflammation is well known to exist as a result of ongoing exposure to stress, and to cause further interference with metabolic function, which can then be something which promotes more inflammation, as well as disease. Inflammation is something which has been shown to be genotoxic and mutagenic.

“…when inflammation persists, the resultant state of chronic inflammation may have a number of secondary consequences associated with increased risk of chronic disease. Among these is an increased rate of mutation…the Inflammatory bowel diseases, Crohn’s disease and ulcerative colitis are associated with enhanced levels of chronic inflammation, and show evidence of enhanced levels of genetic damage…”

“…sustained inflammation may elicit the stem cell insult by inducing a state of chronic oxidative stress…thereby creating a high-risk microenvironment for induction of mutations due to the persistent inflammation-induced oxidative damage to DNA… “

“Nitrative and oxidative DNA lesions with mutagenic properties are formed in various types of inflammation-related cancer tissues….a mechanism for the generation of cancer stem cells by inflammation…Chronic inflammation by infectious agents, inflammatory diseases, and other factors causes various types of damage to nucleic acids, proteins, tissue…Tissue injury under chronic inflammation may activate progenitor/stem cells for regeneration…inflammation can cause multiple mutations, which may generate mutant stem cells and cancer stem cells, leading to carcinogenesis.”

Low level maternal inflammation during pregnancy has an impact upon physiological function (including genes), and when this increases serotonin production, it has the potential to impair fetal brain development. You could say this is a genetic issue, but it probably makes more sense to say that it is an inflammatory stress related metabolic issue.

“…mild maternal inflammation induces a cascade of genetic and enzymatic changes within the placenta that result in increased 5-HT [serotonin] output to the fetus…it appears that prenatal inflammation can lead to increased anxiety and depression-like behaviors in the offspring, behaviors that are influenced by serotonergic function…”

One argument is that it is genetics in the first place, that determines the inflammatory response a person will have when exposed to stress. But there are many things that promote inflammation (and at the same time have an impact upon genes), that can be easily avoided. It’s just as easy to argue that it is these things that are of most significance, and in fact, more and more experimental evidence is backing this hypothesis up.

When stress and chronic inflammation interferes with metabolism, one of the things that is known to happen is that digestive function is impeded, and bacteria are more able to grow in number and move further up the intestines, promoting greater interference. Bacteria and the toxic byproducts of bacteria, are known to directly interfere with metabolism, and cause inflammation and disease. They’ve also been shown to have an impact upon the genes.

“More and more convincing data link bacteria to the development of cancers. How bacteria act as mutagens by altering host genomes…H. pylori is a major risk factor for gastric cancer development. Its oncogenic role is mediated by the chronic active inflammation it elicits in the gastric mucosa…Recent findings on its mutagenic effects at the nuclear and mitochondrial genome and related DNA damage…”

“Previous studies indicate that the co-localization of pro-inflammatory LPS [bacterial endotoxin] with AD [alzheimer’s disease]-affected brain cell nuclei suggests that there may be a contribution of this neurotoxin to genotoxic events that support inflammatory neurodegeneration and failure in homeostatic gene expression.”

“A total of 514 genes was greater than 1.5-fold differentially expressed in the LPS induced lung inflammation model. 394 of the 514 were up regulated genes mostly involved in cell cycle and immune/inflammation related processes, such as cytokine/chemokine activity and signalling…it is the extent of the immune response which drives genetic instability in the inflamed lung.”

Stress and metabolic suppression promote disease, and changing bacterial numbers and composition are known to play a significant part. Dietary, and other environmental changes (more so than genetics) directly impact upon bacterial conditions.

“…this study provides a cautionary note for ongoing efforts to link host genetics to the composition and function of the human gut microbiota. Perhaps more so than any other complex trait, the gut microbiota is shaped by a wide range of environmental factors, including diet…”

Inflammation, stress and increased exposure to bacteria (and the toxic byproducts of bacteria), interferes with thyroid energy metabolism, promoting the release of defensive stress substances such as nitric oxide and estrogen.

Systemic and chronically raised levels of these stress related substances, further suppress energy metabolism and encourage inflammatory, disease promoting conditions. They have also been demonstrated to be responsible for genetic and epigenetic changes which have been said to promote increased disease susceptibility.

“At low levels, nitric oxide (NO) is a signaling molecule required for many physiological functions. However, when produced in excessive amounts, for example, by inflammatory cells, it can cause cell death and mutagenicity…Overproduction…under pathological conditions such as inflammation…increases levels of mutation and carcinogenesis…exposure to NO induces cytotoxicity and mutagenicity in target cells and…inhibition of NO production…is effective at abrogating these properties…”

“…the accumulation of DNA lesions during NO stress may be in part attributed to the inhibition of DNA repair enzymes by NO…Thus, continuous genomic insults due to NO production may have negative effects on genome stability promoting tumor progression.”

“…evidence supports a dual role of estrogen in carcinogenesis as a hormone stimulating cell proliferation and as a procarcinogen inducing genetic damage…Several types of direct and indirect free radical-mediated DNA damage are induced by E2…E2…induces various chromosomal and genetic lesions…and gene mutations…”

“Here we report that estrogen and estrogen metabolites can cause DNA double strand breaks (DSB) in estrogen receptor-α negative breast cells…findings suggest that exposure to estrogen…is capable of driving genomic instability, a well-defined early event in breast cancer development.”

Rising levels of estrogen due to stress, have been shown in numerous different ways to promote mood dysregulation. Excess estrogen can also impact upon the expression of genes, in a manner which is said to increase the likelihood of suffering from stress-induced psychiatric disorders, such as depression and PTSD.

“…evidence for direct estrogenic regulation of CRF gene expression provides a compelling mechanism for sexual dimorphism of stress reactivity and prevalence of stress-related psychopathology in women.”

Ongoing exposure to high amounts of stress, without sufficient energy availability, promotes the release of fat out of storage as an alternative fuel source. Increased use of fat for fuel further suppresses metabolic function, and particularly when the fat composition is made up more of PUFAs, promotes systemic and chronic inflammation and stress.

The breakdown products of PUFAs, such as malondialdehyde and 4-HNE, have been shown to be a significant cause of oxidative stress and inflammatory disease, as well as damage to DNA.

“Malondialdehyde (MDA) is an endogenous genotoxic product of enzymatic and oxygen radical-induced lipid peroxidation…MDA induced up to a 15-fold increase in mutation frequency in the supF reporter gene compared with untreated DNA…biological and biochemical evidence for the existence of MDA-induced DNA interstrand cross-links that could result from endogenous oxidative stress and likely have potent biological effects.”

“When oxidant compounds target lipids, they can initiate the lipid peroxidation process, a chain reaction that produces multiple breakdown molecules, such as MDA and 4-HNE…proteins and DNA are particularly susceptible to modification caused by these aldehydes. MDA and 4-HNE…may induce profound alteration in the biochemical properties of biomolecules, which may facilitate development of various pathological states…”

“Oxygen radicals react with polyunsaturated fatty acid…resulting in the production of…products, many of them reactive toward protein and DNA..One of the most abundant carbonyl products of lipid peroxidation is malondialdehyde (MDA)…also…generated as a side-product of prostaglandin biosynthesis…Lipid peroxidation appears to be a major source of endogenous DNA damage in humans that may contribute significantly to cancer and other genetic diseases…”

“During chronic inflammatory processes an excess of free radicals and DNA-reactive aldehydes from lipid peroxidation (LPO) are produced, which deregulate cellular homeostasis and can drive normal cells to malignancy. Etheno (epsilon)-modified DNA bases are generated by reactions of DNA with a major LPO product, trans-4-hydroxy-2-nonenal…Excess storage of copper/iron causing oxidative stress and LPO-derived DNA-damage, are implicated in disease pathogenesis…”

PUFAs promote inflammation, and directly interfere with digestive function, encouraging bacterial overgrowth. More PUFAs, slower digestion, and increased bacterial issues, promote nitric oxide, estrogen, serotonin production, and other stress related things. All of the above can interfere with liver function, allowing for inflammatory substances to circulate throughout the main system in greater amounts. Systemic inflammation causes more stress, and further interferes with metabolism, increasing levels of all of the above stressful things, including levels of PUFAs in circulation. This can become a vicious circle of inflammation and disease promotion, and each element of the above story can effect the genes.

Excessive exposure to the breakdown products of PUFAs, interfere with the ability of the cell to use sugar for energy, increasing stress and inflammation, potentially promoting chronic hyperglycemia and diabetes. Hyperglycemia has been shown to cause gene mutations.

“…the present study provides the first and direct evidence for HG [high glucose]-induced gene mutations, which provides novel insight into understanding the mechanism of cancer risk in diabetes mellitus.”

Sugar restriction directly interferes with energy metabolism, increasing exposure to the substances of stress and promoting the release of PUFAs into circulation. In this sense (and in other ways) it can be argued that insufficient intake or availability of sugar is anti-metabolic, can encourage inflammation and disease, and can (at least indirectly) impact upon genes.

Sugar promotes cholesterol production, and by increasing metabolic function, sugar also improves cholesterol conversion into the anti-aging anti-inflammatory hormones (pregnenolone and progesterone etc.). Slow metabolism, as well as interaction between cholesterol and PUFAs, has been shown to damage or promote oxidation of cholesterol. Oxidized cholesterol is involved in the progression of disease, including heart disease and alzheimer’s, and is another factor which has been shown to damage genes.

“The presence of unsaturated fatty acids (linoleic and oleic acids) significantly increased the amount of COPs [cholesterol oxidation products]…COPs are considered to be cytotoxic, mutagenic, and carcinogenic…”

The truth is there is plenty of high quality science demonstrating the ways that stress impacts upon metabolic energy system function, and upon genes and their expression. It is not a stretch to argue that it is metabolic interference as a whole that is powerfully deterministic when it comes to disease potential.

“Our findings provide a hitherto-undescribed direct role of increased aerobic glycolysis in inducing the cancer phenotype, in which increased glycolytic activity regulates the canonical oncogenic pathways dynamically and reciprocally…These results may provide additional evidence for how hyperglycemia in diseases such as obesity and diabetes could provide a microenvironment that results in higher risk of some cancers”

“Our results clearly show that most of the glycolysis pathway genes are upregulated…in response to mitochondrial stress…MtRS [mitochondrial retrograde signaling pathway] induces tumor growth independent of HIF-1α pathway…”

“Aberrant DNA methylation has been implicated in the etiology of various mental disorders including, depression, psychotic disorders, post-traumatic stress disorder, autism, eating disorders and substance dependence, but also has an important role in the pathology of physical illnesses, such as cancer…We found that psychosocial experiences are linked to immediate epigenetic modifications in a sample of subjects with early adverse experiences.

“Based on the results and trends of this study, we propose a generalized epigenetic mechanism behind the development of ASD-like characteristics in embryos…exposed to prenatal stress. Since all the embryos were genetically equivalent, all embryonic changes that occur are likely a result of maternal effect stemming from maternal SERT genotype and maternal stress…”

I don’t think the big question is, ‘What role do genes play in the development of disease?’ Rather, I think it makes more sense to understand, how much disease susceptibility is influenced by exposure to stress and it’s impact upon metabolism. Is it really that useful focusing on genetic correlation?

The popular claim goes a bit like this. You inherit a genetic blueprint which determines the diseases you are likely going to get. Random mutations gradually change the blueprint, and the environment can switch genes on and off, but it is the genes that are ultimately in charge. Once it is determined which genes cause what, you will need only go get a reading, then choose a specific course of action, or resign yourself to a predetermined outcome. So far this has not proven accurate, and completely disregards a whole field of science relating to stress, metabolism and disease.

Not only are there specific dietary and lifestyle factors that impact upon genes and significantly increase disease risk, there are also things that can damage or improve health without altering DNA. Is it genes that are responsible?

“…a common soy isoflavone, at dietary concentrations, can influence expression of BRF2 and BRF1… The response may involve an epigenetic component…BRF2 can be oncogenic and prognostic of poor survival.”

“…these age-associated phenotypes found in elderly fibroblasts are regulated reversibly and are similar to differentiation phenotypes in that both are controlled by epigenetic regulation, not by mutations in either nuclear or mtDNA…continuous glycine treatment restored respiration defects in elderly human fibroblasts…”

“…a variety of genetically stable cell types, among which are tumor-associated fibroblasts, endothelial cells, as well as innate and adaptive immune system components, are known to undergo characteristic phenotypic changes as a consequence of residing in the vicinity of a growing tumor…the conditions within the tumor microenvironment have profound effects on the metabolism of a cancer cell.”

Exposure to stress has been shown to be able to promote epigenetic changes which can last for many generations, and increased susceptibility to disease (from exposure to metabolic stress), can be inherited via non-genetic means.

“Stress-induced epigenetic changes in the germ line can be inherited and can have a profound impact on offspring development…DNA methylation, small regulatory RNAs, and histone modifications have been implicated as carriers of epigenetic information across generations.”

“Environmental change can critically affect the lifestyle, reproductive success, and life span of adult animals and their [offspring] for generations…a temperature-induced change in expression…can endure for at least 14 generations…Long-lasting epigenetic memory of environmental change is therefore possible…”

“Multigenerational non-genetic inheritance is often interpreted as the transmission of epigenetic marks, such as DNA methylation…However, information can be carried across generations by a large number of bioactive substances, including hormones, cytokines, and even microorganisms…”

Just imagine what a lifetime of exposure to PUFAs and other stressful things (which can create a cocktail of rising levels of inflammation promoting substances like endotoxin, estrogen, nitric oxide, cortisol, serotonin etc.) can do to the function of metabolism and the risk of disease. And then when it finally happens, they’ll tell you it’s genetic. What they often mean when they say that, is that you were destined to get sick, and that it had nothing to do with anything they told you to do, or not to do.

I’m not a biologist, or a doctor, and I’m not anti-science, but I’m yet to see the value in labeling any health issue genetic, at least not for the patient. Even if there were such a thing as a purely genetic disease, this information makes not one iota of difference, especially when it comes to metabolic approaches to treatment.

A diet avoiding PUFAs and other inflammatory things, with enough protein from milk, cheese and gelatin, and plenty of sugar from sweet fruits, fruit juice, white sugar and honey, is one way to promote metabolic function and protect against any potentially disease promoting effects of your particular genome.

Some other things which can impact upon genes include radiation, carbon monoxide, iron and some other heavy metals, BPA and other estrogenic substances, as well as breakdown products of fish oil such as acrolein, 4-oxo-2-nonenal (4-ONE), 4-hydroxy-hexenal (4-HHE), and crotonaldehyde.

The diseases of stress and aging (cancer, heart disease, stroke, diabetes etc.) are being seen at a rapidly rising rate in younger age groups, for reasons that appear to have more to do with environmental changes, than random genetic mutation.

“…age-specific risk of a CRC [colorectal cancer] diagnosis…escalated back to the level of those born in the late 1800s for current birth cohorts…the proportion of rectal cancer diagnosed in adults younger than age 55 years years has doubled in just two decades…”

“…incidences of both type 1 and type 2 diabetes among youths increased significantly in the 2002-2012 period, particularly among youths of minority racial and ethnic groups.”

“Hospitalization rates for acute ischemic stroke in younger adults continued to increase since 1995-1996, coexistent with increasing prevalence of stroke risk factors.”

I’m not saying DNA doesn’t have a part to play (nor am I suggesting susceptibility to illness is not inheritable), but it’s probably better to focus on the things you can do to protect against metabolic damage or to improve your health, rather than be too distracted by having your tea leaves read. By all means, do some research into genetics, but just imagine where we’d be if only a small percentage of the money that has been put into the genetics industry, went into looking at the metabolic causes of disease.

It’s a little like putting a flame on skin and watching it burn, then saying the type of skin you have, caused the burn. At this stage there is nothing you can do with your genes to help you, but there is plenty you can do if you understand metabolism, and what damages it.

Even if it’s all true, and genes, and gene mutations directly cause disease, the stress promoting things, like the breakdown products of the PUFAs, and many other inflammatory, anti-metabolic things, can change gene expression, and are genotoxic and mutagenic. And they are promoted and sold as health improvement products. Let that sink in.

See more here

Restricted epigenetic inheritance of H3K9 methylation

Epigenetic regulation of the nuclear-coded GCAT and SHMT2 genes confers human age-associated mitochondrial respiration defects

Increased sugar uptake promotes oncogenesis via EPAC/RAP1 and O-GlcNAc pathways

Role of nitric oxide in genotoxicity: implication for carcinogenesis.

Estrogen Drives Cellular Transformation and Mutagenesis in Cells Expressing the Breast Cancer-associated R438W DNA Polymerase Lambda Protein

Germ line-inherited H3K27me3 restricts enhancer function during maternal-to-zygotic transition.

Effect of Hyperglycemia on Gene Expression during Early Organogenesis in Mice

Is estradiol a genotoxic mutagenic carcinogen?

Transgenerational transmission of environmental information in C. elegans

Dietary glycine supplementation mimics lifespan extension by dietary methionine restriction in Fisher 344 rats

Oxidative stress and lipid peroxidation-derived DNA-lesions in inflammation driven carcinogenesis.

Chronic inflammation as a promotor of mutagenesis in essential thrombocythemia, polycythemia vera and myelofibrosis. A human inflammation model for cancer development?

Intrinsic mutagenic properties of 5-chlorocytosine: A mechanistic connection between chronic inflammation and cancer.

Intestinal mucosal inflammation leads to systemic genotoxicity in mice

When bacteria become mutagenic and carcinogenic: lessons from H. pylori.

Nitric Oxide Promotes Resistance to Tumor Suppression by CTLs

How does inflammation drive mutagenesis in colorectal cancer?

DNA Mutations May Not Be the Cause of Cancer

Potential genotoxicity of chronically elevated nitric oxide: a review.

Colorectal Cancer Incidence Patterns in the United States, 1974–2013

Behavioural individuality in clonal fish arises despite near-identical rearing conditions

Hyperglycemia and hyperlipidemia blunts the Insulin-Inpp5f negative feedback loop in the diabetic heart

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Non-genetic cancer cell plasticity and therapy-induced stemness in tumour relapse: ‘What does not kill me strengthens me’

Oxidative stress-induced mutagenesis in single-strand DNA occurs primarily at cytosines and is DNA polymerase zeta-dependent only for adenines and guanines

Induction of proto-oncogene BRF2 in breast cancer cells by the dietary soybean isoflavone daidzein

The role of BRCA status on prognosis in patients with triple-negative breast cancer

Genotoxicity of lipid oxidation compounds.

Genotoxicity and mutagenicity of the alpha, beta-unsaturated carbonyl compound crotonaldehyde (butenal) on a plasmid shuttle vector.

High level glucose increases mutagenesis in human lymphoblastoid cells

Die, selfish gene, die

DNA deaminating ability and genotoxicity of nitric oxide and its progenitors.

Intestinal inflammation induces genotoxicity to extraintestinal tissues and cell types in mice

Mitochondrial DNA oxidative damage and mutagenesis in Saccharomyces cerevisiae.


Inflammation, ROS, and Mutagenesis.

A threshold of endogenous stress is required to engage cellular response to protect against mutagenesis

Endogenous Gradients of Resting Potential Instructively Pattern Embryonic Neural Tissue via Notch Signaling and Regulation of Proliferation

Revisiting telegony: offspring inherit an acquired characteristic of their mother’s previous mate

The role of thyroid hormone and brown adipose tissue in energy homoeostasis

Early-life exposure to endotoxin alters hypothalamic–pituitary–adrenal function and predisposition to inflammation

An Expanded View of Complex Traits: From Polygenic to Omnigenic.

Redox Signaling by the RNA Polymerase III TFIIB-Related Factor Brf2

Interplay between maternal Slc6a4 mutation and prenatal stress: a possible mechanism for autistic behavior development

Assessing the genotoxic effects of two lipid peroxidation products (4-oxo-2-nonenal and 4-hydroxy-hexenal) in haemocytes and midgut cells of Drosophila melanogaster larvae.

Social and physical environments early in development predict DNA methylation of inflammatory genes in young adulthood

Heritable DNA methylation marks associated with susceptibility to breast cancer

Chronic inflammation and mutagenesis.

Maternal serotonin transporter genotype affects risk for ASD with exposure to prenatal stress.

A non-genetic basis for cancer progression and metastasis: self-organizing attractors in cell regulatory networks.

Antidepressant Use During Pregnancy and the Risk of Autism Spectrum Disorder in Children.

DNA damage-induced nuclear factor-kappa B activation and its roles in cancer progression

Complete Genes May Pass from Food to Human Blood

Positive Selection on a Regulatory Insertion–Deletion Polymorphism in FADS2 Influences Apparent Endogenous Synthesis of Arachidonic Acid

DNA damage response impacts macrophage functions

Controlling the Cyanobacterial Clock by Synthetically Rewiring Metabolism

Oxy radicals, lipid peroxidation and DNA damage.

Bioelectric signals spark brain growth

Effects of Dietary Cholesterol and Its Oxidation Products on Pathological Lesions and Cholesterol and Lipid Oxidation in the Rabbit Liver

DNA repair is indispensable for survival after acute inflammation

Cytotoxic versus genotoxic effects of nitric oxide (NO).

Mitochondrial Stress Induced p53 Attenuates HIF-1α Activity by Physical Association and Enhanced Ubiquitination

Chronic cellular hypoxia as the prime cause of cancer: what is the de-oxygenating role of adulterated and improper ratios of polyunsaturated fatty acids when incorporated into cell membranes?


Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism

The cytotoxic and mutagenic properties of cholesterol oxidation products.

A genome-wide systems analysis reveals strong link between colorectal cancer and trimethylamine N-oxide (TMAO), a gut microbial metabolite of dietary meat and fat

Acrolein-induced oxidative stress and genotoxicity in rats: protective effects of whey protein and conjugated linoleic acid.

Influence of nitric oxide on the generation and repair of oxidative DNA damage in mammalian cells

Cholesterol oxidation: health hazard and the role of antioxidants in prevention.

Gut Microbe-Generated Trimethylamine N-Oxide From Dietary Choline Is Prothrombotic in Subjects

Dynamic changes in DNA methylation of stress-associated genes (OXTR, BDNF ) after acute psychosocial stress

Genotoxic effect of iron overload and disease complications in transfused β thalassaemic patients.

Environmental programming of stress responses through DNA methylation: life at the interface between a dynamic environment and a fixed genome

Genotoxicity of vegetable cooking oils in the Drosophila wing spot test

Long-term exposures to ethion and endotoxin cause lung inflammation and induce genotoxicity in mice.

DNA Damage in Inflammation-Related Carcinogenesis and Cancer Stem Cells

Role of nitric oxide in genotoxicity: Implication for carcinogenesis

Iron induced genotoxicity: attenuation by vitamin C and its optimization

Mechanism of genotoxicity induced by targeted cytoplasmic irradiation

Diet dominates host genotype in shaping the murine gut microbiota

Incidence Trends of Type 1 and Type 2 Diabetes Among Youths, 2002-2012

Oxidized cholesterol as the driving force behind the development of Alzheimer’s disease

Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

Prevalence of Cardiovascular Risk Factors and Strokes in Younger Adults

Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans

Transgenerational inheritance of an acquired small RNA-based antiviral response in C.elegans

Monitoring the formation of cholesterol oxidation products in model systems using response surface methodology

Intracellular and extracellular factors influencing the genotoxicity of nitric oxide and reactive oxygen species.

Brain feminization requires active repression of masculinization via DNA methylation

A review of recent studies on malondialdehyde as toxic molecule and biological marker of oxidative stress.

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

Current knowledge on the mechanism of atherosclerosis and pro-atherosclerotic properties of oxysterols

Hepatic inflammation facilitates transcription-associated mutagenesis via AID activity and enhances liver tumorigenesis

The prion protein is critical for DNA repair and cell survival after genotoxic stress

Lipopolysaccharide-induced DNA damage is greatly reduced in rats treated with the pineal hormone melatonin.

Maternal Inflammation Disrupts Fetal Neurodevelopment via Increased Placental Output of Serotonin to the Fetal Brain

Genotoxic effects of neutrophils and hypochlorous acid

Assessment of Hematotoxicity and Genotoxicity among paint Workers in Assiut Governorate: a case control study

Dietary and lifestyle determinants of malondialdehyde DNA adducts in a representative sample of the Florence City population

Nitric oxide-induced genotoxicity, mitochondrial damage, and apoptosis in human lymphoblastoid cells expressing wild-type and mutant p53

Prenatal exposure to famine and the development of hyperglycemia and type 2 diabetes in adulthood across consecutive generations: a population-based cohort study of families in Suihua, China

Malondialdehyde epitopes as targets of immunity and the implications for atherosclerosis

Lipopolysaccharide (LPS) Accumulates in Neocortical Neurons of Alzheimer’s Disease (AD) Brain and Impairs Transcription in Human Neuronal-Glial Primary Co-cultures

Malondialdehyde adducts in DNA arrest transcription by T7 RNA polymerase and mammalian RNA polymerase II

Malondialdehyde, a Product of Lipid Peroxidation, Is Mutagenic in Human Cells

Suppression of transcriptional drift extends C. elegans lifespan by postponing the onset of mortality

Mechanisms of Non-Genetic Inheritance and Psychiatric Disorders

Formation of malondialdehyde (MDA), 4-hydroxy-2-hexenal (HHE) and 4-hydroxy-2-nonenal (HNE) in fish and fish oil during dynamic gastrointestinal in vitro digestion

Mitochondrial metabolism and cancer

Transcriptional profiling of the acute pulmonary inflammatory response induced by LPS: role of neutrophils

The New Genetics and Natural versus Artificial Genetic Modification

A Decade Later, Genetic Map Yields Few New Cures

Darwin’s Pangenesis, the Hidden History of Genetics, & the Dangers of GMOs

Elucidating the Metabolic Plasticity of Cancer: Mitochondrial Reprogramming and Hybrid Metabolic States

Why the ‘Gene’ Concept Holds Back Evolutionary

Epigenetics II: Cellular Memory, Imprinting, and Targeting Genome Configuration With RNA


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