Genetic Supremacy

If you listen to enough conversations or look at enough articles, books and even scientific studies relating to the topics of heredity and evolution or medicine and disease, there’s a good chance you are going to come away with the impression that it is genes that matter and that the solution to understanding life will somehow come from decoding them.

The most deeply entrenched medical/scientific belief is probably that which suggests that your DNA is a kind of blueprint that has your destiny written into it. This idea is central to an extremely powerful and profitable system and yet there has long been evidence contradicting its validity.

“Francis Crick’s Central Dogma of Molecular Biology – that genetic information passes one-way from DNA to RNA to protein – became the ruling paradigm of molecular genetics from the 1950s up to the mid-1970s…This is…the mainstream account…But soon after…geneticists were to find exceptions and violations to every tenet of classical genetics…”

Media reports regularly talk about new discoveries regarding the importance that variations in specific ‘genes’ have in driving disease and the belief being promoted is that we are getting closer and closer to mapping the causes. Meanwhile scientific experiment continues to show otherwise.

“…gene regulatory networks are sufficiently interconnected such that all genes expressed in disease-relevant cells are liable to affect the functions of core disease-related genes and that most heritability can be explained by effects on genes outside core pathways.”

In fact even the NY Times recently admitted that the Human Genome Project has so far been a complete failure and that ‘indeed, after 10 years of effort, geneticists are almost back to square one in knowing where to look for the roots of common disease.’

This failure is not due to a lack of time, effort and financial investment put into untangling the connections in order to find the right answers, but rather because the basic foundations of the mainstream view regarding the relevance of genes to issues of heredity and disease is almost completely wrong.

“Instead of the linear, one-way information flow envisaged in the central dogma from DNA to RNA to protein and “downstream” biological function, there is intricate cross-talk between the organism and its environment at all levels, with feed-forward and feed-back cycles in the epigenetic and metabolic networks of molecular interactions that mark and change genes as the organism goes about its business of living, with effects reverberating and amplified down the generations.”

Regardless, many billions of dollars continue to be spent on the development of technology intended for research, as well as treatment and prevention approaches formed in line with current genetic dogma, no matter how much it is demonstrated to be misleading, unhelpful and even dangerous.

“The entire history of genetics and its continuity with epigenetics need to be truthfully retold, to put an end to the abuses and misuses of the subject that endanger society.”

The mainstream message is that it is essentially DNA determining the diseases a person is likely to get and once it has been properly worked out which genes cause what, people need only go get a reading and work out the appropriate course of action based on individual risk factors.

Attached to this is the assertion that mutations in genes driving specific diseases occur largely as a result of completely random events, rather than due to any possibly intelligent adaptive response to environmental changes.

“One of the strictest dogmas in conventional evolutionary thinking is the explicitly anti-Lamarckist assertion that conditions cannot induce a related genetic change.”

Evidence of epigenetic factors driving the disease and aging process are also generally ignored or rationalised. Meanwhile experiments have demonstrated that glycine supplementation can lead to the reversal of mitochondrial aging without any alteration to the structure of DNA.

“…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…”

Degenerative diseases like cancer and diabetes are increasingly being viewed – and treated – as though they arise simply as a result of genetic predisposition, ignoring high quality evidence regarding the metabolic nature of their onset.

“Our…findings fill a fundamental gap in…understanding…the mechanism by which glucose metabolism is involved in cancer…a…direct role of increased aerobic glycolysis in inducing the cancer phenotype, in which increased glycolytic activity regulates the canonical oncogenic pathways dynamically and reciprocally…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…”

Real science showing the manner in which metabolic factors can impact upon the function of an organism, as well as upon genes and their expression, has enormous implications for issues relating to disease.

Exposure to stress of many different kinds influence physiological biochemical conditions causing rising levels of a number of substances – including bacterial endotoxin, estrogen and serotonin – which have been shown to interact with genes and promote disease.

“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.”

“Prenatal stress has…a significant…impact on neurodevelopment, and has been linked with several…disorders, including ASD [autism spectrum disorder]…Aberrant serotonergic function has been implicated…having the short allele variant of 5-HTTLPR does not appear to increase the likelihood of experiencing stressful events, it does affect the manner in which one responds to stress…carriers of the short allele have significantly less serotonin (5-HT) clearance causing increased levels.”

Psychosocial stressors have been found to have a direct epigenetic impact via methylation, increasing symptoms of the mood disorders as well as other conditions.

“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.”

Estrogen, which tends to rise under stress, can impact upon the expression of genes related to 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.”

Low levels of maternal inflammation during pregnancy increase serotonin production potentially impairing fetal brain development.

“These results demonstrate that a 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…”

Greater exposure to highly inflammatory polyunsaturated fats – released from storage out of tissue under stress – impair cellular function and have been demonstrated to be a factor causing a variety of diseases of degeneration.

“…despite 50 years of intensive cancer research increasingly focused on genetic causes, no single unifying cause for cancer has been established…Over 70 years ago, Warburg showed that cells could always be made cancerous by subjecting them to periods of hypoxia…It is our hypothesis that long-term hypoxia of cells in the body…is the primary trigger for cancer…linked to the incorporation of…polyunsaturated fatty acids (PUFAs) into the…cell…”

Decades worth of evidence regarding the physiological impact of stress upon metabolism long ignored, now needs to be at the forefront of any discussion on medical and pharmaceutical approaches worth investing in.

Evidence continues to mount confirming that metabolic stress is a powerfully deterministic factor and that many substances which tend to rise in the body in relation to stress have an important role in shaping biological outcomes, independent of changes to genes.

“In…the desert locust of Africa, the Middle East and Asia…phase changes…occur when crowding spurs a temporary spike in serotonin levels, which causes changes in gene expression so widespread and powerful they alter not just the hopper’s behaviour but its appearance and form…their genes don’t actually change….they don’t mutate or in any way alter the genetic sequence or DNA.”

In fact stress has been shown to promote epigenetic changes which last for generations.

“Stress-induced epigenetic changes in the germ line can be inherited and can have a profound impact on offspring development.”

“Long-lasting epigenetic memory of environmental change is therefore possible…”

Dietary factors – including sugar restriction causing increasing levels of exposure to polyunsaturated free fatty acids – can have a powerful effect upon stress levels, increasing the substances of stress, influencing metabolic function and impacting genes and their expression.

“…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.”

Issues of stress and metabolism are closely connected to intestinal bacterial conditions and experiments have pointed to diet as an important determining component.

“…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…”

At the very least, it is no longer possible to justify ignoring the Lamarckian proposition regarding the inheritance of acquired traits and to continue to claim that evolutionary adaptations occur purely as a result of random genetic mutations.

“…we describe a set of small RNAs that are induced by starvation. We show that these starvation-induced small RNAs are transmitted transgenerationally, providing a mean for starved worms to control the expression of relevant genes in consecutive generations.”

“Recent advances in our understanding of inheritance have revealed that offspring-parent resemblance cannot be explained solely by the transmission of parental genes… both genetic and non-genetic sources of variation (and the interactions between them) can influence phenotypic variation and evolutionary outcomes…”

The diseases of aging – cancer, heart disease, stroke, diabetes etc. – are being seen at a rapidly rising rate in younger age groups, ruling out any possible rational explanation based upon so called classical genetic theory.

“…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.”

Mae-wan Ho – a Ph.D. in biochemistry, postdoctoral fellow in biochemical genetics, visiting professor of biophysics and author of numerous publications  – spent decades researching and writing on this topic and has for a long time warned of the inherent dangers in blind acceptance of deterministic dogma.

“Feedback from the environment not only determines which genes are turned on where, when, by how much and for how long, but marks, moves and changes the genes themselves. By the early 1980s, ‘the fluid genome’ had emerged to make genetic determinism obsolete.”

See more here

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

Why the ‘Gene’ Concept Holds Back Evolutionary
Thinking

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

Restricted epigenetic inheritance of H3K9 methylation

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

The New Genetics and Natural versus Artificial Genetic Modification

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

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

Transgenerational transmission of environmental information in C. elegans

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

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

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

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

Die, selfish gene, die

Helping a cagemate in need: empathy and pro-social behavior in rats

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

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

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

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

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

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

Controlling the Cyanobacterial Clock by Synthetically Rewiring Metabolism

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?

BRCA1 DEFICIENCY EXACERBATES ESTROGEN INDUCED DNA DAMAGE AND GENOMIC INSTABILITY

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

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

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

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

Diet dominates host genotype in shaping the murine gut microbiota

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

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

Brain feminization requires active repression of masculinization via DNA methylation

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.

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

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

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

A Decade Later, Genetic Map Yields Few New Cures

#yourgenesarenotyourfuture
#Haidut
#MaeWanHo
#raypeat

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