Pathology Prevention with Environment

Pathology Prevention with Environment

When it comes to your health, the environment is often underestimated or even forgotten. The emergency first responder, is trained that the first step is to get the victim out of harms way. You need to look around an be sure that there is no immediate danger, then proceed to what ever steps are mandated. But first, we check the environment. At every level this is true. Check the environment if your working at the township level with interrelationships of the citizens. Check the environment within an individual as you examine internal organs. Tissues also are impacted by their environment. At the Cellular level, and even the organs within the cell body have environments. At every level, the environment is crucial in pathology prevention.

At the micro-cellular level, the meaning of the term epigenetics has evolved considerably over time. Conrad Hal Waddington coined the term in the 1940s to describe the “casual mechanisms” that give rise to phenotypes from genotypes in the developmental and differentiation processes of humans. It is at this level, the environment can impact the way DNA is replicated and control our responses to yet a larger, external environment.

Nowadays, the term is used to explain stable heritable chemical modifications to DNA and histones that affect gene expression without altering nucleotide sequence. This new concept has allowed the consideration of a new perspective from which the complexity of many cellular processes such as genetic regulation, cellular development and differentiation, genomic imprinting, embryology, aging and cancer, and other diseases is understood.

Also, epigenetic alterations may occur due to chance or under environmental influence. In the latter case, epigenetics moderates the genetic expression of a trait depending on the prevailing environmental conditions, a phenomenon which could confer us with the necessary plasticity to adapt to our environment and the capacity to induce alternative phenotypes from the same genotype through the regulation of gene expression patterns.

Environmental epigenetics emerges from the idea that the interaction between the environment and the epigenome may alter the phenotype and might be related to disease susceptibility. And most importantly, these alterations could be transmitted down through generations.

The epigenome is at risk of changes and alterations over time, and it will be dependent on internal, external, and/or stochastic factors. In this article we describe how external factors affect the epigenome and the consequences for health and disease during lifetime.

Recent works demonstrate how epigenetic mechanisms are affected by environmental aspects, such as different chemical and physical environmental stressors, diet, unhealthy habits, and pharmacological treatments.

It is well known that maternal tobacco smoke exposure is one of the most important risk factors during pregnancy for many diseases such as asthma, cancer, obesity, and type II diabetes. Tobacco smoke is known to produce epigenetic changes that can affect birthweight and fetal programing in children exposed to prenatal smoking compared to children who were not.

In adults’ tobacco use has been related to an increase in promoter gene-specific DNA processes, which in turn is linked to increased predisposition to diseases such as cancer. Methylation is a chemical reaction in the body in which a small molecule called a methyl group gets added to DNA, proteins, or other molecules. The addition of these methyl groups can affect how some molecules act in the body. For example, methylation of the DNA sequence of a gene may turn the gene off so it does not make a protein. Changes in the methylation patterns of genes or proteins can affect a person’s risk of developing a disease, such as cancer.

To investigate in more depth the effect of tobacco smoking on DNA, researchers have performed genome-wide DNA analyses. As a result, tobacco use has been related to changes in DNA methylation sites related to the development and function of the cellular, cardiovascular, detoxification, hematological, immune, tumorigenic, and reproduction systems.

High alcohol consumption is also widely recognized to have many negative effects which lead to a deterioration in an individual's health. Alcohol can interfere with cellular metabolism through the inhibition of methionine synthase. Other studies have revealed that the use of alcohol alters DNA patterns in hepatocarcinogenesis and neural stem cell differentiation.

Apart from DNA changes, ethanol induces gene activation through an increase in histone, which may lead to immune system dysfunction. Interestingly, epigenetic changes due to ethanol seem to be different depending on whether there is chronic or binge ethanol intake. Furthermore, prenatal alcohol exposure also significantly affects the correct development of the fetus.

Substantial stress during early life can be a risk factor in the initial appearance of symptoms for individuals susceptible to bipolar disorder and other mental disorders. Many studies have reported a relationship between early life stress and the aberrant DNA of many genes. Also, stress is able to produce changes in histone modifications. In this regard, there is an interesting study showing how prenatal maternal stress, generated by a natural disaster, was related to changes in DNA patterns of blood cells, which could influence the immune function of the offspring.

Physical exercise enhances or maintains physical fitness and is beneficial for human health in several ways. Little is known about the molecular mechanisms responsible, but several studies have shown that epigenetics is related to the effects of exercise on human health, since epigenetic changes in germ cells, skeletal muscle, and brain have been observed following a period of exercise.

In conclusion, our pathology prevention efforts should consider the environment, both in the short-term, long-term, and generational perspectives.

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