Anyone suffering Hashimoto’s Thyroiditis, Lupus, Graves, Rheumatoid Arthritis or other autoimmune spondyloarthritic conditions, or any autoimmune condition, you may be interested in the plethora of research into possible causation.
We are a unique, symbiotic array of cells, tissues, organs and organ systems with biofeedback mechanisms and cross talk.
We speak about the Gut Brain axis, the HPA – Hypothalamus Pituitary Axis or HPG Hypothalamus Gonadal axis; the bidirectional crosstalk between controls and recipient organs.
Our bodies are interdependent, finely tuned and biodynamicly designed to work synergistically and given adequate fuel, healthy genes, environment, exercise , rest, mindset and balance, tend toward healthy longevity.
We do know, however the impact of epigenetics , often largely impacted by various Snps and triggers also play an integral role in our health.
The microbiome is a large component contributing to our healthy function and well-being.
“Here, we present evidence linking gut microbiota dysbiosis with autoimmune mechanisms involved in disease development to identify future effective approaches based on the gut microbiota for preventing autoimmune diseases.
The gut microbiota maintains the homeostasis of our immune system. Innate and adaptive immunity plays an important role in the containment and clearance of microbial pathogens.
The gut microbiota in the human body forms a barrier to resist invasion of pathogenic bacteria and synthesis of nutrients, such as proteins and vitamins, changes in the intestinal microbiota impair intestinal mucosal barrier function.
Manipulation of the dense gut microbiota has broad implications for host health. The diverse human gut microbiota plays a fundamental role in the well-being of hosts and is closely correlated with the growth, development, substance metabolism, and immune function of the host.
Indeed, the gut microbiota is intimately connected to numerous facets of host biology, and beneficial microbiota organisms play an important role in the processes of food digestion, immune system homeostasis maintenance, anti-infection immunity support, lipid metabolism modulation, and other.
The main groups of the gut microbiota in the human intestinal lumen include Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria.The human gut-resident commensal microbiota is a unique ecosystem associated with various bodily functions, especially immunity.
Gut microbiota dysbiosis plays a crucial role in autoimmune disease pathogenesis as well as in bowel-related diseases. However, the role of the gut microbiota, which causes or influences systemic immunity in autoimmune diseases, remains elusive.
The human gut is colonized by various microorganisms collectively termed the gut microbiota, which has a mutualistic relationship with the host. The gut microbiota is the major source of microbes that may exert beneficial or pathogenic effects on host health.Moreover, the gut microbiota hosted in the gastrointestinal tract, which is the largest host interface exposed to the external environment, comprises approximately two-thirds of the human microbial commensal community. “
What is Epigenetics?
“Your genes play an important role in your health, but so do your behaviors and environment, such as what you eat and how physically active you are. Epigenetics is the study of how your behaviors and environment can cause changes that affect the way your genes work. Unlike genetic changes, epigenetic changes are reversible and do not change your DNA sequence, but they can change how your body reads a DNA sequence.
Gene expression refers to how often or when proteins are created from the instructions within your genes. While genetic changes can alter which protein is made, epigenetic changes affect gene expression to turn genes “on” and “off.” Since your environment and behaviors, such as diet and exercise, can result in epigenetic changes, it is easy to see the connection between your genes and your behaviors and environment.
How Can Your Epigenetics Change?
Your epigenetics change as you age, both as part of normal development and aging and in response to your behaviors and environment.
Epigenetics and Development
Epigenetic changes begin before you are born. All your cells have the same genes but look and act differently. As you grow and develop, epigenetics helps determine which function a cell will have, for example, whether it will become a heart cell, nerve cell, or skin cell.
Example: Nerve cell vs. Muscle cell
Your muscle cells and nerve cells have the same DNA but work differently. A nerve cell transports information to other cells in your body. A muscle cell has a structure that aids in your body’s ability to move. Epigenetics allows the muscle cell to turn “on” genes to make proteins important for its job and turn “off” genes important for a nerve cell’s job.
Epigenetics and Age
Your epigenetics change throughout your life. Your epigenetics at birth is not the same as your epigenetics during childhood or adulthood.
Example: Study of newborn vs. 26-year-old vs. 103-year-old
DNA methylation at millions of sites were measured in a newborn, 26-year-old, and 103-year-old. The level of DNA methylation decreases with age. A newborn had the highest DNA methylation, the 103-year-old had the lowest DNA methylation, and the 26-year-old had a DNA methylation level between the newborn and 103-year-old.
Epigenetics and Reversibility
Not all epigenetic changes are permanent. Some epigenetic changes can be added or removed in response to changes in behavior or environment.
Epigenetics and Health
Epigenetic changes can affect your health in different ways:
Germs can change your epigenetics to weaken your immune system. This helps the germ survive.
Certain mutations make you more likely to develop cancer. Likewise, some epigenetic changes increase your cancer risk. For example, having a mutation in the BRCA1 gene that prevents it from working properly makes you more likely to get breast and other cancers. Similarly, increased DNA methylation that results in decreased BRCA1 gene expression raises your risk for breast and other cancers.
While cancer cells have increased DNA methylation at certain genes, overall DNA methylation levels are lower in cancer cells compared with normal cells. Different types of cancer that look alike can have different DNA methylation patterns. Epigenetics can be used to help determine which type of cancer a person has or can help to find hard to detect cancers earlier. Epigenetics alone cannot diagnose cancer, and cancers would need to be confirmed with further screening tests.”
For anyone that has experienced methylation issues, or chronic health conditions such as inflammatory bowel disease, cancer, or metabolic disorders, here is a simple explanation that highlights the importance of a healthy, diverse microbiome.
“The intestinal microbiota is known to produce B9 (folate) & B12, essential nutrients in methylation.
Short Chain Fatty Acids, produced in the intestine exclusively by commensal microbes through fermentation of complex non-digestible carbohydrates and fibre. We know SCFA promote intermediates that modulate enzyme activity directly related to DNA methylation.
The gastrointestinal tract is continuously exposed to trillions of commensal microbes, collectively termed the microbiota, which are environmental stimuli that can direct health and disease within the host. In addition to well-established bacterial sensing pathways, microbial signals are also integrated through epigenetic modifications that calibrate the transcriptional program of host cells without altering the underlying genetic code. Microbiota-sensitive epigenetic changes include modifications to the DNA or histones, as well as regulation of non-coding RNAs.
While microbiota-sensitive epigenetic mechanisms have been described in both local intestinal cells and as well in peripheral tissues, further research is required to fully decipher the complex relationship between the host and microbiota. This Review highlights current understandings of epigenetic regulation by gut microbiota and important implications of these findings in guiding therapeutic approaches to prevent or combat diseases driven by impaired microbiota-host interactions.”