When the doctor says you have a genetic disease, what does this mean?
Does it mean that the downward progression of your health is out of your hands?
You may be surprised to know that the progression of many genetic diseases can be stopped by living a certain lifestyle that changes internal cellular environments, by using natural medicines, shutting down the action of superantigen pathogens, removing constant contact with specific toxic chemicals and responding differently to stress.
Progress in research is indicating that chemicals in the air we breathe and the food we consume, the pathogens to which we are continually exposed, and the stress we experience, can affect the way our genes work, to progress or stem disease throughout our lives.
This is a relatively new area of science and is easily misunderstood. Many people confuse genetics (involving our DNA genome) with epigenetics, which involves collections of protein chemicals that attach to parts of the DNA and tell the DNA how to behave. This chemical influence is known as the epigenome. This prefix “epi” means above. So, epigenetic means control above the genes. These epigenetic mechanisms change the readout of genes but do not change the original genetic code. Understand that a gene is a blueprint to make a body part, a protein. Epigenetics is the study of the ways environmental factors can rewrite the gene’s blueprint.
A human body is composed of trillions of cells, specialised as muscles, bones, nerves, different organs and other tissues, however each and every one of your body cells carries the same genetic makeup (genome) in its nucleus. The human genome is the complete assembly of DNA (deoxyribonucleic acid)—about 25,000 genes—assembling as 23 pairs of chromosomes inherited from your biological parents, that contain the codes for making the cells of your body.
The way a cell becomes specialised is determined by how and when different sets of genes in the genome are turned on or off to produce specific proteins. For example, the cells that compose the retina of the eye turn on genes that make proteins for detecting light, while the red blood cells make proteins that carry oxygen from the air to other cells throughout the body.
During the growth of a fetus, the epigenome turns genes on or off to control the production of the proteins—”marking” them. These chemical compounds do not change the DNA. Rather, they change the way different cells can use the DNA’s coding instructions. The epigenome is like a conductor, directing when and where DNA instructions are read in the types of cells of the different organs that enables them to function in unison in a body.
However environmental chemicals not associated with the body; pathogens that invade the body, such as viruses; and electromagnetic radiation, have been found to pressure the epigenome and influence the behaviour of body’s cellular function during fetal growth. These lifestyle/environmental factors can also trigger “silent” genetic disease states, that can evolve to become chronic and even terminal, at sometime after birth.
Turning on and off epigenetic switches can create more than 30,000 different proteins from a single gene. Epigenetic mechanisms can alter the readout of normal genes and create the equivalent of mutated proteins even though there will be nothing wrong with the genes. This epigenetic mechanism is the primary way that a cancer cell is created. More than 98% of cancer cells do not result from mutations in the DNA but from mutated proteins that cause epigenetic responses for gene expression in vulnerable cells—which switches-off their ability to behave as community cells.
On the other hand, while epigenetic mechanisms can modify and disrupt the blueprint of normal genes, they can also modify abnormal gene (mutant) expression to create normal and healthy proteins. Thus it is possible for a person with a birth disease to override their “mutation” to experience a mostly normal life. And the most natural way to do this is by changing exposure to certain common environmental factors.
Understanding epigenetics is crucial to understanding chronic diseases. Consider autism, which is a disease now affecting about one in thirty-five people. Autism is an immune-related disease that affects the central nervous system. The emerging body of evidence demonstrates that autism (and many other neurological/immune diseases, neurodegenerative disorders, and most noncommunicable diseases) are all diseases of epigenetically predisposed adaptive immune-nervous systems, which are poorly coping with constant and long-term pressure from pathogens and toxins, in utero. These diseases are triggered later in life by constant exposure to related environmental factors that overwhelms body homoeostasis.
Epigenetic changes can also occur when a growing fetus in the womb is affected by Mum’s autonomic nervous responses, Mum’s disease state, and her body’s responses to constant exposure to environmental factors such as cigarette smoke, alcohol, industrial toxins, or specific defence toxins in plant foods (natural or commercial). Most children begin to show the typical symptoms of autism in the second year of life (usually around eighteen months) once they have started consistently eating plant-derived foods linked to the standard Western diet. This can happen, however, much earlier or much later depending on the timing and severity of exposure to these toxins, and the activity of other environmental influences such as superantigen producing pathogens such as the Epstein-Barr virus.
While DNA is a major influence in the development of autism and other chronic diseases in children, it is certainly not the only influence. Consider identical twins. They have identical genes. If one identical twin has autism, the other twin usually does also, but not always. That is the crucial point, because normal epigenetic patterns are overridden in only one of the twins. There is some control by the mother on the health of her offspring by her lifestyle and how she exposes herself to environmental conditions. Identical twins, who share the exact same DNA, don’t always both have the same severity of autism either, nor do they experience identical illnesses throughout life, nor develop the same chronic diseases later in life.
Researchers are still finding new ways that epigenetic changes unfold at the biochemical level. One form of epigenetic change physically blocks access to the genes by altering what is called the “histone code”. The DNA in every cell is tightly wound around proteins known as histones and must be unwound to be transcribed. Alterations to this assemblage cause certain genes to be more or less available to the cell’s chemical activity, and this determines if those genes will be expressed or silenced.
A second, well-understood form of epigenetic influence, called DNA methylation, involves the addition of a methyl group—a carbon atom plus three hydrogen atoms—to particular bases in DNA sequences. Contact with this methyl group can interfere with the chemical signals that would put a gene into action—thus effectively silencing the gene.
An Example of Epigenetic Processes
The system of controlling our gene expression is affected by both outside influences (the environment—chemicals, electromagnetic radiation and pathogens), as well as internal ones, the genes themselves.
In 2000, Randy Jirtle, a professor of radiation oncology at Duke University, and his postdoctoral student Robert Waterland designed a genetic experiment in which they demonstrated how changes in the womb environments can dramatically affect genes in mice. They experimented with mice that had a mutation of the agouti gene. This is a gene which creates yellow fur, leads to obesity, diabetes, cancer and poor survival health for the mice.
Typically, when agouti mice breed, almost all of the offspring are identical to their poorly adapted parents. The parent mice in Jirtle and Waterland’s experiment, however, produced litters with most of the offspring being slender, and brown, with no health problems—normal mice which lived to normal old age. The effects of the agouti gene had been virtually erased—amazing.
What they simply did to create the transformation, was to alter the normal laboratory diet for mice. Starting just before conception, Jirtle and Waterland fed a test group of mother mice a diet rich in methyl donors—epigenetic assisting chemicals. These molecules are common in the environment and are found in many foods, including onions, garlic, beets, and in food supplements.
The methyl donors worked their way into the developing embryos’ chromosomes and affected the critical agouti gene. The mothers passed along the agouti gene to their offspring intact, but the methyl-rich pregnancy diet, stopped the switching of the gene, and this resulted in most of the litter being born as normal mice with brown fur, normal weight and normal health (with an occasional mouse showing the typical agouti symptoms, and a few with a mottled look and increased weight but not really obese—”halfway” symptoms). The experiment did not change the DNA. The epigenetic influencing chemicals just changed how the agouti gene was expressed in the bodies of the offspring mice.
What is becoming obvious is a growing body of evidence suggesting that the epigenetic changes wrought—by a person’s diet; their responses to stress; toxic environments and superantigen pathogens; and gut flora in their bodies—can work their way into the germ line and pass the epigenome to future generations.
More and more, researchers are finding that a diet high in sugars and natural plant defence toxins, and even social stress, can tweak the epigenome—and trigger inappropriate responses of our genes in ways that can continue for life, when the exposure to these environmental/lifestyle influences is unrelenting.
In 2004 Michael Skinner, a geneticist at Washington State University, discovered epigenetic effects in rats can continue for at least four generations. He was studying how a commonly used agricultural fungicide, when introduced to pregnant mother rats in their food, affected the development of the testes of fetal rats. He was not surprised to discover that male rats exposed to high doses of the chemical while in utero had lower sperm counts later in life.
The surprise came when he tested the male rats in subsequent generations that were not exposed to the pesticide. Although the pesticide had not changed the DNA, these second-generation offspring also had low sperm counts. The same was true of the next generation (the great-grandsons) and the next.
Examples of Environmental Triggers
A number of toxic environmental chemical triggers have been shown to affect the behaviour of an organism’s epigenome, causing genes to be switched “off” when they should be “on”. One well-tested trigger is a chemical found in many plastic drink bottles, called bisphenol-A. Pregnant agouti mice exposed to bisphenol-A, give birth to greater numbers of yellow, obese offspring than normally occurs in litters. Bisphenol exposure doesn’t guarantee yellowness and obesity in mice, rather, it simply increases the risk of developing these traits through secondary effects.
The implications of this discovery are chilling, because bisphenol-A has been used for 40 years in our water pipes, and as coatings on the inside of many food and beverage cans. There has been suggestions that this could be one of the environmental factors contributing to modern diseases such as obesity, however, an association between the rise of obesity throughout the world coinciding with the widespread use of bisphenol-A has yet to be definitively demonstrated.
When gene expression goes amiss during fetal development, as in bisphenol-exposure to mice, the consequences can cause changes in adult mice that are not obvious at birth, and these limiting survival traits only trigger later in life. This phenomenon is called “fetal programming”.
These delayed changes are believed to play a role in the development of many chronic health conditions, including heart disease, diabetes, obesity, cancer, autoimmune diseases and noncommunicable chronic diseases, through overwhelming and consistent exposure to specific environmental toxic chemicals.
The key appears to be the consistency of exposure, day after day, week after week, as occurs in cigarette smoking and eating types of staple foods, week after week for years—grain based foods are the likeliest contender for fetal programming.
Emotional Stress as an Epigenetic Driver
When we are subjected to stressful situations, the sympathetic nervous system is activated. If the physical tension persists and we cannot turn it off, the hypothalamic-pituitary-adrenal axis—a network involving the hypothalamus and pituitary gland in the brain and the adrenal glands near the kidneys—along with the brain-intestine axis, will become more involved. Steroid hormones called glucocorticoids will be produced by this axis. This has the effect of pressuring people to respond impulsively and with anxiety. This is where physical and breathing exercises in yoga classes, dancing and sports, help remove the physical tension of the hypothalamic-pituitary-adrenal axis response.
It is known that an excess amount of glucocorticoids in the body can impact some epigenetic brain processes and increase the risk of experiencing chronic psychological illnesses and subsequent quality of life. People who prolong anxiety, post-traumatic stress, depression and other emotionally-related attitudes to their life circumstances, could be adjusting chemical tags on their DNA. When we are experiencing stress we produce higher amounts of the cortisol hormone. There are cortisol-sensitive genes that play a role in the plasticity and development of the brain.
Michael Meaney, a biologist at McGill University has pursued an idea that some epigenetic changes can be induced after birth, through a mother’s physical behaviour toward her newborn. Meaney sought to explain some curious results he had observed involving the nurturing behaviour of rats. He compared two types of mother rats: those that patiently licked their offspring after birth, and those that neglected their newborns. The licked newborns grew up to be reasonably brave and calm. The neglected newborns grew into nervous rodents that skittered into the safest corner when placed in new environments.
Traditionally, researchers have offered explanations for one side or the other of the nature-versus-nurture debate. Either newborns inherited a genetic propensity to behave in certain coded ways (nature), or they were learning to behave from their parents (nurture). Meaney results didn’t fall neatly into either camp. However, after analysing the brain tissue of both licked and non-licked rats, the researchers found distinct differences in the DNA methylation patterns in the hippocampus cells of each group.
Remarkably, the mother’s licking activity had the effect of removing dimmer switches on a gene that shapes stress receptors in the newborn’s growing brain. The well-licked rats had better-developed hippocampi and released less cortisol, making them calmer and appearing more confident with opportunities. In contrast, the neglected newborns released much more cortisol, had less-developed hippocampi, reacted nervously, and were overly careful. Through a simple maternal licking behaviour, mother rats can shape the brains of their offspring.
Licking and grooming release serotonin in the newborn’s brain, which activates serotonin receptors in the hippocampus. Serotonin modulates cognition, reward, learning, memory, and various physiological processes, although it has a popular image of being a contributor to feelings of well-being and happiness. These serotonin receptors create proteins called “transcription factors”. These turn on the gene that dampens stress responses.
Researchers now think that transcription factors also carry methylation chemicals that have the ability to alter gene expression. In subsequent studies, Meaney and his colleagues were able to reverse the epigenetic signals by injecting the drug “Trichostatin-A” into the brains of adult rats. In effect, they were able to simulate the effect of good (and bad) parenting with a pharmaceutical intervention. Trichostatin is chemically similar to the drug “Valproate”, which is used clinically in people as a mood stabilizer for bipolar disorder and headaches.
The link between parental nurturing and brain development is more than just a curious cause and effect. Making postnatal changes to an offspring’s epigenome can offer adaptive advantages. Mothers and fathers of social animals can mold their progeny to increase survival potential in the environment into which they were born. This idea challenges some of the theories of biology and psychology, and suggests that adaptive survival responses are not necessarily innate or passively emerge from the genome, but can be moulded by lifestyle and environment.
Magnetic resonance imaging brain scans of adult people who believe they have had a poor and hateful relationship with their parents have hippocampi that are significantly smaller than the average. Adults who believe they have had a close and loving relationships with their parents, show normal size hippocampi. This adds to the understanding that the quality of parenting, along with the perceptive attitude of the offspring, is responsible for the different development potential of brains.
Historically, genetics has not meshed well with discussions of social policy. It is too easy to view disadvantaged groups—criminals, the poor, the ethnically marginalised, sexually compromised—as somehow fated by DNA to their condition. The advent of epigenetics offers a new focus, and an opportunity to more comprehensively understand how nature and nurture combine to shape the individual and our sociocultures.
You Can influence your Genes
Researchers used to think that once your epigenetic code was laid down in early development—well, that was it for life. More and more researchers are now accepting that the epigenetic patterns that controls our DNA can be influenced after birth by our environment/lifestyle. Unlike genetic mutations, epigenetic changes are potentially reversible. A mutated gene is unlikely to ever mutate back to normal, and the only recourse is to destroy or cut out all the cells carrying the defective gene, to eliminate chronic illness. This is what oncologists do with tumours.
A gene with a defective methylation pattern can be encouraged to reestablish a normal pattern to change disease into health. This will occur when certain environmental conditions are removed and others imposed over a reasonable time frame. This is the new direction research is exploring to find a drug “cure” for cancer and other neuro-immune diseases.
There are now cancer researchers who suggest that once we understand the connection between our epigenome and diseases like cancer, lifelong “methylation diets” may be the lifestyle change required to stay healthy. Such diets would need to be tailored to an individual’s genetic makeup, their exposure to specific toxins or cancer-causing agents, along with the attitude to themselves and their community.
More than 15 years ago, in 2003, biologist Ming Zhu Fang and her colleagues at Rutgers University published a paper in the journal Cancer Research on the epigenetic effects of green tea. In animal studies, green tea prevented the growth of cancers in several organs. Fang found that epigallocatechin-3-gallate (the major polyphenol from green tea) can prevent deleterious methylation dimmer switches from turning on (and shutting down) certain cancer-fighting genes. The researchers demonstrated that a herbal medicine can inhibit DNA methylation. Long term exposure to specific herbal medicines (there are more than 200 of them) has been suggested as a method to regulate the epigenome.
Fang and her colleagues have since gone on to show that “genistein” (an angiogenesis inhibitor and a phytoestrogen) and other compounds in soy, show similar epigenetic effects. While this is an example of isolating one chemical compound from many in soy, and suggesting by implication that soy is a healthy food. There is, however, much more to plant chemicals and their effects on the epigenome—some will be beneficial, some will just be toxic—but the overriding decider is the individual’s body and their overall epigenetic competency.
Assisting the Epigenome as you Age
For generations, through science, we have been led to believe that through our DNA we are destined to have particular body shapes, personalities, and diseases. Some scholars have even contended that the genetic code predetermined intelligence, and has been the root cause of many social ills, including poverty, crime, and violence. “Gene as fate” had become conventional wisdom until epigenetic studies outdated that concept. For better or worse, as individuals, we appear to have a measure of control over our genetic legacy.
We have known that environmental influences make us sick, but now we know that, as we contact toxic chemicals in our foods/drinks, through breathing and touch, and when we suffer pathogenic infections, our gene expression throughout life can be compromised and lead to chronic illnesses. Epigenetics has introduced the concept of “free will” into our understanding of genetics. It is more obvious now that we need to be mindful of our actions and thoughts, for they can reduce the competency of our epigenome which can switch and cause us to suffer chronic mental and physical health, and die before our potential longevity.
In human ecology relating to immune competency, there are nine categories of lifestyle/environment that determine health and will have effects on the epigenome to varying degrees in different people. They are:
Being competent in:
• Emotional health and wellbeing.
• Obtaining sleep quality.
• Regulating toxic phytochemicals.
• Controlling superantigen pathogens.
• Maintaining physical movement (strength, flexibility, balance, static-dynamic endurance, relaxation, joint alignment, fascia release).
• Having a strong ability to denature, detoxify and remove chemicals from the body.
• Taking care to buffer vaccination complications.
• Maintaining a normal gastrointestinal tract to uptake macro and micro-nutrition.
• Understanding where you, as an individual, need to live on the nature-culture spectrum.