Nutritional Genomics in Clinical Practice – Part 3
A Developing Relationship
Nearly everything about the emerging science of nutritional genomics points to a developing relationship with the science behind adrenal fatigue syndrome (AFS). AFS is the condition that arises from the body’s natural response to stress. Adrenal fatigue research shows the typical sequence of processes that lead to AFS.
Once the body is faced with stress from any source, the hypothalamic-pituitary-adrenal (HPA) axis is activated. Hormones released set in motion a cascade of processes as a response to stress. At one end of that cascade is the release of cortisol by the adrenal glands. Cortisol is the stress fighting hormone of the body. Normally, once the stress is gone, cortisol levels return to normal and the adrenals rest.
However, in this stress-filled world in which we live, stress continues. This puts an additional burden on the adrenals to continue secreting cortisol to fight the stress. Eventually, adrenal fatigue sets in. No more cortisol is available to deal with the effects of stress, and the symptoms associated with adrenal fatigue set in.
Often, these symptoms are difficult to assess by traditional methods, so they are not always recognized as all related. Some of the symptoms are similar to those encountered by practitioners using research into nutritional genomics.
The Inflammation Circuit and Nutritional Genomics
One of the most frequently seen symptoms in both AFS and nutritional genomics is an increase in inflammation. This increase in AFS comes when the lining of the gut system becomes more permeable due to imbalances in the metabolic system, allowing toxins and bacteria to enter the bloodstream. This brings an inflammatory response, prompting the immune system to activate.
Inflammation is a major factor in nutritional genomics research.
Another major part of this developing relationship has to do with a more comprehensive approach to remediating health conditions called the NeuroEndoMetabolic (NEM) stress response model. Current medicine focuses on illness conditions and their symptoms. Remediation efforts typically are directed toward single organs or individual symptoms.
This is too narrow a model to follow if healthcare professionals desire to get to the root of health problems. The NEM model views organ systems as being interrelated. What affects one, affects others.
This model also recognizes the importance of imbalances in organ systems that are due to environmental factors that include diet, nutrition, exercise, and toxins. These imbalances and their causes are filtered through a set of unique genetic predispositions, beliefs, and attitudes of the individual, as well as lifestyle choices made by individuals.
Markers such as the TNF gene can affect inflammation levels in your body. Genes such as APOE4 and PPARGC1 that influence your weight and insulin resistance may affect inflammation levels in your body as well. All of these factors must be considered in order to find the underlying pathology that causes the health conditions of people.
Metabolism is an essential aspect of this approach. Not only does it convert food into energy for our bodies to use, it also directs the body’s inflammatory response and makes sure our bodies can detox themselves. Healthy metabolism keeps our bodies safe from oxidative stress by lowering the number of toxins in the body and preventing stress from damaging our bodies.
On the other hand, a weak metabolic system reduces the ability of our bodies to absorb nutrients from foods and slows down the detoxification efforts of our bodies. This is a direct link to the new research being carried out in nutritional genomics as seen with metabolic gene markers FTO, LEPR, and ADRB2 for example.
Other Health Conditions
This emerging science of nutritional genomics is concerned with other health conditions in addition to obesity. These other conditions are very significant in our culture today.
Possibly the number one diet-related chronic health condition today is cardiovascular disease (CVD). Inflammation at least partially due to diet is a major risk factor. CVD is said to be a group of conditions made up of many factors that include obesity, atherosclerosis, high blood pressure, and thrombosis. All of these are influenced by dietary considerations and genetics. A strong relationship between diet and CVD has been well established.
This condition is a combination of lipid transport and disorder of metabolism, along with high levels of inflammation. High levels of LDL cholesterol, overall cholesterol level, and triglycerides are the triggers for plaque formation that leads to atherosclerosis. High levels of HDL cholesterol are protective against this condition. People with apolipoprotein E4 and a high-fat content in their diets are at risk of developing this condition.
High blood pressure is affected by both genetic and dietary factors, also. Some genetic patterns have an effect on primary hypertension. The relationship between high blood pressure, obesity, and diet is well known. A decrease in blood pressure is seen when obese individuals lose weight.
There appears to be a relationship between diet, genetics, and the emergence of cancers. Certain mutations in genes can be inherited, increasing the risk of developing cancer. This risk increases with the consideration of a diet-gene relationship. Twin studies have shown a ten percent chance of identical twins developing the same type of cancer. This suggests strongly that environmental factors (such as diet) play an important part in whether cancers develop or not.
Diet has been shown to be either a source of carcinogens or protectants for the development of cancers. It has also been shown that genetic mutations that affect metabolism can modify the chances of carcinogens coming in contact with target cells. This would occur at the initiation of the cancer process.
The influence of gene mutations on hormonal regulation is shown in those cancers that are related most closely to hormones. Breast, prostate, ovarian, and endometrial cancers are in this category. Dietary considerations also interact a great deal with hormone regulation. Obesity very much so.
Some food factors, like phytoestrogens, are metabolized by the same pathways as the sex hormones and may be affected by the mutations mentioned here.
Diet and Its Effect on Cancers
Research has shown all of the major signaling pathways detrimentally affected in different types of cancers to be influenced by nutrients. Some of these pathways include inflammation, DNA repair, oxidant/antioxidant balance, and more. To this point, over 1,000 phytochemicals have been shown to have anticancer properties.
Long-chain polyunsaturated fatty acids have been shown to have a benefit on physiological processes that are involved in nearly all chronic and degenerative illness conditions. Fish oil, with its Omega-3 fatty acids, has been shown to slow down the growth of colon tumors.
The biologically active factors in fruits and vegetables can prevent the onset of cancers through several mechanisms. They can increase detoxification efforts and thus block the metabolic activation of carcinogens. Plant foods can also increase the action of detoxification enzymes.
Diet can also increase the risk of developing some kinds of cancers. A diet high in consumption of red meat increases the risk of colorectal cancers. N-Acetyl Transferase (NAT) is implicated in acetylation of the heterocyclic aromatic amines present in muscle meat cooked at high temperatures. These amines can be activated through acetylation to ultimately bind DNA and lead to cancers. Through this process, there is an increased risk of developing colon cancer in those people who eat large quantities of red meat.
Excess body weight and lower activity levels combine to bring about one-fifth to one-third of the most common cancers. These cancers include breast, colon, endometrium, kidney, and esophagus.
Some salts and preservatives have been linked closely with the development of gastric cancer. Low levels of folate ingestion, vitamin B12, vitamin B6, or methionine have been implicated in the development of cancer in CC or TT phenotype of MTHFR gene.
The new science of nutritional genomics appears to hold great promise for limiting or even preventing the most common chronic illness conditions. Clearly, diet and genes are interrelated and affect each other for either good or ill.
We are what we eat, and we eat what we are. This is the relationship between diet and genes stated generally. We can choose to eat foods that improve the expression of our genes to boost our human potential. We also can eat foods that lead to better health and possibly longer life.
© Copyright 2017 Michael Lam, M.D. All Rights Reserved.