The following top five risk for CHD has been identified: hypertension, diabetes mellitus, dyslipidemia, obesity and smoking. In many cases CHD can be prevented when these risk factors are optimally treated and monitored.
Recent clinical studies suggest that a limit has been reached in the ability to reduce the incidence of CHD while adressing only the top five risk factors. Approximately 50% of non-smoker patients continu to have CHD despite normal blood pressure, normale lipids levels, normal weight and normal blood sugar levels. Based on new information other CHD risk factors must be redefined and treated. These factors include hyperuricemia, renal disease, elevated fibrinogen, elevated serum iron, lack of sleep, lack of exercise, stress, anxiety, depression, homocysteinemia, subclinical hypothyroidism, hormonal imbalances, chronic infections, micronutrient deficiencies, heavy metals, and environmental pollutants.
To achieve further reduction of the incidence of CHD the three finite responses of the coronary arteries to the infinite insults must be adressed. They are vascular inflammation, vascular oxidative stress and vascular immune dysfunction ( MC Houston, MD. The Truth About Heart Disease. 2023).
Vascular inflammation plays an important role in causing CHD. Inflammation in the coronary arteries can be measured by scientifically validated blood tests, such as the high-sensitivity C-reactive protein ( hs-CRP). There are many nutritional recommendations and lifestyle changes that can effectively reduce vascular inflammation.
Oxidation ( free radicals formation), if is not balanced by antioxidants, may damage coronary arteries and cause CHD. Oxidative stress can be measured by numerous blood and urine tests. 8-Hydroxydeoxyguanosine (8-OHdG) is the most widely used marker for oxidative stress. There are many nutritional recommendations that will treat oxidative stress.
Vascular immune system dysfunction is one of the primary causes of CHD, hypertension, high cholesterol and atherosclerosis. Immune system dysfunction of the arteries involves T cells and elevated white blood cells ( WBC). T cells ( a type of WBC monocytes) cross the endothelium ( a thin layer of cells that separate the blood from the muscle of the artery), invades into the underlying layer, and transforms into various immune cells, that promote vascular damage. The more damage that occurs in the artery, the faster and more severe this process progress.
Vascular inflammation, vascular oxidative stress and vascular immune dysfunction occur at the same time and lead to the atherosclerotic plaque formation which may rupture causing clot formation and myocardial infarction.
Identification of vascular inflammation, vascular oxidative stress and vascular immune dysfunction (they can be measured in the blood or urine) is very important because they can be treated to prevent or slow the progression to CHD.
There are numerous genes that have been identified that cause CHD. These genes cannot be changed, but they may respond in a good way or a bad way. That response could be an increase or decrease in CHD depending on nutrition, supplements, lifestyle or medications. Genetic testing allows us to measure many of the genes that cause CHD and provide an integrated, precision and personalized treatment program.
There is a proven connection between human gut and the risk of CHD. We can test, measure and treat gut microbiome (GM, a collection of bacteria, fungi, viruses and other organisms that inhabit the human intestine) to prevent CHD.
CHD can be identified with an advanced testing and correct measurements of all CHD risk factors. A combination of targeted and integrated, personalized and precision treatments will be needed to reduce CHD.
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