Updated: Sep 19, 2020
DNA Diligence™ is a process developed to discover root cause issues by condensing past history, previous diagnosis, and current symptoms, then, cross-referencing that information with the most updated medical research in order to discover the genes and pathway signaling systems most impacting you on a cellular level. Once completed, we begin targeting the negative effects of these specific genes and pathways to reverse engineer your adverse health condition. HOW DOES IT WORK?
First, we gather information based on your history/background, current symptoms, and/or previous diagnosis.
Then, by cross referencing and analyzing several databases and comparing that information to the most updated medical research we are able to pinpoint that exact gene and it's related interactions that are most relevant to your adverse health condition.
Finally, we build a tailor made custom protocol to reverse engineer the negative impact those genes and pathways are causing using holistic approaches.
An estimated 7.5 million Americans have psoriasis. Psoriasis typically develops after an environmental trigger, which can include an infection, such as strep throat, or injury to the skin, including a cut or bug bite. Certain medications, smoking and heavy alcohol consumption also are triggers.
This type of psoriasis accounts for 80 percent of all cases and is characterized by dry, raised, red patches covered with silvery scales that can be itchy and painful.
Psoriasis is a common skin condition that speeds up the life cycle of skin cells. It causes cells to build up rapidly on the surface of the skin. The extra skin cells form scales and red patches that are itchy and sometimes painful.
Specialized skin cells called keratinocytes, a malfunction in CARD14 increase the activity of NF-kappaB, a protein that turns on genes. This protein increases the production of certain signaling molecules that attract inflammatory cells to the skin, unleashing a vicious cycle of inflammation that is so notable in psoriasis.
The NF-κB protein complex regulates the activity of multiple genes, including genes that control the body's immune responses and inflammatory reactions.
Inflammation is a normal immune system response to injury and foreign invaders (such as bacteria). The NF-κB protein complex also protects cells from certain signals that would otherwise cause them to self-destruct (undergo apoptosis).
The CARD14 protein is found in many of the body's tissues, but it is particularly abundant in the skin. NF-κB signaling appears to play important roles in regulating inflammatory reactions in the skin and in promoting the survival of skin cells.
According to the Mayo Clinic, psoriasis signs and symptoms are different for everyone. Common signs and symptoms include:
Red patches of skin covered with thick, silvery scales
Small scaling spots (commonly seen in children)
Dry, cracked skin that may bleed
Itching, burning or soreness
Thickened, pitted or ridged nails
Swollen and stiff joints
There are several types of psoriasis. These include:
An autoimmune reaction thought to be related to an immune system problem with T cells and other white blood cells, called neutrophils, in your body.
T cells normally travel through the body to defend against foreign substances, such as viruses or bacteria.
But if you have psoriasis, the T cells attack healthy skin cells by mistake, as if to heal a wound or to fight an infection.
Overactive T cells also trigger increased production of healthy skin cells, more T cells and other white blood cells, especially neutrophils. These travel into the skin causing redness and sometimes pus in pustular lesions. Dilated blood vessels in psoriasis-affected areas create warmth and redness in the skin lesions.
The process becomes an ongoing cycle in which new skin cells move to the outermost layer of skin too quickly — in days rather than weeks. Skin cells build up in thick, scaly patches on the skin's surface, continuing until treatment stops the cycle.
Researchers believe both genetics and environmental factors play a role.