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Inflammation Control Factor

Take action and build a lifetime of better, healthier skin!

Sensitivity + Inflammation
The regulation of inflammation is largely regulated by your genes. Genetic variations found in vital genes can lead to excessive inflammation.

Excessive inflammation is one of the most common themes in early onset aging.1,2 Often subtle, the signs include skin sensitivity, redness and irritation.

 
Explore other Test Categories:1. Firmness + Elasticity
2. Sun Damage + Pigmentation
3. Free Radical Damage
4. Wrinkling (A.G.E.)
5. Sensitivity + Inflammation
Background
  Genes tested in this category
 

Inflammation is the skin’s first line of defense against foreign invaders such as bacteria and viruses. Inflammation also initiates the tissues healing processes and limits the damage to skin cells caused by everyday chemicals and pollutants. Excessive inflammation is one of the most common themes in early onset skin aging. While it is a helpful response in the short term, if inflammation continues on-going, it can play a negative role.3 Often subtle, the signs include skin sensitivity, redness and irritation.3

The genes that make up your ICF™ score play a key role in signalling the release of inflammatory proteins and help in the detoxifying of Environmental Pollutants and Xenobiotics. Having variations in this category can signal an over-reactive inflammatory signalling mechanism. This can cause heightened inflammation and trauma that is unnecessary to skin cells, result in prolonged irritants, increased redness and enhanced sensitivity to Environmental pollutants and everyday chemicals.


Did you know?
8 in 10 people have a genetic variation that can cause an over reactive inflammation response.

   
SkinDNA™ Gene Name/
Descriptor
Genotype Description
s100286/
Inflammatory Signalling
GG
Responsible for signalling the release of inflammatory proteins to help defend skin cells against invaders.
Chromosome Location: 6q21.3
s100773/
Xenobiotic Detox
AA Involved in efficiently detoxifying Xenobiotic compounds so that they can be safely metabolised and converted to water.
Chromosome Location: 11q13
s100921
s100922/
PAH Protection
TT
AA
Regulates the detoxification of Epoxides found in PAH’s into a more water soluble so that they can be safely broken down.
Chromosome Location: 1q42.1

Glossary of Terms   References
  

Harmful toxins that are found in pollutants such as PAHs. These harmful toxins surround us in our day to day living. If not broken down epoxides can be extremely harmful to the body releasing a wave of free radical mayhem.

Polycyclic Aromatic Hydrocarbons (PAH’s). Highly toxic chemical compounds released from everyday pollutants such as the burning of wood, coal, diesel, and waste, industrial activities, exhaust fumes and cigarette smoke5. Belonging to the Xenobiotic family they can cause a great deal of trauma and damage to skin cells if not efficiently metabolised.6

Chemical compounds which cause trauma and damage to skin cells.4 They can set the foundation for free radical havoc, increase cellular damage, cause collagen to breakdown and enhance skin sensitivity.4 These chemical compounds can stem from air pollution, cigarette smoke and exhaust fumes.

    

1. Girolamo. N., et al., (1997). "Expression of TNF-alpha by human plasma cells in chronic inflammation." Journal of Leukocyte 61(6): 667-678.

2. Rein. P., et al., (2001). "Factors of skin ageing share common mechanisms." Biogerontology 2(4): 219-229..

3. Sawatzky. D., et al., (2006). "The Involvement of the Apoptosis-Modulating Proteins ERK 1/2, Bcl-xL and Bax in the Resolution of Acute Inflammation in Vivo." American Journal of Pathology 168: 33-41.

4. Cleveland, C. J. (2007). "Cells." Encyclopedia of Earth.

5. Berko, D. H. N. (1999). Polycyclic aromatic hydrocarbons (PAHs) in Australia. Environment Australia. Western Australia, Department of Environmental; Protection: 63.

6. Jean. D., et al., (2003). "Health Risks of Residential Exposure to Polycyclic Aromatic Hydrocarbons." Archives of Environmental Health: An International Journal 58(2): 111-118.