Have you heard of inflammaging before? A portmanteau of “inflammation” and “ageing”, it’s an evolving medical term used to describe the foremost cause of fine lines, wrinkles and age spots. In other words, it stands for chronic low-grade inflammation which plays a big part in the ageing process, resulting in changes in body tissues. Unfortunately, once the damage is done, it’s nearly impossible to reverse.
(I’m going to dig really deep into the science of it all, to give you all the information you need to make a clear & informed decision but if you’d rather just read the quick and easy version, skip straight to page 2 by clicking here)
Inflammation is the body’s response to cellular aggression or injury. It represents a defence mechanism designed to heal cells from injury and protect the body from the consequences of that injury. Cell injury may occur due to trauma, genetic defects, physical and chemical aggressions, tissue death, foreign bodies, immune reactions and infections. Inflammation also facilitates early tissue healing and repair and allows the body to restore itself to a normal form and function.
Most people are familiar with the visible inflammation that can be seen on the surface of the skin, with redness representing a sign of infection, irritation or discomfort. However, inflammation can also be invisible. All skin—and certainly weakened or aged skin—is subject to inflammation, even at low intensities. It is this underlying inflammation that ultimately exhausts the body’s defence system, dismantling key youth-sustaining skin structures, and resulting in collagen and elastin degradation, as well as a breakdown of the skin’s barrier function.
When it comes to skin ageing, there are two types of ageing. Intrinsic & extrinsic skin changes.
Intrinsic ageing is accompanied by cell loss, thinning of the outer layer of skin, called the epidermis, and flattening of the area that joins the epidermis to tissue below its surface. This leads to the appearance of fine lines and wrinkles.
Extrinsic ageing is caused by external factors such as UV radiation from excess sun exposure, which causes inflammatory reactions in the skin, as well as oxidative damage from pollution in the environment. This oxidative stress injures cell membrane proteins and fats, and the genetic blueprint of the cell (DNA), which can increase skin cancer risk.
Inflammation + Skin Ageing = Inflammaging
Today, the direct link between extrinsic skin ageing and inflammation is well-established and documented. In the early 90’s, Elias and Feingold demonstrated the reciprocal effect of many chronic inflammatory diseases—such as psoriasis, and atopic and seborrheic dermatitis—on the stratum corneum barrier, which maintains healthy hydration levels in the skin. [1,2]
The integrity of your skin barrier is maintained by a metabolic balance, such as the synthesis of collagen fibres and the replacement of old, worn out fibres by enzymes called metallop-roteinases, regulated by tissue inhibitors of matrix metalloproteinases.
Inflammaging destroys this balance, decreasing cellular metabolic activity and collagen renewal. Externally, the skin loses its suppleness and elasticity, and becomes flaccid. It is also known that inflammaging generates reactive oxygen species (ROS), causing age-accelerating oxidative damage, which further perpetuates a chronic, pro-inflammatory state. 
Epigenetics of Inflammaging
Remember when I said inflammaging is next to impossible to reverse? Well you can partly thank epigenetics for that. Epigenetics, as a simplified definition, is the biological mechanism that will switch genes on and off in your DNA, the instruction book on how each cell will direct their activities. Genes are specific sequences of bases that provide instructions on how to make important proteins – complex molecules that trigger various biological actions to carry out life functions.
Epigenetics affects how genes are read by cells, and subsequently whether the cells should produce relevant proteins. For example, the COL1A1 gene in DNA is present in all types of cells but “expressed” in skin cells to produce Type 1 Collagen proteins.
What you eat, where you live, who you interact with, when you sleep, how you exercise, even ageing – all of these can eventually cause chemical modifications around the genes that will turn those genes on or off over time. It’s what makes us unique. Why do some of us hate the taste of mushrooms or marmite? Why are some of us more sociable than others? The different combinations of genes that are turned on or off is what makes each one of us unique.
Just like epigenetic markers record a whole host of information about the environment you are in, it also records inflammaging sources during your life. In essence, your body remembers the inflammaging and how it was caused. Some clues indicate that inflammaging and epigenetic recording can sustain each other, likely feeding vicious circles and representing a significant contributor to age-related physiological decline and diseases. 
Inflammaging and the body
Scientists have already outlined a relationship between inflammation and a range of conditions, including type 2 diabetes, atherosclerosis, Alzheimer’s disease, and osteoporosis.
In the past, scientists thought that the immune system or the liver drove inflammaging. However, according to a new study that the Journal of the European Academy of Dermatology and Venereology recently published, the skin might play a significant role, too.
“The inflammation must come from an organ big enough that very minor inflammation can affect the whole body. Skin is a good candidate for this because of its size.”
– Dr. Mao-Qiang Man
Dr. Man, who is a research scientist in the Department of Dermatology at UCSF, continued, “Once we get old, we have dermatological symptoms like itchiness, dryness, and changes in acidity. It could be that the skin has very minor inflammation, and because it’s such a large organ, it elevates circulating cytokine levels, the messengers of the body which stimulate the movement of immune cells towards sites of inflammation, infection and trauma.”
This story continues on Page 2
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