A fat fitness curriculum.
Adipose tissue, also known as fat, has come a long way. It is no longer viewed simply as a repository, where lipids are deposited or withdrawn. Metabolism researchers are now evolving a concept of adipose tissue health that emphasizes its quality, not just its quantity.
The idea that adipose tissue fosters the skin's health is very new. The skin's adipose tissue was only formally named in 2014. The name "dermal white adipose tissue" (dWAT) was selected to emphasize its many skin-specific functions. Last year, Yale researchers stunned some experts by revealing that facial adipose volume increases, rather than decreases, as we get older.
It is not surprising, then, that the concept of facial fat fitness is not well or widely understood. To address this, we are initiating a "fat fitness" curriculum, with help from experts in dermatology, plastic surgery and basic science. The goal is to connect silos of knowledge so that facial fat fitness can be understood in a larger health context.
We are grateful for your interest and welcome your feedback.
Fat fitness 101: The basics
The fit or healthy state of fat tissue is one where there are sufficient fat cells (e.g., adipocytes) to handle the tasks the tissue needs to perform and where adipocytes produce and secrete factors (e.g., adipokines) that support surrounding cells and tissues.
The unfit or unhealthy state of fat tissue is one where there are insufficient numbers of adipocytes to handle necessary tasks and/or adipocytes produce factors (e.g., adipokines) that harm surrounding cells and tissues.
Adipocytes store and release lipids as necessary to support metabolism, energy expenditure and other functions. Adipocytes are uniquely equipped to store lipids without sustaining damage. Adipocytes also influence the function of surrounding cells and tissues.
Adipocytes make and release more than 1000 different factors. These factors are involved in metabolism, new blood cell formation, extra-cellular matrix remodeling, new adipocyte formation, inflammation and more.
Like other cells, adipocytes have cell surface and intracellular receptors that convey information. In response to signaling at these receptors, adipocytes can alter the factors that they secrete.
Adipocytes can increase their size by up to four fold. They are the only cells in the body that can do that. Adipocytes increase size by taking up more lipids from the surrounding environment.
The number of adipocytes can change as a function of the rate at which new cells are being created and the rate at which existing cells are dying or transforming.
The rate of adipocyte turnover has been estimated to be between 10% new cells per year and 100% new cells per year. The big range in the estimate is due to difference in methodology but also to differences in which tissues are sampled.
There is a main genetic switch or regulator that needs to be turned on within a pre-adipocyte for it to convert to a mature adipocyte (i.e., PPARγ). This switch turns or transcribes other genes that are needed to complete the process.
No, they can get stuck in the process of converting and never mature, a phenomenon that is called senescence. Or they can convert into fibroblasts instead.
There are a lot of factors that influence new adipocyte formation (e.g., adipogenesis), ranging from the stiffness of the structure in which pre-cursors are nested to signals received from other cells, including mature adipocytes and keratinocytes.
No, adipocytes do not stop being formed as we get older. The process is just less efficient. For example, older pre-adipocytes require a stronger signal to become mature adipocytes than younger pre-adipocytes.
No, there are three types of adipocytes, white, beige and brown. White adipocytes have one large lipid pool, beige have a few lipid pools and brown have many smaller lipids pools. Even within a single type, adipocytes may behave very differently depending on their location in the body.
Yes, facial adipocytes turn over faster than adipocytes from the abdomen. They also are less responsive to signals telling them to tone down or free up lipids (e.g., less lipolytic).
Fat fitness 201: The skin
Yes, there are adipocytes (e.g., dermal adipocytes) that are an inherent part of the skin. Dermal adipocytes convert from a pre-cursor cell type that produces fibroblasts, which are another key skin cell type.
There are three layers of skin. The epidermis, the dermis and the dermal white adipose tissue (dWAT). The term dWAT was coined in 2014. Prior to that , the dWAT was referred to as hypodermis. The dWAT is still often mistakenly referred to as "subcutis" or "subcutaneous", meaning underneath the skin.
Dermal adipocytes have a number of skin-specific functions such as supporting hair growth, responding to infection and helping wounds to heal. Hair will not grow and wounds will not heal in the absence of dermal adipocytes.
Yes, loss of fat fitness (e.g., reduction in numbers, cell enlargement or lower levels of good adipokines) is associated with both common (e.g., rosacea) and rare skin diseases (e.g., systemic scleroderma).
The majority of dermal adipocytes are found below the skin's dermis layer. Importantly, dermal adipocytes also extend into the dermis, forming cone shapes that encase the bottom portion of hair follicles (e.g., the bulb).
Dermal adipocytes are sustained, in part, by factors secreted by the skin's keratinocytes in the top skin layer. Damage to the skin's keratinocytes thus impacts the adipocytes.
Adipocytes regulate the productivity of fibroblasts by secreting factors (e.g., adipokines) that either promote or retard their production of collagen, elastin and hyaluronan, the key building blocks that determine the core strength of the skin. Adipocytes also make collagen and collagen-degrading enzymes.
Adipokines have a decisive impact on fibroblast production of skin building blocks. Fibroblasts exposed to enlarged fat cells reduce production of collagen, elastin and hyaluronic acid by 50 to 80%.
Loss of fat fitness through cell enlargement is associated with a less organized, weaker and less resilient dermis, which manifests as sagging skin. Loss of fat fitness through reduced numbers manifests as thinner skin.
Yes, adipocytes help the skin's epidermis retain moisture and maintain barrier function, in part, by secreting adiponectin, a beneficial adipokine.
Fat fitness 301: Facial aging
The face has dermal, subcutaneous and deep fat. The dermal and subcutaneous fat together make up the superficial fat.
There is no physical barrier to separate dermal and superficial fat.
A thin collagen-rich tissue -- the superficial muscular aponeurotic system (SMAS) -- separates the subcutaneous and deep fat.
The concept that the health of one fat tissue influences surrounding fat tissue is both intuitive and enticing. We know that fat cells can promote or retard new fat cell formation. We are not aware, however, of experimental evidence documenting how changes in one tissue (e.g., dermal) influences another (e.g., subcutaneous).
The fat tissue in the face is organized in puzzle-piece like compartments. Together the dermal and subcutaneous fat make up the superficial fat compartments. The deep fat compartments are separate from the superficial compartments.
Most people simultaneously lose and gain facial fat. 50% of dermal fat is lost as a result of sun exposure. At the same time, weight gain increase subcutaneous facial fat, which can result in a net gain in superficial fat.
Loss of fat cells manifests as hollowing. This is most prominent under the eyes where the epidermis and dermis are especially thin and where, consequently, sun exposure is more damaging. This loss is also more prominent at the borders between superficial fat compartments.
Enlarged fat cells cause the dermis to become weaker and thus contributes most prominently to the sagging of the face.
The fat fitness landmarks are common features of the "aging" face restated in terms of adipocyte biology. We focus on six: strength under the eyes, cheek bone definition, cheek projection, cheek definition, jaw strength and jaw definition.
Yes, unlike the loss of time, loss of fat fitness can be restored. In animal models, exercise or calorie restriction can undo the damage that enlarged fat cells convey to the skin. Adipeau has initial evidence that long-standing skin damage can be similarly undone in humans.
Fat fitness 401: the landmarks
The groove between the lower eyelid and cheek is narrow or non-existent. The lower eyelid runs into the cheek in an upward sloping ridge. The skin of the lower eyelid does not drape or furl upon smiling or squinting. Smiling does not reveal significant cavities or indentations, especially toward the ear-side corner of the eye. The skin is thick and covers up the ligament-structures underneath.
The cheekbone area is defined by a single convex curve with a clear start and end and no breaks or inflections in between. The bottom of the cheekbone area does not sag or obscure the jaw muscles. The cheekbone adjacent to the ear-side corner of the eye has a maximal convex shape and is not planed down.
The top of the cheek forms a concave arc or cup shape under the eye without any breaks or effacement. Specifically, the ear side corner of the arc should be full and erect. The lower branches of the underlying ligament network should not be visible. Upon smiling, the line running from the middle of lower eyelid to the upper edge of the nasolabial fold should follow an unbroken convex arc. Upon smiling, the line running from nostril toward the ear should follow an unbroken convex arc.
Upon pouting, the cheek bottom is bordered by a diagonal line at the corner of the mouth (nose side) and a concave arc extending inward parallel to the upper vermillion (or higher). At rest, the cheek bottom forms an acute triangle.
The area covering the buccinator muscles adjacent to the corner of the mouth is full and defined by a subtle convex arc. Upon smiling, this area is not bisected or interrupted by vertical (accordion) lines.
The masseter musculature of the mid-jaw is maximally revealed. An S-curve runs from the lower mouth to the ear, inflecting below the zygomatic arch or cheekbone.