Skin laxity

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Revision as of 19:46, 27 January 2015 by RRM (talk | contribs) (Water Retention)

Skin laxity may be caused by ...

  • redundant skin after rapid weight loss
  • damaged collagen and reduced collagen production in aging
  • reduced muscle tone due to immobility

... in combination with heavy skin due to:

  • water retention in the true skin
  • subcutaneous fat accumulation


Collagen is the most abundant protein in the extracellular matrix of the skin and due to its slow turnover rates it is a frequent target of modifications by reactive compounds.[1] Collagen is damaged by sunlight exposure, endogenous- and dietary AGEs/ALEs and free radicals in general. Elevated exposure will accelerate age-related exhaustion of collagen production. Solar UV irradiation causes photoaging, characterized by fragmentation and reduced production of type I collagen fibrils that provide strength to skin.[2] Long-term exposure to sunlight, including ultraviolet A and B, produces signs associated with photoaging and photodamage, including laxity.[3] Exposure to UV-B irradiation suppresses collagen synthesis. Daily life low-dose UV-A1 exposures promote photoaging by affecting collagen breakdown. Responsive darkening of the skin does not prevent UV-A1-induced collagenolytic changes.[4] Resveratrol has antioxidant properties and promotes autophagy, stimulating mitochondrial biogenesis. Topically applied Resveratrol (1%) in combination with vitamin E (1%) and baicalin (0.5%) may reduce skin laxity in 12 weeks.[5] Topically applied Pogostemon cablin may inhibit UV-induced photaging, due to its antioxidative property.[6] Radiofrequency produces thermal effects at various depths, promoting collagen remodeling while sparing the overlying tissue.[7] Precise and controlled subdermal heating may promote subdermal skin tightening.[8] Radiofrequency may be more effective than cutaneous and subcutaneous administration of CO2[9]

AGEs/ALEs accumulate in aged skin.[10] AGE accumulation is associated with age, smoking and obesity.[11] AGEs (advanced glycation end products) and ALEs (advanced lipoxidation end products) are ingested with diet and formed endogenously. In diabetes, endogenous formation of AGEs is elevated, and may lead to 5-fold higher collagen glycation.[12][13] Creatinine is a potent precursor of specific AGEs (HCAs), and creatinine clearance is negatively associated with accumulation of AGEs in the skin.[14] Skin AGEs are robust long-term markers of microvascular disease progression.[15] AGEs and ALEs are associated with age-related NADH oxidase, which may generate free radicals (superoxide), creating oxidative damage leading to cross-linking of skin proteins [16], such as collagen and elastin.[17] Collagenase naturally degrades damaged collagen, but it may be unable to degrade collagen damaged by cross-linking too heavily.[18] Crosslinking may cause the increased age-related stiffness of the skin [19] and stiffening of blood vessels.[20]

Water Retention

Water may be retained in the true skin due to elevated levels of hydrophylic compounds, such as salt, sugars and proteins. Levels of electrolytes are maintained within relatively narrow margins, as both too high and too low levels of sodium, chloride, potassium and calcium inhibit muscle functioning and cell functioning in general. The renin-angiotensin system regulates the amount of fluids and sodium in the body. Sodium is the most prominent cation in extracellular fluid [21], available for local swelling of the skin. Sodium levels are normally maintained between approximately 135-145 mmol/L. Lower levels may reseult in spasms, cramps, seizures and eventually coma.[22] Mildly elevated levels may result in lethargy and edema, levels over 157 mmol/L are considered severe.[23] Values above 180 mmol/L are associated with a high mortality rate.[24] Thus, normal serum sodium fluctuations are 25% maximally.

Glucose levels in the blood are also maintained within a relatively narrow margin. Glucose is the primary source of energy for the brain. When glucose levels are too low, you will faint. A range 70 to 99 mg/dl before a meal is normal. Levels of 101–125 mg/dl may be an indication of possible prediabetes. Levels over 126 mg/dl constitute a risk of diabetes. After a 12‑hour fast, a range of 70.2 to 100 mg/dl is normal; a level of 100 to 126 mg/dl is considered a sign of prediabetes. A level of less than 140 mg/dl, 90 minutes after a meal is considered normal.[25] Normal serum glucose fluctuations may be about 100% maximally, taking in consideration that the total amount of sugar in the blood is only 5 grams (2 sugar packets for coffee or tea).[26] Hence the role of sugar in water retention in the skin is very small.

Protein levels may vary much more widely, as it is the main structural component of cells, and cells desintegrate and are (re)constructed continuously. Differences between upper and lower serum reference values for some individual amino acids are 271% (taurine), 289% (glycine), 625% (hydroxyproline), 769% (glutamic acid), 1000% (methionine) and 3067% (cystine). [27] During the day, protein degradation remainders may accumulate in the skin, prior to deportation by the lymphe system during the night. Edema fluid is high in protein.[28] Edema of the skin may occur when the colloid osmotic pressure (protein level) in the skin is lower than the serum colloid osmotic pressure.[29] The relationship between serum oncotic pressure and interstitial edema is non-linear, i.e. edema becomes progressively greater per mm decrease of the oncotic pressure.[30] The serum protein level (the serum colloid osmotic pressure) determines the excretion/retention ratio of a given water and sodium load. Of the total fluid retention, fat and muscle each may accommodate 25%, whereas the skin, which contributes only 7% to the total body weight, may accounted for 37%, and may increased its volume by roughly one third.[31] The skin is particularly susceptible to the development of edema because its extracellular space is three times larger than the average whole-body value.[32]