- Cellular Blebbing: an effect of UV exposure
- Epidermal Strength and Adhesion
- Endocrine System, Hormones and the Skin: An overview
I recently read an advertisement made by a sun-bed manufacturer that stated "some sceptics still damn the use of sun-beds". To make it worse this was in a trade magazine, which is supposed to educate and support the beauty therapy industry.
Research has proven the damaging effects of UVA, the primary UVR source of sun-beds. Enough to convince some states in America to ban the use of sun-beds, and to be universally rejected by those involved in skin cancer research, this also includes skin treatment therapists who specialise in skin ageing.
Advances in research techniques
The sophisticated methods now used by scientists to culture cells represents a major breakthrough in the biological sciences. Biochemical analysis of growing cultures can investigate, for instance the mechanisms of cellular replication, cell to cell communication, cellular energy production or DNA repair. Furthermore, the development of powerful electron microscopes allows the study of cell morphology, these advances have proven without doubt the damaging effects of UVR on the skin cell, in particular UVA.
This article describes the differences in cell deformation due to the damaging agents UVA & UVB IRRADIATION.
The cell membrane structure
Life is based on a vast continuous series of chemical changes that take place in and around our cells. This series of chemical changes takes place in any living thing and is called metabolism.
Each cell, a microscopically small unit, is surrounded by a delicate membrane some sixty-millionths of inch thick called the cell wall. This cell wall membrane surrounds the protoplasm of the cell and helps maintain its shape and structure.
The cell membrane comprises of a double layer of lipid molecules interspersed with protein molecules, the lipids that make up the bulk of a cell membrane fall into three classes namely phospholipids 45%, steroids and glycolipids. Each phospholipid has a hydrophilic (water seeking) phosphate head and two flexible hydrophobic (water avoiding) lipid tails. In the surface membrane, phospholipids are arranged in a bi-layer with the phosphate heads touching the watery interior and exterior of the cell and the lipid tails buried in the middle layer.
The main function of the cell membrane is to regulate active and passive transport of nutrients and oxygen. This process selectively allows certain substances to enter and leave the cell while barring others, this selectivity is done by receptors that are coded to recognise certain substance required for cell metabolism. (Example: Vit A receptors)
Appearing like finger-like projections, these receptors increase the surface area of the cell and so help the exchange of materials that is constantly occurring between the cell content and the surrounding tissue fluids.
The health and well being of the cell membrane is paramount to the metabolism of the cell interior and all its functions. Without a healthy permeable membrane the cell could be compromised, causing impaired DNA replication and become a rogue or damaged cell. Because of the high phospholipid content of the cell membrane, a constant supply of Essential Fatty Acids by dietary or topical source is required to ensure this permeability and transport of life sustaining nutrients.
What would happen if the cell membrane were compromised by UVR?
Cellular Blebbing: A description for a type of damaged caused by UVA & UVB.
Blebs: The formation of protrusions on a cells surface is called zeiosis" from the Greek term for boiling water (bubbling)
Extensive plasma membrane blebbing is prominent in a process leading to cell death. Because blebbing is induced by free-radical generators and by DNA damaging agents, studies were done with UVR to induce blebbing in human keratinocytes (in vitro). UV is currently accepted as triggering an oxidative process (free radicals). Human epithelial cells exposed to UVA or UVB showed an interesting blebbing pattern.
Blebbing caused by UVB
80% of cells underwent blebbing within 7 hours of exposure producing many small blebs per cell. The cells eventually detached from the plastic dish (and died) about 24 hours after UVB irradiation.
Blebbing caused by UVA
After UVA the cells developed one single large bleb per cell. (These cells also died)
The two modes of bleb induction point out, beyond reasonable doubt, that UVA and UVB exert their harmful actions in different ways. Whether it is single or multiple blebbing that occurs, when the cell wall is jeopardised, free radicals have a direct pathway to the interior of the cell.
Blebs may be a consequence of direct or indirect molecular damage impairing the cyto-skeletal scaffolding. Blebs and resultant cell segmentation can affect the nucleus and the mitochondria. Cytoplasmic material is entrapped in the blebs, which can either rupture or be shed. If shed, cytosolic enzymes and other materials in the released vesicles can interact with another cell, fusing with its membrane and transferring cytosolic material from the first to the second cell.
This means cell death or mutation, end of story.
We have always known of the harmful effects of UVB, but have been kidding ourselves about UVA. The blebbing induced by UVR justifies the argument that protection against UVA & UVB is desirable in skin care and anti-aging products. It may finish the story once and for all about the damaging effect of sun beds.
In the end, it is our professional responsibility to educate our clients about this newly found information and that sun protection must have the highest priority over any skin product we sell. These sun protection products must have a high anti free radical profile of actives that should include Vitamins A, C & E to help counteract the free radical formation caused by cellular blebbing. Because more recent research has proven that a sun block will not prevent cell damage.
About the Author:
New Zealand born Florence Barrett-Hill is an internationally acclaimed independent dermal scientist, aesthetic technical educator, practitioner, researcher, and author with a vast experience covering all aspects of professional aesthetic therapy and paramedical skin care. Florence's internationally respected "Advanced Skin Analysis" training program is a breakthrough post-graduate curriculum launched in 1994, and was the first to recognise and teach the importance of linking skin structure and function to skin condition. It is the core of this training program that has provided the content for the book of the same name, first published in 2004.
More information about her e-learning and seminars can be found here: www.pastiche-training.com
Her books "Advanced Skin Analysis" and "Cosmetic Chemistry" can be purchased direct from the publisher: www.virtualbeauty.co.nz
Have you ever wondered what it is that your peeling solutions are affecting or how they work?
The old saying "softening and loosening the bonds that hold the corneocyte in place" didnt do it for me. I wanted to know more, hence my research into cell junctions and the role they play in skin adhesion. In addition I wanted to know the effect that different acids had on those cell junctions.
This article is part one of a two part series.
The cell does not end at the cell membrane
Bricks in a building must be stuck together and also tied somehow to the foundation. Similarly, cells within tissues and organs must be anchored to one another and attached to components of the extracellular matrix. Cells have developed several types of junctional complexes to serve these functions. In each case, anchoring proteins extend through the plasma membrane to link cytoskeletal proteins in one cell to cytoskeletal proteins in neighbouring cells as well as to proteins in the extracellular matrix.
The human body is composed of cells organised together with extracellular matrix into tissues having specific characteristics relating to specific functions. Each tissue is composed of several cell types and supporting extracellular matrix.
About 200 cell types are found within the human body, and this article is discussing the cell junctions found within the epidermis. This article concentrates on the cell junctions in the adult epidermis.
Cells within a tissue must communicate with one another, and this may be facilitated by a signalling mechanism or by direct cellular contact. In tissues where wear and tear is a regular occurrence like the skin and heart, cells are held tightly together by a series of cell junctions to form a barrier.
Cells are held together by the adhesive forces of cellular membrane molecules called desmosomes and hemidesmosomes.
Epithelial cells communicate and adhere to each other and/or to the underlying basement membrane by diverse junctions, which are presented schematically in the diagram at left.Specialised junctions provide attachment and mechanical strength to the epithelial cells, and mediate signals from the neighbouring cells or from the extracellular matrix to the cyto-skeleton and the cortical cell cytoplasm.
The epidermis consists of four different layers: stratum basale, spinosum, granulosum, and corneum.
Depending on the epidermal layer, the keratinocytes express a selected pattern of cell junctions. The expressions of different junctions and junctional molecules have been shown to vary also during development.
The intercellular junctions characterised so far in the epidermis are desmosomes, adherens and gap-junctions.
The hemidesmosomes connect the basal keratinocytes to the basement membrane.
The tight junctional molecules have been described to occur in the stratum granulosum.
More about the types of Cell Junctions
Anchoring Proteins occur in three structurally and functionally different forms: Anchoring Proteins also known as Adhesive junctions for Cell to Cell or Cell to Extracellular Matrix. The anchoring junctions enable groups of cells to function as robust structural units by connecting the cyto-skeletal elements of a cell either to those of another cell or to the extracellular matrix.
They are most abundant in tissues that are subjected to severe mechanical stress, such as heart muscle and skin epithelium (epidermis).
Desmosomes are cell-cell junctions, which are attached to the intermediate filaments.
These junctions are complex disc shaped structures, usually a few hundred nanometres in diameter. The surface on one cell is matched with an identical structure on the surface of the adjacent cell. Within each cell, in close approximation to the junction is a circular plaque made of some 12 proteins called the attachment plaque, the plaques have numerous intermediate filaments (keratin) entering and leaving them.
These junctions seem to function as points of especially firm adhesion between adjacent cells.
Desmosomes are very abundant in the skin and mediate a strong adhesion between the epidermal keratinocytes from the basale cell layer to the stratum corneum.
These junctions can rapidly respond to environmental changes, and allow the dynamic processes such as wound healing to occur. The lack of desmosomes is associated with skin cancer. It is suggested that the absence of this junction account for a tumors ability to grow.
However, they are not found solely in the skin and may vary in structure depending on the structure being examined. Hemidesomosomes (Connecting sites for intermediate filaments).
There is also such a thing as a hemidesmosome, meaning half desmosome. These are not necessarily found between two cells. Hemidesmosomes, instead, connect epithelial cells to the basement membrane (basal lamina ) where they serve to bind the cell to the membrane.
Adherens junctions (Connecting sites of actin filaments). This type of junction encircles the cell and provides for the adhesion of one cell to another. These junctions are rich in actin, myosin, tropomyosin and vinculin microfilaments.
Another type of plaque bearing junction is the adherens junction, and it is associated with actin filaments. The actin filaments are connected to catenins. Because of their association with actin filaments, adherens junctions help to mediate coordinated movements and shape change of neighbouring cells.
The main protein of an adherens junction is vinculin. Vinculin functions to bind adherens junctions to the actin filaments. Cadherins are also present and are the transmembrane proteins that connect the cells. Adherens junctions are found primarily in cardiac muscle and epithelial tissues and are responsible for maintaining contact inhibition. Adherens junctions mediate the cell-cell contacts of all living cell layers of the epidermis.
These junctions are connected to microfilamentous cytoskeleton. The transmembrane molecules of the adherens junction are the calcium-dependent E- or P-cadherins, while the plaque consists of plakoglobin and α- and β catenin. The assembly of adherens junctions seems to be a driving force for the formation of other cell junctions (e.g. desmosomes). In addition to their adhesive function in epidermis, the adherens junctions have been assumed to participate in cellular communication, migration, and tissue.
Focal adhesions have been shown to appear in keratinocytes in vitro, and these molecules may play a role in e.g. the migration of the cells during wound healing. Focal adhesions mediate the cell-matrix interactions (such as between keratinocytes and the cell culture substratum) and are linked to the microfilaments.
Communication Junctions (Gap junctions)
Communication junctions also known as Gap junctions provide direct chemical and electrical communication between cells by allowing the passage of small molecules and ions from one cell to another.
Gap junctions are numerous in all layers of the epidermis and have an important role in the coordination of the keratinocyte growth and differentiation and in cell-cell communication.
The gap junctions form a hydrophilic pathway for passive diffusion of nutrients, metabolites, ions, and small signalling molecules up to ~1000 Da in size between adjacent cells, which would include ions, some hormones, cAMP and cGMP causing cells in many tissues to act in a coordinated manner.
Structurally, each gap junctional channel is composed of pair of connexons / hemichannels, which leave a narrow intercellular gap between the neighbouring cell membranes. Each connexon is composed of a hexameric assembly of connexin proteins lining the transmembrane channel. Many different types of the connexins can join to form a wide diversity of gap junctional channels, depending on the tissue and the functional status of the cell.
Also known as Tight junctions, Occluding Junctions create an impermeable seal between cells, thereby preventing fluids, molecules, or ions from crossing a cell layer via the intercellular space. These junctions are seen as a band that encircles the cell and fuses adjacent cell membranes closing off the intracellular space. The principle function of the tight junction is to form a more or less tight seal that prevents the flow of materials between cells. The membranes may have many fusion sites within the junction and therefore be more impermeable or have only a few and be relatively "leaky". The tight junctions are one of the cells first lines of defence against unwanted molecules entering the body through the side door.
The keratinocyte cell and desmosomes
Desmosomes basically provide strength and integrity to the epidermis by tethering the cells of the stratum spinosum (spiny layer). Desmosomes link adjacent cells together.
Keratin intermediate filaments link one desmosome on a cell to another desmosome on a second cell.
The whole epidermis (i.e. the stratum spinosum) is basically strung together by this system of desmosomes and intermediate filaments.
As the cells move into the granular layer a number of changes to the keratinocyte take place. These changes contribute to the skin barrier defence systems, the dissolution of the desmosomes and the formation of NMF.
As mentioned, granular cells are important in synthesising material for the stratum corneum namely the permeability barrier. One type of granule that is made by the granular cell layer is called a lamellar body. These lamellar bodies contain ceramide, free fatty acids and cholestrol sulfate, which are secreted as a huge complex, (bilayers) which become part of the acid mantle and create a permeability barrier to protect us from the environment. (acid mantle)
Another type of granule contained in the granular cell layer is the keratohyalin granule. Instead of lipid, his granule contains a protein called profillagrin, which is subsequently digested to fillagrin. Further digestion of fillagrin by different peptidases makes the amino acid constituents of the natural moisturizing factor (NMF).
Dissolution of the desmosomes also begins in the granular layer as the keratinocyte prepares for desquamation This dissolution of the desmosomes requires a percentage of free water for the enzyme activity that is needed to allow normal cell desquamation. The enzymes (glycosidase and proteases) that break apart these desmosomes are not only dependent on the presence of water, the protease enzymes are also sensitive to the pH, or acidity, of the skin. So it makes sense that when the pH becomes more acidic, these enzymes are activated to break apart the desmosomes, allowing skin cells to be shed more easily.
Having dry skin, an impaired acid mantle or insufficient amounts of natural moisturising factor, can lead to decreased water content of the stratum corneum. This in turn leads to dysfunction of these degradative enzymes, which then leads to these residual desmosomes not getting degraded (so cells stick together) and therefore abnormal desquamation or scaling of the skin. Therefore, if it is not well hydrated, the enzymes functioning in destruction of the desmosomes do not work properly and the skin becomes dry and flaky.
An example: When you have dandruff, however, the flakes consist of "aggregates of cells," so you can see these this also indicates that there is something wrong with the normal desquamation process. In psoriasis, as well as any scaly dermatoses, there is something wrong with the granular cell layer and the process of desquamation is not functioning properly.
We examined the mechanism of desquamation, to establish what factor influence the mechanism and what treatments might be effective for skin care. We have revealed that desmosomes play a key role in the adhesion of epidermal cells, and the digestion of desmosomes by two types of serine proteases leads to corneocyte desquamation.
The water content in the epidermis influenced the digestion of desmosomes by the proteases. Thus, low humidity in winter may cause insufficient digestion of desmosomes and this may lead to a scaly skin surface.
About the Author:
Florence Barrett-Hill is an internationally acclaimed dermal science educator, practitioner, researcher and author with a vast experience covering all aspects of professional aesthetic therapy and paramedical skin care. Florence holds over a dozen diplomas and international qualifications covering every aspect of modern skin treatment therapy, and is well respected by her industry peers for her 30+ years of knowledge she loves to share.
Florence is the programme director of Pastiche Resources, an Internationally recognised postgraduate beauty industry education provider.
Janine Tait is an internationally qualified beauty therapist with over 30 years experience in the beauty industry, a dermo-nutrition expert, and educator with a particular interest in skin health and wellbeing.
Janine says: Giving nutritional advice is now an accepted part of a therapists recommendation for the clients home care program.
If beauty therapists want to move towards involving nutrition in their salon Janine recommends that they start to increase their knowledge base by reading and taking courses in those relate subjects.
The agony of adolescent acne, the irritation of pre-menstrual breakouts, the burden or bloom of our skin during pregnancy and the changes experienced at menopause. What do these skin conditions have in common? Sex hormones.
As therapists we are aware of the huge influence sex hormones have on the appearance of the skin. For men their influence is most apparent during puberty when acne strikes. For women, whose blood hormone levels are constantly fluctuating, their influence is experienced throughout their adult lives. Not only this, the difference we see between the skin of men and women is due to the dominant hormones of each sex.
What are hormones?
Hormones are chemical messengers that have specific effects on certain cells of the body. Hormones, which are produced by endocrine glands, are released into the bloodstream where they are carried to all parts of the body. But they will only effect cells that have specific receptors for that particular hormone. The tissue acted upon by each hormone is known as the TARGET TISSUE. The cells that make up these tissues have receptors in their cell membrane or within the cytoplasm to which a specific hormone attaches. The purpose of the receptor is to recognise the presence of the hormone. Once it is attached it then conveys the message to the nucleus, where the required action takes place through the regulation of the manufacture of proteins and enzyme synthesis.
Hormones can only have an effect if they are able to bond to a receptor. If they cannot bond it will not matter how high the hormone levels are, they will have no effect. The more receptors in a certain area the more sensitive that area will be to that particular hormone.
The skin contains receptors for several types of hormones:
- Oestrogenic Hormones Female-like effect
- Androgenic Hormones Male-like effect
- Progesterone A precursor hormone to both androgens and estrogens.
Many endocrine diseases and disorders effect the hormonal balance throughout our bodies. This can result in an imbalance of sex hormones, which can affect the appearance of the skin.
The effects of hormones on the skin
- Increases the rate of cell turnover in the basal layer of the epidermis.
- Reduces the size and activity of the sebaceous glands.
- Keeps sebaceous secretion thin and less fatty.
- Slows the rate of hair growth.
- Increases the action of the enzyme hyaluronidase, which produces hyaluronic acid.
- Keeps the skin metabolically active.
- It also appears to stimulate fibroblast activity however study is continuing into this area. (Fibroblasts contain oestrogen and produce hyaluronic acid.)
The influence of oestrogen is easily seen in women's skins. Its regulatory effect on the size and action of the sebaceous gland means that compared with men, women generally have finer pored and drier skins.
Oestrogen also stimulates the production of hyaluronic acid. Hyaluronic acid is one of the chief components of the base substance in the dermis and it enables the dermis to hold moisture. It provides the skin with its ability to resist stretching and keeps the skin firm and moist, giving it the smooth, soft feel we so often associate with the skin of a woman. Androgens, on the other hand, stimulate collagen production resulting in the stronger, coarser skin of a man.
The skin contains receptors for progesterone but its action on the skin is unknown. However, it has been shown that progesterone can interfere with the action of oestrogen receptors in the skin.
- Increase the rate of cell turnover in the basal layer of the epidermis.
- Increase the size and activity of the sebaceous glands.
- Increase collagen production through the stimulation of fibroblast cells to produce the proteins needed for collagen synthesis.
- Increase hair growth.
Males have a far higher level of androgen hormones than females and because of the effect the sex hormones have on the skin, this means there is a huge difference in the skin of the sexes. Because of the effect of the androgens the sebaceous glands are larger and therefore the pores appear larger. In the dermis, the androgens stimulate the action of the fibroblast cells, responsible for the production of collagen and elastin. Little is known about the effect of hormones on elastin production but much research has been carried out on their influence on collagen synthesis. This has shown that testosterone increases collagen production resulting in a very strong skin.
We can now apply these hormonal influences to the different stages our skin passes through during times of hormonal change.
Androgens increase the rate of cell turnover in the basal layer resulting in a thickening of the skin surrounding the opening of the pilosebaceous duct.
One of the most undesirable effects of hormones on the skin is acne. This can range from the odd spot to Grade IV acne. Even though the actual cause of acne is unknown some facts have been established. Acne in puberty is the result of defective sebum production, abnormal cornification (thickening) in the top of the pilosebaceous duct, abnormal microflora of the skin and inflammation as a result of the presence of this micro-flora.
The androgen hormones influence two of these. Androgens increase the rate of cell turnover in the basal layer resulting in a thickening of the skin surrounding the opening of the follicle. This increases the likelihood of blockages forming in this area. Androgens also increase the flow of sebum. However, we often observe acne conditions that show signs of lipid dryness. This could be due to the fact that an androgen dominance would negate the thinning, liquefying effect oestrogen would normally have on sebaceous secretions, resulting in a thick, viscous sebum that is more likely to block the pilosebaceous duct. Because of this the sebum would not be secreted onto the surface of the skin and the skin would appear lipid dry as a result.
This suggests that all acne sufferers have high levels of androgens circulating in their blood. But research shows that this is only true for 50-70% of women with acne. So not all acne sufferers have disturbed androgen levels. It is also interesting that not all people with hormonal imbalances get pimples. It seems that one factor that can determine whether or not a person will develop acne is their sensitivity to androgens and this sensitivity can be an inherited trait. Studies show that the same acne type will equally affect identical twins whereas this is not the case for non-identical twins. There are also racial tendencies with the Japanese being less affected than the Chinese and Caucasians more affected than Blacks.
To further complicate the issue, we must also consider that the ovaries and adrenal glands produce only 50% of our androgens. The other half is produced locally in tissue such as the skin. Weak androgens can be converted into stronger ones in the hair follicle. This results in an increased androgenic influence in the skin without high levels circulating in the blood. This also tends to be an inherited trait.
In summary, androgen hormones certainly contribute to the problem of acne by increasing the turnover of cells and the flow of thick, fatty sebum. However, the person must have inherited sensitivity to androgens in order for them to have this influence.
During the first half of the menstrual cycle the hormone oestrogen is dominant and it exerts its control over the sebaceous glands, limiting sebum production and ensuring that it is thin and less fatty. After ovulation the corpus luteum is formed in the ovary and starts to produce increasing amounts of progesterone making it the dominant hormone in the second stage of the menstrual cycle. The effect of progesterone on the skin is unknown even though we know that our skin cells do have receptors for this hormone. However, progesterone can interfere with the action of the skins oestrogen receptors and the regulating effect that oestrogen would normally have on the secretions of the sebaceous glands. This would result in an increase in the flow of thick, viscous sebum, explaining why women suffer from pre-menstrual breakouts.
The effect of progesterone on the skin is still unknown, but we do know it interferes with the regulating effect that oestrogen would normally have on the sebaceous glands.
Women often find that their skin can respond to pregnancy in a number of different ways. Some women find to their delight that their skin is radiant and glowing while others, to their despair, find their skin is unsettled and they develop pimples.
The dominant hormone during pregnancy is progesterone with the placenta churning out quantities ten to twenty times higher than normally experienced during a usual menstrual cycle.
The exact effect of progesterone on the skin is still unknown but we do know that it interferes with the regulating effect that oestrogen would normally have on the sebaceous glands. To further complicate the issue, whenever progesterone levels are high in our bodies, androgen levels are low. Perhaps these two conflicting influences explain why some women have wonderful skins during pregnancy and others do not. Obviously, more research is needed in this area.
Unless surgically induced, the hormonal changes at menopause often occur gradually. The menstrual cycle becomes increasingly erratic and ovulation occurs less and less. Eventually ovulation ceases completely.
At this time a number of things happen. Progesterone production stops because the corpus luteum, which is the source of this hormone, only forms if ovulation occurs. The ovaries production of oestrogen greatly diminishes and oestrone becomes the dominant oestrogen in the body.
Oestrone is formed by the conversion of androgens in the fatty tissue (peripheral oestrogen conversion). It is a very weak estrogen (twelve times weaker than oestradiol the oestrogen produced by the ovary). Because the ovary produces only minute amounts of oestradiol, the main source of estrogen available to the body is now oestrone and even the formation of this weak hormone drop to two-thirds of the usual level found in menstruating women. The net result of these changes is a much-reduced oestrogen and progesterone influence in the body.
Meanwhile, testosterone production by the ovary continues after menopause at much the same levels as in menstruating women. The effects of testosterone now become more apparent as normally oestrogen would balance out its effect. This unopposed testosterone often stimulates the hair germ cells causing facial hair growth. It can also cause acne to return or the development of seborrheic dermatitis.
The lack of oestrogen also causes a reduction in the action of the enzyme hyaluronidase, which produces hyaluronic acid. The low dermal GAGS (hyaluronic acid makes up a large percentage of these substances) mean that the skin becomes thinner and loses its supple texture. The skin can remain soft to touch but can feel less smooth. There is also a decrease in the reflection of light from the skin leaving the surface looking dull and dry. Stress can also disrupt the delicate hormonal balance, upsetting the menstrual cycle or even stopping it completely.
When Things go Wrong
Many endocrine diseases and disorders effect the hormonal balance of our bodies. This can result in an imbalance of sex hormones, which can effect the appearance of the skin in the following ways:
- Too much androgen causes the epidermis to become coarse and thick. The sebaceous glands enlarge and acne can develop. The hairline of both males and females can recede.
- Too little androgen results in a dull, thin epidermis that becomes finely wrinkled. The skin can become dry and there is no facial, pubic or axillary hair. The skin can have a pallor due to fewer blood vessels and decreased pigment levels.
- Too little oestrogen in women causes changes to the skin that are very similar to a lack of androgens but not to the same extreme. The skin will appear dull, thin and finely wrinkled with some loss of tone.
- Too much oestrogen causes pigmentation changes and the appearance of spider nevi.
Stress can also disrupt the delicate hormonal balance, upsetting the menstrual cycle or even stopping it completely. That stress can be emotional, as in the break-up of relationships, exams or moving away from home. Stress can also be physical, such as serious illness or extreme physical exercise. Often women who are involved in such physically demanding sports as triathlons or bodybuilding can develop acne conditions because of the effect this has on their bodies endocrine system.
As we know, the sex hormones can have a powerful effect on the skin and any upset in their delicate balance can have a dramatic effect on the appearance of the skin. Is there anything that we can do to positively influence these hormones and help our clients through their times of change?
Pugliese, P. (1996). Physiology of the Skin. Allured Publishing Corporation.
Trickey,R. (1998). Women, Hormones & Menstrual Cycle. Allen & Unwin.
About the Author:
ITEC, CIDESCO, CIBTAC, ABThNZ
Janine Tait is an internationally qualified beauty therapist with over 30 years experience in the beauty industry, a dermo-nutrition expert, and educator with a particular interest in skin health and wellbeing.