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PRODUCTS FOR PREVENTION, CURE OR SUPPORT BY A LOT OF DISEASES: Acne, aging symptoms, AIDS, allergies, Alzheimers disease/dementia, angina, arthritis (osteoarthritis), arthritis (rheumatoid arthritis), asthma, attention deficit disorder (ADD), breast cancer, burns, carpal tunnel syndrome, cholesterol, cronic bronchitis, chronic cough, chronic fatigue sydrom, cognitive problems, colds and flue, congestive heart failure (CHF), Crohn`s disease, depression, diabetes mellitus type 1, diabetes mellitus type 2, eczema, edema, endometriosis, fatigue, fibromyalgia, hair loss, herpes simplex, hyperlipidemia, hypertention, obesity, otitis media.

ALL SKIN CARE PRODUCTS

PRODUCTS TO FIGHT SPECIFIC DISEASES

The skin is the largest organ of the body. As our major interface with the environment, the skin, composed of specialized epithelial and connective tissue cells, has many protective and synthetic functions.

1. Layers of the Epidermis

The epidermis forms the external surface of the skin and is mainly composed of keratinocytes which differentiate to form 4 layers, the Stratum Basale (basal layer), Stratum Spinosum (spinous or prickle cell layer), Stratum Granulosum (granular layer), and Stratum Corneum (surface layer).

-- a. Stratum Basale:

The basal layer consists of 1 cell layer of cuboidal cells attached by hemi-desmosomes to a thin basement membrane which separates it from the underlying dermis. Mitotic figures are usually in this layer, and the cells are interconnected by desmosomes and gap junctions.

-- b. Stratum Spinosum:

Above the basal layer is the spinous or prickle cell layer so named because of the prickly appearance at high magnification due to the fine cell processes containing desmosomes attaching one polyhedral-shaped cell to another. ( NOTE: If these desmosomes are damaged, as in the autoimmune disease pemphigus, the epidermal cells become separated, a process called acantholysis, and an intraepidermal blister results). Active protein synthesis occurs in this layer, producing a fibrillar protein keratin which aggregates to form tonofibrils. These tonofibrils migrate to the granular layer to eventually become part of the keratin complex (see Stratum Granulosum).

-- c. Stratum Granulosum:

Above the spinous layer is the granular layer, in which each keratinocyte contains basophilic keratohyalin granules. The protein filaggrin is a major component of these granules, and it is thought to bind to the keratin filaments (a modified form of the tonofibrils produced in the spinous layer) to form the keratin complex. The cells also synthesize lipids which are believed to serve as "intercellular cement".

-- d. Stratum Corneum:

The outer layer of the epidermis is the corneal layer which consists of fully keratinized, flat, fused cells bound together by lipids synthesized in the granular layer. The protein involucrin is produced in the stratum granulosum and corneum and forms a thickened protein layer on the inner surface of the plasma membrane.

2. Cellular Components of the Epidermis

-- a. Keratinocytes:

The Basal keratinocyte is a mitotically active cell (analogous to the stem cell of bone marrow), which differentiates terminally from the basal (least keratin) to the cornified cells (most keratin). As it migrates upward, there is progressive synthesis of keratin proteins, which constitute part of the protective interface between the body and the environment. The migration process normally takes approximately 28 days (NOTE: This cell turnover process is abnormally rapid in psoriasis).

-- b. Melanocytes (pigment cells):

Produce melanin for skin pigmentation, which is partially protective against UV radiation. These cells are derived from the neural crest and migrate to the basal layer of the epidermis during fetal development, where they become interspersed among the keratinocytes by 8-10 weeks of gestation in the cephalic skin and by the 4th month of gestation in the caudal regions. Melanosomes (pigment containing granules produced within melanocytes) are present in melanocyte dendrites and are transferred to surrounding keratinocytes. The melanocytes tend to form a cap over the keratinocyte nucleus and partially protect it from UV radiation. Melanin synthesis is controlled by melanocyte-stimulating hormone (MSH) from the pituitary gland. (NOTE: Some pigment cells fail to remain in their basal destination, instead re-entering the dermis as nests of pigment cells (*gross photo). These nests form the melanocytic nevi which may be acquired during postnatal life or may be congenital. Some uncommon melanocytic nevi arise by failure of migration into the epidermis. Nevi will be discussed in the section titled "Disorders of Melanocytes").

-- c. Langerhans' cells:

These are dendritic antigen-presenting cells intimately involved in immunological responses in the skin.

-- d. Merkel cells:

Merkel cells are neuroendocrine cells which form a small percentage of the cells in the basal layer. They have contact with small unmyelinated nerve endings and may function as a slow mechanoreceptor.

B. dermis

1. Layers of the dermis:

The dermis is separated from the epidermis by the basement membrane and this junction consists of the interlocking rete ridges and dermal papillae. The dermis is divided into 2 layers, the papillary dermis and the reticular dermis.

2. Components of the dermis:

-- a. Cellular

Fibroblasts(synthesize collagen, elastin, and reticulin), histiocytes, endothelial cells, perivascular macrophages and dendritic cells, mast cells, smooth musce, and cells of peripheral nerves and their end-organ receptors.

-- b. Fibrous

This consists largely of collagen (Type I collagen) and reticulin (Type III collagen), which provide tensile strength. Elastic fibers provide for restoration of shape after a deformation

-- c. Ground substance

This constantly undergoes synthesis and degradation, and consists largely of glycosaminoglycans: hyaluronic acid, chondroitin sulfate, and dermatan sulfate.

sexual attractiveness may be dependent upon appearance and smell of skin

Keratins are the cytoskeletal components of all cells of epithelial origin, varying in molecular weight depending on the type of epithelia. Keratin is one of the 5 classes of intermediate filaments, each found in a different cell type.

Intermediate filaments (10nm)

Serve a distinct cytoskeletal function. Three of the 5 classes of intermediate filaments are found in the skin: Keratin, Vimentin, and Desmin. Keratin is composed of both acidic keratin and basic keratin, which together function to strengthen and stiffen the intercellular junctions and laminate to form protective layers. Vimentin is the major cytoskeletal protein of connective tissue cells, melanocytes and Langerhans cells. Desmin filaments hold myofibrils in place in muscle cells.

Keratin Products

The differentiated state of epidermal cells--basal or granular layer-- determines which of the 20 various polypeptides will be produced. There are keratin polypeptides which can be recognized only in the basal cell layer--the low molecular weight (50,000-58,000)-- and others,which are of high molecular weight (57,000-67,000) and appear first in the spinous and granular layers. Other keratin polypeptides are found in all epidermal cells. Several different keratins are made in nails, hair, and stratum corneum.

The processes of aging differ in male and female skin.
In men, there is a gradual thinning of male skin with increasing age of approximately 1% per year. On the other hand the thickness of most women's skins remains surprisingly constant until the menopause, after which there is a significant and sometimes dramatic thinning with increasing age.
There is a relationship between skin thickness and collagen content in men of all ages. A similar relationship exists among women over 60 years of age, but it is less evident in younger women.
In adult skin, the features of aging are closely related to the total collagen content, which in both sexes decreases with increasing age, but at different rates. In later life women may look

older than men of the same age and similar experience of sun exposure, partly because their skin has a lower collagen content to start with. Another reason for the gender difference in skin collagen content may be the difference in male hormone production between men and women.
In women, estrogen and androgen output from the ovaries and adrenal glands falls after menopause, resulting in decreased collagen synthesis and repair.
Aging related to the failure of estrogen production at the menopause accentuates intrinsic aging, and together with photoaging may dramatically increase the apparent age of a menopausal woman.
Estrogen deficiency particularly affects the fibroblasts of the dermis, and thinning of the skin is primarily related to a decrease in the production of collagen. This decrease is relatedto a decline of bone mineral content with age, which can lead to the condition of osteoporosis. The fibroblasts are also responsible for the synthesis of the dermis ground substance, particularly glycoproteins and hyaluronic acid (which is able to bind water). The decrease in fibroblast activity with age accounts for the decreased dermal hydration.
Skin elasticity decreases with age, but the effect is more marked in women than in men.
In the epidermis, a lack of estrogen slows down the activity of the basal keratinocytes,and consequently leads to epidermal atrophy. This atrophic fragile skin is less well protected by the normal surface film of lipids, because of the slow decline in sebum secretion experienced by everyone as they age. The stratum corneum barrier is less effective, and the skin may develop reactions to irritants, particularly if skin care has been inadequate or too aggressive.

SUN EXPOSURE AS A MAJOR CAUSE OF SKIN AGING AND POSSIBLE PREVENTION STRATEGIES

The skin is subject to the same aging process as other body tissues. The skin is also   directely influenced by  additional environmental facors accelerating the aging process, of which sunlight is the most important

Repeated exposure to ultraviolet radiation in sunlight causes skin to age prematurely-a condition called photoaging. Photoaged skin has wrinkles, brown spots, changes in pigmentation and surface roughness. These skin changes are not part of the natural, normal aging process.

The most likely cause for the visible wrinkling associated with photoaging is the breakdown of collagen-the major structural material in skin. Ninety-five percent of the dermis, or underlying layer of skin, is made of collagen.

Ultraviolet radiation in sunlight triggers a molecular chain reaction which produces large amounts of enzymes called matrix metalloproteinases (MMPs). MMPs break apart and degrade collagen. While skin has a natural ability to repair damaged collagen, these repairs are never perfect.

Tiny amounts of at first invisible scar tissue build up over time and eventually become visible as wrinkles (photoaging).

U-M scientists found that MMP levels in dermal skin were directly associated with the length and frequency of exposure to ultraviolet light. Exposure to small amounts of UV (too small to cause skin redness) every other day was enough to induce sustained MMP production at high levels in the individuals in this study.

Pretreating skin with retinoic acid before UV exposure inhibited production of MMPs and resulting collagen damage by 70 to 80 percent in the U-M study. Because it blocks MMP production, retinoic acid should also prevent photoaging, although more research will be needed to know for sure.

The possibility of photoaging prevention is a surprising outcome of this study. Retinoic acid is already approved by the FDA to treat photoaging that has already happened. But until now, the possibility that vitamin A and retinoic acid might prevent photoaging has not been seriously considered.

While retinoic acid blocks MMP production, it has no effect on the skin's ability to produce enzymes called Tissue Inhibitors of MetalloProteinases (TIMPs) which naturally prevent MMP-induced collagen damage. Retinoic acid may prevent photoaging by reducing amounts of harmful enzymes in the dermis, while maintaining normal levels of tissue-protecting proteins (TIMPs).

Future research will attempt to discover how retinoic acid blocks MMP activation when skin is exposed to ultraviolet light. U-M scientists are exploring the role played by a protein called AP-1, which "turns on" genes in skin cells causing them to produce both MMPs and TIMPs.

These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease. This information is nutritional in nature and should not be construed as medical advice. This notice is required by the Federal Food, Drug and Cosmetic Act.