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Aging Skin
By: Michael Lam, MD, MPH

Table of Contents

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Information presented here is for general educational purposes only. Each one of us is biochemically and metabolically different. If you have a specific health concern and wish my personalized nutritional recommendation, write to me by clicking here.

Aging Skin

The aging of our skin can be divided into two broad processes:
Chronological Aging and Photo-Aging.

1. Chronological aging represents the structural, functional, and metabolic changes in the skin that parallel the aging and degenerative changes in other body organs. Symptoms of chronological aging include:

Dry and Thin Skin. While young skin renews itself every three to four weeks, older skin takes four to six weeks to renew itself. The top layers lose more moisture due to the aging process, and older skin has a dryer and more dehydrated appearance.

Fine Wrinkles. Diminished production of collagen leads to fine wrinkles initially observed around the eyes (commonly known as "crow's feet"), forehead, and other sun-exposed areas. More pronounced effects include furrows at the site of facial expression lines and sagging folds over the eyelids, neck, jaw, and arms.

Abnormal Blood Vessels. Within the many small, delicate blood vessels supplying nutrients to the skin, abnormalities develop. This is particularly conspicuous over the nose and cheeks.

Age Spots. These are pigmentations that surfaced as a result of a decrease in the number and function of pigment cells in sun-exposed areas.

Benign and malignant skin tumors due to the deterioration of the skin's immune system.

Successful restoration of youthful skin from this perspective must address a variety of key issues including: collagen replacement, strengthening the vascular walls of small blood vessels that supply the skin, increasing vascular supply for oxygenation and detoxification purposes, increasing immunity to reduce cancer risks, and reducing oxidative damage to the skin

2. Photo-aging is a separate process and largely involves damage to the collagen and elastin fibers in the skin. While genetics play a significant role, the amount of wrinkles present is highly dependent on the amount of sun exposure. The lines in a "lived-in face," especially for those who spend a considerable amount of time outdoors, is a consequence of oxidative damage due to overexposure to ultraviolet (UV) sunlight - both UVA (responsible for tanning, wrinkling, and melanoma) and UVB (responsible for sunburn and basal and squamous cell carcinoma). UV light may further damage skin by increasing the production of proteolytic enzymes that break down collagen, the connective tissue located beneath the dermis.

Successful retardation of photo-aging can be achieved by wearing a sunscreen of SPF of 15 or more, and by avoiding direct and indirect exposure to the sun for extended periods of time.

How Wrinkles Develop

The skin is made up of multiple layers of cells that are constantly going through self shedding and regeneration once every 30 days or so in repeated cycles. The layers can be broadly divided into two sections - the top epidermis and the underlying dermis.

Histological studies of the skin show that a wrinkle is formed following a series of major cellular changes:

During the sub-clinical phase of aging (from age 35-45), there is a gradual and progressive slowing of cellular turnover and regeneration. This results in the skin getting thinner. As a result, the normally undulating ridge-like dermal-epidermal interface (DEI) becomes flatter. This flatness reduces the surface area of nutritional exchange between the underlying dermis on the bottom and the epidermis on top.

Reduced nutrition to the epidermis from aging is one factor that causes cellular exhaustion and weakness. Without proper nutrition to the epidermis, cellular metabolism of the epidermal cell is slowed. Furthermore, the transportation of certain unwanted byproducts of cellular metabolism such as free radical is reduced. The accumulation of such free radicals within the cell can lead to undesirable mutational damages in the cell and ultimately cancer.

The adhesion between in the DEI is normally supplied by collagen IV (a multi-sheet structure or basal layer) and collagen VII (anchored to the sheets structure). The progressive loss of nutrients to this area slows the circulation of the messengers that serve to promote the neo-synthesis process of such collagen. A vicious cycle is set up. Without an optimal amount of collagen, the skin sags even more, propagating the dearth of nutrients.

Paradoxically, matured aging skin contains more elastin, which the body uses to fill in the empty space left by the deficiency of collagen. Such elastin, unfortunately, is fragmented, calcified, and contains excessive lipids.

In addition to the loss of skin thickness due to lack of collagen support, the aging skin is more loose and lacks elasticity. These two properties are hallmarks of wrinkles.

This process of aging and appearance of wrinkles is accelerated during the clinical phase of aging (age 45 and higher). By age 50, very few women can escape wrinkles. The difference only lies in the degree of the blemish.

A wrinkle, very simply, is caused by the reduction of collagen.


Collagen is a major body protein. There are 19 forms of collagen, and it accounts for almost 20% of the total protein in our body. In addition to its critical role in forming support structure of the skin, it is also the main constituent of the extra-cellular matrix.

Collagen is characterized by its high proline content, which constitutes about one third of the amino acids. Its triple helix, rope-like structure contains protein organized in bundles that are anchored to each together at right angles and held in place by inter-fiber cross linkages. The most abundant collagen is Type I Collagen.

The spatial arrangement of the collagen network also depends on the presence of supporting macromolecules known as proteoglycans and glycoaminoglycans (GAGs).

Collagen is a much better support structure than GAGs. GAGs are a water-saturated gel in which water soluble molecules, hormones, peptides, and ions circulate. During the aging process, the diminished amount of collagen is gradually replaced by the weaker GAGs. This reduction in the quantity of collagen and replacement with alternative but weaker macromolecules results in skin that is less thin and less elastic. With age, this gel, due to its weak support structure, tends to sag, and cellular metabolism and mitosis is compromised. Furthermore, if water intake is insufficient, the links in the collagen network, like those of a net cast into the sea, collapse as the net is only "kept open" in the presence of water and collapses upon itself in a dehydrated environment.


Fibroblasts are mesanchymatous cells within the dermatological meshwork. They are the basic building blocks involved in numerous mechanisms, including fibrogenesis, tissue contraction, and tissue skeleton building. They also have a role in epithelial differentiation, leading to collagen formation. After tissue damage has occurred, whether it be through acute forces such as trauma, or chronic forces such as aging, stress, and oxidative damage, the fibroblasts possess an unique ability to change their phenotype and become myofibroblasts, thereby contributing actively to the repair process. In the case of wound injury, it would form granulation tissue to enhance wound contraction and synthesis of macromolecules in connective tissue such as GAGs.

Researchers have observed for years that fibroblasts in aged tissue do not produce as much collagen. However, after they have been isolated from their tissue and exposed to endogenous stimulating factors such as TGFb, they once again produce significant amounts of collagen, especially Type I Collagen (the predominant collagen in reconstructed healthy skin) based on a good DEI (where collagens IV and VII are abundant).

Message from Dr. Lam

I hope you have enjoyed reading this article. If you have areas you don't understand,
or if you have a specific health concern, feel free to write to me by clicking here.

About The Author

Michael Lam, M.D., M.P.H., A.B.A.A.M., is a western trained physician specializing in nutritional and anti-aging medicine. Dr. Lam received his Bachelor of Science degree from Oregon State University, and his Doctor of Medicine degree from the Loma Linda University School of Medicine in California. He also holds a Master’s degree in Public Health. He is board certified by the American Board of Anti-Aging Medicine where he has also served as a board examiner. Dr. Lam is a pioneer in using nontoxic, natural compounds to promote the healing of many age-related degenerative conditions. He utilizes optimum blends of nutritional supplementation that manipulate food, vitamins, natural hormones, herbs, enzymes, and minerals into specific protocols to rejuvenate cellular function.

Dr. Lam was first to coin the term, ovarian-adrenal-thyroid (OAT) hormone axis, and to describe its imbalances. He was first to scientifically tie in Adrenal Fatigue Syndrome (AFS) as part of the overall neuroendocrine stress response continuum of the body. He systematized the clinical significance and coined the various phases of Adrenal Exhaustion. He has written five books: Adrenal Fatigue Syndrome - Reclaim Your Energy and Vitality with Clinically Proven Natural Programs, The Five Proven Secrets to Longevity, Beating Cancer with Natural Medicine (Free PDF version), How to Stay Young and Live Longer, and Estrogen Dominance. In 2001, Dr. Lam established as a free, educational website on evidence-based alternative medicine for the public and for health professionals. It featured the world’s most comprehensive library on AFS. Provided free as a public service, he has answered countless questions through the website on alternative health and AFS. His personal, telephone-based nutritional coaching services have enabled many around the world to regain control of their health using natural therapies.

For More Information

For the latest Anti-Aging and Adrenal Fatigue related health issues, visit Dr. Lam at
Feel free to email Dr. Lam by clicking here if you have any questions.

© 2012  Michael Lam, M.D. All Rights Reserved.

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