Skin Care and Treatments of Melbourne Dermatology - Oxidative Stress and Free Radical Damage

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Oxidative Stress and Free Radical Damage

Oxidative Stress and Free Radical Damage

As research into aging continues, more and more evidence seems to support the "Free Radical Theory" of aging, first proposed in 1956.

Tuesday, 8 September 2009

Theories of Aging

The National Institute of Health recognizes 20-30 different theories of aging.

It is important to realize that all these mechanisms are still classed as theories.

Many theories of aging, such as the "Wear and Tear Theory" (simply stated — as body parts are used, they wear out as a car wears out with use) have been abandoned as incorrect.

Two theories are favored presently because scientific research has given them support.

These are the "Free Radical Theory" and the "Neurohumoral Theory".

Tuesday, 8 September 2009

The "Free Radical" Theory of Aging

The "Free Radical Theory" states that, with accumulated free radical damage and oxidative stress biochemical and cellular processes begin to do more "incorrect" things as aging damage accumulates.

Most free radical damage occurs during times of the most active metabolic turnover.

In the human, this would be in early puberty for males and in pre-puberty and early puberty for females.

Also during this time, we possess the most physiologic reserve.

However, as damage accumulates, our physiologic reserve becomes depleted.

Thus, a 20-year-old faced with a trauma or biochemical assault can accommodate and recover faster than an 80-year-old, whose physiologic reserve has been depleted.

The "Free Radical Theory" was originally postulated by Denham Harman.

Monday, 29 October 2007

"Neurohumoral" Theory of Aging

The "Neurohumoral Theory of Aging" says that our biochemical processes, especially enzymatic and other hormonal reactions, begin to give incorrect or incomplete messages as we age.

This increases over time as we age and damage accumulates.

Many experts have pointed out that free radical damage is the cause of this biochemical decline.

Thus, this theory may really be viewed as a subset of the "Free Radical Theory".

Wednesday, 5 March 2008

The Cause of Disease

Diseases begin to develop as more and more oxidative stress accumulates in one organ system.

When a critical amount of damage occurs, we can identify an actual disease, such as diabetes, atherosclerosis, stroke, cancer, etc.

These diseases just mentioned are all "diseases of aging".

Some diseases are the result of simple insult to the organism, such as infections or injury from predators or trauma.

Infections and predation are not the result of aging, but involve the risks of living in one’s environment.

As the average lifespan of our species has increased, we have seen the appearance of the diseases of aging.

These particular diseases occur in the older members of our population and are really not seen with any frequency in younger persons.

But, as our average lifespan increased, we began to develop these diseases, all of which are caused by free radical damage.

Probably more than any other disease, cancer is a disease of aging.

Old lab animals, such as mice and rats, in very controlled environments, mostly all die with cancer.

Wednesday, 19 August 2009

Inflammation

Presently, there are two hot topics in medical literature regarding the development of disease.

One of these involves free radical damage.

The other is inflammation.

As free radical damage occurs and cells and tissues are damaged, the organism attempts to clear away the damaged cells.

In order to do this, various inflammatory pathways are activated.

  1. The body’s own cells are sent to the site of damage to "clean up".
  2. These cells release various chemicals that cause inflammation.
  3. The inflammation further destroys and liquefies the damaged tissue so it may be removed.

However, inflammation is never restricted only to the damaged cells but also spills over to involve surrounding healthy tissue.

Thus, inflammation, although designed for a specific task that is helpful, may actually cause harm itself.

In the medical literature, more research is being published regarding the limiting of oxidative stress and inflammation as a way of ultimately protecting functional tissue.

Thursday, 8 October 2009

Sources of Free Radical Damage

By far, most free radical damage comes from the cell’s own metabolism.

Our cells take the oxygen inspired by the lungs and use it in enzymatic reactions to burn fuel (glucose, fat, or even protein) and create energy.

Each cell uses its energy to perform its own individual function.

Nature did not make us totally efficient in the use of energy, however. Each cell makes extra energy to insure it will be able to perform its function.

As energy is created, radicals (very high-energy molecules) are created.

More are generated than are needed. The extra ones "spin off" into the interior of the cell, combining with whatever structure they strike, damaging that structure.

These extra packets of energy are termed "free radicals" because they are not committed to any particular ongoing biochemical reaction.

Being of very high energy, they combine with whatever they first touch.

Free radical damage can be thought of as a natural consequence of living and breathing in an oxygen-rich environment.

Sunday, 11 October 2009

The Skin and Free Radical Damage

The skin, being the body’s first environmental defense, is also exposed to other sources of free radical damage.

Still, the vast majority of each cell’s damage comes from its own internal metabolic creation of energy.

Other sources of free radical damage to the skin include solar damage, ozone, pollutants, applied substances (for example, some sunscreens) and other toxins.

Also, smoking is critical in damaging cells and tissues.

Every puff of cigarette smoke contains enough free radicals for a "free radical hit" to every cell of the body.

Thursday, 8 October 2009

Definition of Oxidative Stress

Nature has created each organism with mechanisms to deal with free radical damage.

These biochemical reactions that absorb free radicals can be classified in a variety of ways.

Intrinsic antioxidants include superoxide dismutase (SOD), glutathione, catalase and peroxidase.

These are manufactured within the cells of the organism itself for the purposes of cellular protection.

A condition of "oxidative stress" exists when more free radicals exist than can be neutralized by the various types of antioxidants.

We are always in a state of "oxidative stress" since the number of free radicals is never exactly matched by the number of antioxidants.

There are always excess free radicals causing damage and the slow decline of the organism, also known as aging.

Thursday, 31 July 2008

Antioxidants Can Be Harmful

Antioxidants Can Be Harmful

Antioxidants can potentially prevent the cellular cycle of free radical damage to skin that produces skin cancer, visible symptoms of aging skin (mainly photoaging) and a variety of other skin diseases.

Oral and topical antioxidant supplements are popularly thought beneficial or harmless, however a mounting body of evidence and clinical experience suggests non-dietary and topical antioxidants can indeed be harmful.

Raising antioxidant levels in the skin and body can be pro-oxidant, accelerating aging, damage and the likelihood of cancer, yet increasing numbers of consumers believe ingesting and applying more antioxidants to their skins can only be better:

By any measure, some individuals utilizing purportedly antioxidant skin care regimes have some of the worst skin we have ever seen — skin that improves when said regimes are stopped.

Whether their skin be visibly and chronically red, dull, unusually reactive or appearing different or unusual but not better, individuals often persist in using unsuitable antioxidant skin care products.

Beauty therapy, word of mouth, overly simplistic cosmetic analyses and mass media advertising's endless propagation of false ideas about skin and aging are the root source of antioxidant-stimulated skin problems which would never have otherwise emerged.

In the past, beauty therapy and the department store's niche had been to spend an exorbitant amount of time and effort spinning their clients' wheels in the mud with nonsensical ineffective treatments that were made to ring true due to their expense, luxurious, clinical or international flavour.

Luckily, most of the "treatment" supplied was not actively harmful, but it did distract skincare users enough to prevent them from ever attaining actual care of their skin, securing technically unnecessary, permanent deterioration under an ever-changing, disingenuous guise of "skin care."

In the present day, clinics often push cosmeceuticals and antioxidants as the latest penultimate and universally-suitable thing, despite the unchanging organic nature of skin, and despite a flagrant (usually total) lack of expertise required to avoid harm.

Similarly, consumers find "clinically-trialled" and apparently scientific products desirable, however the real-world efficacy of even medically trialled products is often below popular expectations.

Trials and comparisons surrounding idebenone, for example, are inherently flawed — Allergan's Prevage frequently causes acne and irritation, and CosmeceuTechs' Priori are unable to prove actual and consistently superior antioxidant protection.

The skin disease of people applying oxidized and home-made antioxidant skincare is a niche epidemic among obsessive skincare users — fostered online — that is yet to be fully appreciated.

Undesirable effects may not be visible to the untrained eye because topical antioxidant formulas can also produce exfoliation and moisturisation which can mask underlying changes.

Indeed, many cosmetics users are happy to see any change occurring and are often told that temporarily worse skin is a requirement to progress, however not all side effects are appropriate.

Strivectin's Facial Antioxidant marketing claims "facial anti-oxidants can virtually reverse the hands of time" however antioxidants simply do not treat existing skin damage, such as wrinkles.

Guidelines for Antioxidant Use

  • Avoid indiscriminate oral antioxidant supplementation — speak to your health care provider before taking supplements to treat or prevent any condition or disease.

  • Topical antioxidants do not actively reverse existing skin aging and cannot replace sunscreens to prevent aging.

  • Compounding biologically active antioxidants (or other ingredients) at home for topical application is a foolhardy practice.

  • Most mild and low-dose topical purported antioxidants are not irritating, however their users don't appear to avert considerable aging either — particularly if antioxidants are chosen by brand rather than individual relevance or if use is inconsistent.

  • Effective use of topical antioxidants generally requires higher concentrations of multiple antioxidant ingredients and is highly dependent on:

    • skin type;

    • condition;

    • the nature of the patient's environmental exposure;

    • overall skin care and procedure use;

    • initial specialist analysis and ongoing follow up.

Realising more than a small degree of benefit and avoiding undesirable effects from antioxidants requires ongoing specialist assessment and care.

Considerably effective antioxidant skin care protocols are substantially revised over time and make use of multiple brands — a practice which greatly increases results while typically lowering cost.

Until more is known, medically unmonitored use of antioxidants in skin care should be restricted to one gentle formula amidst sunscreen.

Tuesday, 17 March 2009

The Free Radical Cascade / The Importance of Antioxidants

The abbreviated chemical reactions below illustrate the accumulation of free radical damage and oxidative stress.

For our first free radical, we’ll use the oxygen radical, written with an asterisk (*) indicating it contains very high energy.

The O* is of such high energy that it immediately combines with whatever structure it first touches.

  • In combining with this structure, it damages it and, in the process, another free radical is created.
  • This second free radical, being also of very high energy, combines with the first structure it touches.

The process continues as shown below.

  1. O* + cell membrane / damaged cell membrane + A*

    cell membrane protects integrity of cell.

  2. A* + mitochondria / damaged mitochondria + B*

    mitochondria produces energy for the cell.

  3. B* + DNA damaged DNA + D*

    DNA is the genetic mechanism of the cell which directs all cellular function and reproduces itself to create another cell — damaged DNA leads to a cancerous or malignant cell.

  4. D* + cellular protein/collagen/elastin / damaged elastic tissue (wrinkles) + E*

This process continues forever as cellular structures are damaged by free radicals and more free radicals are created.


However, an antioxidant combines with O* at the beginning of this process, neutralizing this entire cascade and preventing all of the ensuing damage.

For this reason, antioxidants are crucial to maintaining cellular function as we age (and, from the time of birth, we are all aging).


Below is a very simple drawing of a cell to illustrate the location of the cellular components mentioned above in the reaction describing damage from oxidative stress.

Any of the body’s cells could be used to illustrate these general principles, but a skin cell is illustrated here.

Remember that a skin cell, being near the surface of the body, is bombarded with additional stressors from the environment that fail to reach other cells far within the organism’s interior.

IS Clinical Skin Cell Diagram

Saturday, 23 August 2008

Cell Structure / Oxidative Damage / The Importance of Antioxidants

IS Clinical Skin Cell Diagram

A few additional facts should be noted about the structure of the cell as it pertains to oxidative damage and antioxidants.

They are listed here:

  1. All membranes are designed to enclose a part of the cell (as mitochondria, nucleus) or the cell itself.

Membranes are lipid-soluble (fat-soluble).

If they become damaged, they have difficulty protecting their interior structures, as well as letting the right substances in and keeping other substances out of cellular components.

Lipid-soluble antioxidants protect these and all other lipid-containing structures.

An example of a lipid-soluble antioxidant is Vitamin E, although there are also many other lipid-soluble antioxidants.

  1. The interior of cellular structures, including the interior of the cell itself, contain much water. Therefore, aqueous (water-soluble) antioxidants protect these areas. An example of an aqueous antioxidant would be Vitamin C.
  2. The DNA portion of the cell in the chromosomes of the nucleus not only directs the cell’s function but also directs the reproduction of the cell so that other similar cells can be made.

    In the case of the example above, the function of this cell is to make collagen.

    If the DNA is damaged, it may direct the formation of collagen containing "mistakes".
  3. Biochemically inaccurate collagen would be unable to function properly; it might have poor elasticity (causing wrinkles) or be unable to bind with other collagen chains (causing wrinkles, loss of resilience, improper scarring).
  4. If the mitochondria is damaged, the cell is unable to produce energy as it should. Energy is required for the cell and all of its parts to function. Also, the mitochondria, in producing energy, creates radicals as an energy source. Nature designed us to make extra energy and this unused energy begins cellular damage inside the cell’s boundaries.
  5. Once any free radical (such as solar rays, oxygen free radicals, radicals from smoking, etc.) touches the cell, the cascade of free radical damage begins, as illustrated in the above reactions.

Primary antioxidants can quench free radicals before they touch the cell or inside the cell.

It is important to have antioxidant protection at all cellular layers because it is impossible to stop all free radicals at the surface.

Many of them get through the initial skin barrier or come from inside the cell itself via cellular metabolism.

Saturday, 29 December 2007

The Importance of The RIght Antioxidants (Highly Individualized Medically Managed Protocols)

Antioxidants can be ingested (taken orally) or applied topically to the skin.

Of ingested antioxidants, only about 1% reach the surface of the skin.

To increase antioxidant protection, it is also necessary to apply effective topical antioxidants to the skin.


Good antioxidants for the skin must be of high:


There are also unique issues in formulating antioxidants to be used topically.

  • Remember that the skin’s primary function, simply put, is to keep some substances in and to keep other environmental agents out.

This makes the design of topical antioxidants particularly challenging.

The skin’s own nature works against allowing formulated topical antioxidants to pass to the interior of the cell, where they can do the most good.

Wednesday, 7 November 2007

The Lifespan Curve

In 1900, the average lifespan was about 45 years.

For someone born today, it is about 85.

There are some differences between populations in various parts of the world and between males and females.

The biggest increase in "average life expectancy" came with the development of sewage systems.

As our average lifespan has increased, sweeping social changes have resulted.

A life plan and the individual life events for a person expecting to live to be 85 or 90 is much different than that for an individual who will most likely die before 45.

Society’s challenges are much different as we face an aging population, many of whom will maintain excellent health into their later years.


Each species has a "species-specific maximum lifespan".

The maximum lifespan is the age at which the mitochondria inside the organism’s cells shut down and stop producing energy.

Although there must be some terminal event, individuals reaching the maximum lifespan for their particular species will die.

  • For humans, the maximum lifespan is 120 years.
  • For chimpanzees, it is about 45.
  • For rats, it is about 3 years.
  • For some types of parrots, it is about 105 years.

There is some interesting work discussing why some species can live longer than others.

Interestingly, there are also species that do not really age. Examples would be the Galapagos tortoise and the rockfish.

These species don’t seem to get "older"; they simply get bigger. Of course, they are living in the wild so they have a high rate of death from predation and natural events.

Breaking through the species-specific lifespan involves genetic manipulation.

In the last few years, Michael Rose at UC Irvine has extended the maximum lifespan of fruit flies and Cynthia Kenyon at UCSF has done the same for Nematode worms.

This research has received a tremendous amount of attention because, in the past, we thought the maximum lifespan for a species could not be exceeded.

The Lifespan/Survival Curves A, B, C and D illustrates these principles.

These survival curve is for the human species.

Each species has a species-specific maximum lifespan, or the longest any member of the species can live before its mitochondria shut down, cellular energy production stops and the organism dies.

For humans, the species-specific maximum lifespan is 120 years...

IS Clinical — The Lifespan Curve

Friday, 5 June 2009

Lifespan Curve A — Neanderthal Wo(Man)

IS Clinical Lifespan Curve

Curve A is for Neanderthal Man who, on average, lived about 17 years.

This was enough to reach puberty, mate and produce offspring, thus passing on the genetic material of the species.

Infant mortality was very high as were death rates from predation, accidents and infections.

Mother Nature has designed us, and other species, primarily to live long enough to pass on our DNA so the species continues.

After that, it’s up to us.

In zoos, where predation and natural accidents have mostly been removed, the average lifespan of animals easily doubles immediately.

Tuesday, 30 October 2007

Lifespan Curve B — Sewers and Household Plumbing

IS Clinical Lifespan Curve

Sewers and household plumbing helped increase the average lifespan of humans to 45 years about 1900.

This is shown by Curve B on the graph.

Tuesday, 30 October 2007

Lifespan Curve C — Contemporary Wo(Man)

IS Clinical Lifespan Curve

Curve C is our present survival curve.

Since 1900, we have:

  • developed antibiotics;
  • work has become less hazardous;
  • other social developments have occurred that prolong life.

Wednesday, 7 November 2007

Lifespan Curve D — Virtually Utopic?

IS Clinical Lifespan Curve

Curve D is the "ideal" lifespan curve for man.

Here, all members of the species would reach the maximum lifespan of 120 years.

In order to do this, disease would have to be eliminated.

Sick animals (and humans) die; healthy ones life longer than their ill counterparts.

At 120 years, all members of the species die because the mitochondria quit.

Monday, 29 October 2007

Hindsight and Empowered Knowledge: From Curve C to D

Getting a species to Curve D involves a number of sweeping social changes as byproducts of "squaring the lifespan curve".

When almost everyone lives to 120, individuals have time for several careers, perhaps several families, may live in a variety of locations, etc.

Finding cures for all diseases can alternately be described as curing aging or curing the diseases of aging, such as diabetes, heart disease, stroke, cancer, etc.

It also probably involves considerable lifestyle modification, such as dietary changes, not being sedentary, etc.


Getting past Curve D and increasing the maximum lifespan involves genetic manipulation.

  • Michael Rose of UC Irvine has increased the maximum lifespan of fruit flies;
  • Cynthia Kenyon of UCSF has increased the lifespan of Nematode worms.

Even though it may seem that work with fruit flies or worms would not apply to humans, the same principles are applicable to all species to some degree.

Others have also manipulated maximum lifespan.

Much of this work has centered around genetically helping the organisms cells to make more intrinsic antioxidants, such as SOD (superoxide dismutase).

Monday, 29 October 2007

Oxidative Stress and Free Radical Damage — Reference List

Available from Melbourne Dermatology — Oxidants and Antioxidants in Cutaneous Biology, J Thiele and P Elsner (eds.), Current Problems in Dermatology, G. Burg (ed.), Vol. 29, Karger: Basel, London, NY, 2001.

The Biology of the Skin, RK Freinkel, DT Woodley (eds.), Parthenon Publishing: NY, London, 2001.

Oxidative Stress and Aging, RG Cutler, L Packer, J Bertram, A Mori (eds.), Molecular Biology Updates, Birkhauser Verlag: Basel, Boston, Berlin, 1995.

Friday, 13 March 2009

Oxidative Stress/Damage Theory of Aging Disproven by Study

The National Institute of Health recognizes 20-30 different theories of aging, among which the "Free Radical" and "Neurohumoral" theories have been given the most support.

Supplement, food and cosmetics industries (a category encompassing cosmeceutical brands) and their consumers have come to regard the Free Radical Theory of Aging as universally accepted.

This acceptance has led to rapid expansion and uptake of products and services with little or no realization that the mechanisms by which antioxidants may work are all still classed as theories.

In reality, science increasingly disproves the current free radical theory of aging and moreover has pointed to harmful effects of some antioxidant use.

Antioxidant skin care use is sometimes clearly deleterious, yet users will maintain their use due to some degree of inattention, reliance on poor or inadequate information, unrealistic product passion, peer factors or a plain inability to equate a relatively high purchase price with uselessness for skin.

One of the prime dermatologic proponents of the free radical theory of aging and moreover it's role in inflammation is Dr. Nicholas Perricone, founder of N.V. Perricone Cosmeceuticals and author of The Wrinkle Cure, among a growing collection of books.

The Free Radical Theory holds that, with accumulated free radical damage and oxidative stress, biochemical and cellular processes begin to do more "incorrect" things as aging damage accumulates.

Researched published by Dr. David Gems of University College London's Ageing Laboratory in the Journal of Genes and Development (see below) finds that antioxidants themselves are not "anti-aging".

In contrast with the universal acceptance of the free radical theory of aging, Dr. Gems states that:

"The fact is that we don't understand much about the fundamental mechanisms of ageing... The free radical theory of ageing has filled a knowledge vacuum for over fifty years now, but it just doesn't stand up to the evidence... One of the hallmarks of ageing is the accumulation of molecular damage, but what causes this damage?... It's clear that if superoxide is involved, it only plays a small part in the story. Oxidative damage is clearly not a universal, major driver of the ageing process. Other factors, such as chemical reactions involving sugars in our body, clearly play a role... It really demonstrates finally that trying to boost your antioxidant levels is very unlikely to have any effect on ageing."

Examples of Superoxide-Scavenging Antioxidants

Skin care products, supplements and foods containing alpha-tocopherol (Vitamin E), ascorbic acid (Vitamin C), propyl gallate and Trolox. (Vitamin E Analogue).

Some Recommendations for Antioxidant Skin Care Use

  • Antioxidants do not reverse aging and increasingly do not appear to prevent aging by themselves, however optimal, careful and managed use may help stimulate your skin's own defenses;

  • If using antioxidants, avoid over-emphasizing the use of any one kind (for example, do not apply a serum containing only Vitamin E or C alone, as these can increase damage) — this usually means using a variety of brands, rather than just one or two;

  • Analogues and derivatives of naturally-occurring antioxidants increasingly appear to be of much less value than nature-identical forms;

  • Avoid use of oxidized antioxidant skin care products — unfortunately, these appear to comprise a significant proportion of those used (stock should be fresh, packaging should omit air — many Vitamin C products should be used within weeks of manufacture, not months);

  • Keep in mind that commonplace use of antioxidant skin care products do not replicate, or only very mildly and transiently reproduce the results of trials published into the ingredients contained within said products;

  • Avoid excessive antioxidant or cosmeceutical skin care use unless your skin is scientifically assessed for irritation (laser doppler allows for this measurement);

  • Never attempt to make your own antioxidant skin care products by purchasing raw materials and combining them into bland base creams or other products — more or stronger is not necessarily better.

Further Information

Antioxidants "Cannot Slow Ageing" — BBC.

Dr. David Gems of University College London's Ageing Laboratory.

A Year of Photoprotection — Results from Topical Vitamin C (as Ascorbic Acid) and Sunscreen Use.

Against the oxidative damage theory of aging

Against the oxidative damage theory of aging: superoxide dismutases protect against oxidative stress but have little or no effect on life span in Caenorhabditis elegans

Doonan R, McElwee JJ, Matthijssens F, Walker GA, Houthoofd K, Back P, Matscheski A, Vanfleteren JR, Gems D.

Institute of Healthy Ageing and Research Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, United Kingdom;

The superoxide radical (O(2)(-)) has long been considered a major cause of aging. O(2)(-) in cytosolic, extracellular, and mitochondrial pools is detoxified by dedicated superoxide dismutase (SOD) isoforms. We tested the impact of each SOD isoform in Caenorhabditis elegans by manipulating its five sod genes and saw no major effects on life span. sod genes are not required for daf-2 insulin/IGF-1 receptor mutant longevity. However, loss of the extracellular Cu/ZnSOD sod-4 enhances daf-2 longevity and constitutive diapause, suggesting a signaling role for sod-4. Overall, these findings imply that O(2)(-) is not a major determinant of aging in C. elegans.

PMID: 19056880

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