Cosmetic
`ermatology
`
`EUNSUNG 1013
`
`Cheryl M.Burgess Editor
`
`) Satta
`
`1
`
`EUNSUNG 1013
`
`

`

`Cheryl M. Burgess (Ed.)
`
`Cosmetic Dermatology
`
`2
`
`

`

`Cheryl M. Burgess (Ed.)
`
`Cosmetic
`Dermatology
`
`With 35 Figures and 33 Tables
`
`3
`
`

`

`Cheryl M. Burgess, M.D., F.A.A.D.
`2311 M Street
`NW Suite 504
`Washington, D.C. 20037
`USA
`
`Library of Congress Control Number: 2004115994
`
`ISBN 3-540-23064-5 Springer Berlin Heidelberg New York
`
`This work is subject to copyright. All rights are reserved, whether the whole or part of the
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`
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`
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`
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`
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`
`4
`
`

`

`Preface
`
`Two years ago, this book was merely a concept,
`fueled by the clinical needs of a new and young-
`er generation seeking cosmetic procedures and a
`desire to share my own clinical experiences with
`botulinum toxin and soft tissue augmentation.
`As the concept evolved, the number of topics did
`likewise, expanding the book’s scope. With mul-
`tiple topics, additional contributing authors
`were recruited. In contemplating the level of
`writing effort required, I had to ask myself:“How
`will this book differ from existing cosmetic der-
`matology textbooks”? Patients’ changing demo-
`graphics coupled with technological advance-
`ments and new FDA product approvals for der-
`matology have created an overwhelming need
`for cutting-edge information. This book at-
`tempts to fill the information deficit.
`Today’s demographics are transforming rap-
`idly.Aging is no longer associated with frailty and
`impaired ability; growing old no longer means
`looking old.While the stigma associated with be-
`ing “old” is decreasing, patient demand for cos-
`metic enhancements is increasing,particularly in
`the younger generation who seek interventions at
`the earliest signs of aging. Additionally, by 2050,
`the U.S. Census Bureau predicts non-Caucasian
`populations will comprise greater than 50% of
`the total population. Ethnic, racial, and gender
`differences present new challenges and necessi-
`tate changes in clinical techniques: practitioners’
`skills must accommodate demographic shifts lest
`clinical interventions falter.
`This book’s eight chapters focus on cutting-
`edge approaches to assessment and treatment
`of the earliest signs of aging. Topics selected
`represent areas where technology and im-
`proved understanding of cellular biology have
`advanced considerably in the past two decades.
`Chapters, although distinct, are unified by sev-
`eral important themes:
`
`쐽 Newer, noninvasive clinical interventions
`and therapeutics offer viable alternatives
`for younger patients seeking cosmetic
`enhancements. These entry-level proce-
`dures often accommodate patients’ clini-
`cal needs as well as life styles (e.g., time
`away from work).
`쐽 With changing patient demographics,
`matching clinical technique to patients’
`unique skin type, tone, and color is cru-
`cial. When possible, recommendations
`reference the Fitzpatrick rating scale.
`쐽 Patients seeking cosmetic enhance-
`ments have definite expectations, and
`patient counseling is imperative. Manag-
`ing patient expectations is medically
`ethical and essential. Apart from discuss-
`ing obvious issues of procedures, contra-
`indications, and potential adverse ef-
`fects, dermatologists must convey a re-
`alistic assessment of predicted outcome
`and determine if patients have similar
`expectations. Although time-consuming,
`informed consent procedures cannot be
`short circuited.
`쐽 Cosmetic dermatology is a field with few
`established treatment algorithms. Unlike
`other medical specialties where clinical
`guidelines are standardized by expert
`consensus panels, dermatologists must
`evaluate each patient on a case-by-case
`basis and strategize accordingly. Detailed
`treatment planning must include patient
`participation.
`
`5
`
`

`

`VI
`
`Preface
`
`The chapters are also united in another impor-
`tant but unique dimension: all authors are
`women and each has had one or more of the
`procedures discussed. Equally significant is the
`authors’ diverse ethnic and racial mix: African
`American, Latino, Jewish, and Caucasian. Why
`female authors who are ethnically and racially
`diverse? These experiential characteristics add
`a depth of understanding and insight that tran-
`scend technique and credentials. Each author
`firmly believes her experiences strengthen
`therapeutic relationships with patients. Authors’
`personal self-selected dermatological proce-
`dures coupled with their gender, racial, and eth-
`nic experiences resulted in each refining, modi-
`fying, and improving clinical techniques within
`their specialties, bringing an experiential clini-
`cal richness that otherwise would be lacking.
`Chapter 1,“Anti-aging Medicine As It Relates
`to Dermatology,” by Rafaela M. Quiroga, dis-
`cusses the clinical science of anti-aging medi-
`cine emphasizing the physiological impact of
`free radical damage and the importance of diet,
`exercise, and lifestyle changes in the aging pro-
`cess. Jeannette Graf continues the discussion of
`anti-aging in Chap. 2,“Anti-aging Skin Care In-
`gredient Technologies,” focusing on molecular
`changes at the cellular level and the impact of
`nutrients upon physiological processes. Topic
`discussion goes beyond antioxidants and free
`radical damage and focuses on the role of pep-
`tides, beta-glucan, polyphenols, and other mo-
`lecular structures of cell life.
`“Photoaging and Pigmentary Changes of the
`Skin”(Chap. 3), by Susan C. Taylor, begins by first
`differentiating clinical characteristics between
`intrinsic aging and photoaging and then pro-
`ceeds to a comprehensive discussion of the
`clinical characteristics of photoaging and pig-
`mentary changes in Asians, African Americans,
`and Caucasians.
`The history of chemical peels dates back to
`the Egyptians and has become increasingly
`popular in the arena of anti-aging medicine.
`Chapter 4, “Chemexfoliation and Superficial
`Skin Resurfacing,” by Paula E. Bourelly and An-
`gela J. Lotsikas-Baggili, reviews chemical peel-
`ing agents and techniques. Since its introduc-
`tion in 1995, microdermabrasion has gained
`popularity and is also covered.
`
`In Chap. 5, “Botulinum Toxin,” I cover the
`history, science, and treatment of botulinum
`toxin. Indications, patient selection, pretreat-
`ment considerations, postinjection considera-
`tions, complications, and adverse reactions are
`highlighted. Along with botulinum toxin, my
`specialty includes tissue augmentation. Tissue
`augmentation offers an alternative to invasive
`surgical procedures for facial aging and is the
`fastest growing segment among plastic and
`dermatologic procedures. In “Soft Tissue Aug-
`mentation” (Chap. 6), I discuss numerous aug-
`mentation options, ranging from natural to
`synthetic fillers, which confront practitioners.
`Treatment considerations surrounding perma-
`nent and temporary fillers are also highlighted.
`Chapter 7, “Laser Skin Resurfacing,” by Tina
`S. Alster and Seema Doshi, details ablative and
`nonablative technologies. Ablative technology
`has historically led to excellent clinical out-
`comes, particularly with one or a combination
`of the CO2 and Er:YAG lasers, although these
`procedures usually require significant down-
`time. Younger patients desiring less aggressive
`methods of photo rejuvenation or procedures
`resulting in less downtime are good candidates
`for the rapidly evolving nonablative proce-
`dures. Results achieved with nonablative tech-
`nology, however, are subtler and take several
`months. Side-effects profiles can be significant
`with both approaches, and the importance of
`clinical technique, postoperative treatment, and
`patient selection are detailed.
`“Sclerotherapy,” Chap. 8, by Jonith Breadon,
`first reviews physiological factors involved in
`the development of varicose veins, a condition
`affecting up to 60% of the population, which is
`associated with pain, lipodermatosclerosis, ve-
`nous ulcerations, thrombophlebitis, and deep
`vein thrombosis. Jonith Breadon’s discussion of
`specific techniques, treatment planning, and
`patient evaluation offers insights that even vet-
`eran practitioners will find useful.
`Collectively, these eight chapters meet the
`needs of a diverse target audience. Those wish-
`ing information on a single topic only will find
`the chapters can be read independently. Der-
`matologists seeking to broaden their expertise
`will find the presentations up to date, well re-
`searched, and clinically relevant. The chapters
`
`6
`
`

`

`Preface
`
`VII
`
`do not offer “how to” instruction, but practi-
`tioners will find a plethora of issues to consider
`that will assist them in clinical decision mak-
`ing. Dermatologists by no means have a
`monopoly on cosmetic enhancements. Other
`cosmetic specialties will find much useful in-
`formation that will enrich their patient consul-
`tations and clinical practice. Finally, this book
`will benefit dermatology residents and medical
`students alike as these topics are core to most
`medical training curricula.
`Many of today’s treatment interventions were
`nonexistent just 20 years ago. Like other medi-
`
`cal specialists, today’s cosmetic dermatologists
`are practicing in a time when diagnostics and
`treatment advances are exploding at an expo-
`nential rate. It is truly an extraordinary time for
`dermatologists and their patients – a time filled
`with exciting challenges and options. And I
`hope this book in some small way conveys both
`the excitement and the challenge!
`
`Cheryl M. Burgess, M.D.
`November 2004
`
`7
`
`

`

`Contents
`
`1 Medicine As It Relates
`to Dermatology   .  .  .  .  .  .  .  .  .  .
`Rafaela M. Quiroga
`
`2 Anti-aging Skin Care Ingredient
`Technologies   .  .  .  .  .  .  .  .  .  .  .  .
`Jeannette Graf
`
`3
`
`Photoaging and Pigmentary
`Changes of the Skin   .  .  .  .  .  .  .  .
`Susan C. Taylor
`
`4 Chemexfoliation and Superficial
`Skin Resurfacing   .  .  .  .  .  .  .  .  .  .
`Paula E. Bourelly,
`Angela J. Lotsikas-Baggili
`
`Botulinum Toxin   .  .  .  .  .  .  .  .  .  .
`Cheryl M. Burgess
`
`Soft Tissue Augmentation   .  .  .  .  .
`Cheryl M. Burgess
`
`83
`
`93
`
`Laser Skin Resurfacing   .  .  .  .  .  .  . 111
`Tina Alster, Seema Doshi
`
`Sclerotherapy  .  .  .  .  .  .  .  .  .  .  .  . 127
`Jonith Breadon
`
`5
`
`6
`
`7
`
`8
`
`1
`
`17
`
`29
`
`53
`
`Subject Index   .  .  .  .  .  .  .  .  .  .  .  .  .  . 167
`
`8
`
`

`

`List of Contributors
`
`Tina Alster, M.D., F.A.A.D.
`(e-mail: Tina.alster@skinlaser.com)
`2311 M Street, NW Suite 200
`Washington, D.C. 20037, USA
`
`Jeannette Graf, M.D., F.A.A.D.
`(e-mail: JOG88@aol.com)
`88 Bayview Ave.
`Great Neck, NY 11021, USA
`
`Paula E. Bourelly, M.D.
`(e-mail: pbourelly@yahho.com)
`2412 Norbeck Farm Place
`Olney, MD 20832, USA
`
`Angela J. Lotsikas-Baggili, M.D.
`(e-mail: lotsikaa@yahoo.com)
`1610 Grace Church Road
`Silver Spring, MD 20910, USA
`
`Jonith Breadon, M.D.
`2525 N. Lincoln Ave.
`Chicago, IL 60614, USA
`
`Cheryl M. Burgess, M.D., F.A.A.D.
`(e-mail: Cheryl.burgess@
`ctr4dermatology.com)
`2311 M Street, NW Suite 504
`Washington, D.C. 20037, USA
`
`Rafaela M. Quiroga, M.D.
`(e-mail: rafaeladermdoc@hotmail.com)
`5353 Columbia Pike Suite #604
`Arlington VA 22204, USA
`
`Susan C.Taylor, M.D.
`(e-mail: Drstaylor1@aol.com)
`932 Pine Street
`Philadelphia, PA 19107, USA
`
`Seema Doshi, M.D.
`Washington Institute of Dermatologic Laser
`Surgery, Washington, D.C., USA
`
`9
`
`

`

`Chapter 1
`
`Anti-Aging Medicine As It Relates
`to Dermatology
`Rafaela M. Quiroga
`
`1
`
`Core Messages
`
`쐽 Anti-aging medicine physicians, scien-
`tists, and researchers are dedicated to
`the belief that the process of physical
`aging in humans can be slowed, stop-
`ped, or even reversed through existing
`medical and scientific interventions.
`
`쐽 Possible theories of the aging process
`include the free radical theory of
`aging, oxidation, cell senescence, and
`cleavage of telomere during DNA syn-
`thesis.
`
`쐽 A good diet slows the aging process
`and adds healthier years to life.
`
`쐽 A therapeutic guide for vitamin sup-
`plements and recommended anti-
`aging doses is provided.
`
`Contents
`
`1.1
`
`1.2
`
`1.3
`
`1.4
`1.4.1
`
`1.5
`
`1.6
`1.6.1
`1.6.2
`1.6.3
`1.6.4
`
`Introduction . . . . . . . . . . . . . .
`
`The Clinical Science
`of Anti-Aging Medicine
`
`. . . . . . . .
`
`The Aging Process
`
`. . . . . . . . . . .
`
`Free Radical Theory of Aging . . . . .
`Antioxidizing Processes . . . . . . . .
`
`Diet and Nutrition . . . . . . . . . . .
`
`Hormonal Regulation of Aging . . . .
`Adrenopause . . . . . . . . . . . . . .
`Menopause . . . . . . . . . . . . . . .
`Andropause . . . . . . . . . . . . . . .
`Somatopause . . . . . . . . . . . . . .
`
`2
`
`2
`
`2
`
`3
`3
`
`3
`
`4
`5
`5
`5
`6
`
`1.7
`
`1.8
`
`1.9
`
`1.9.1
`
`1.10
`
`1.11
`
`Growth Hormone in the Aging Process
`
`Consequences
`of Reduced Growth Hormone Secretion
`on the Skin . . . . . . . . . . . . . . .
`
`Can Human Growth Hormone Reverse
`. . . . . . . . . .
`the Effects of Aging?
`. . .
`Growth Hormone Secretagogues
`
`Side Effects
`of Growth Hormone Therapy . . . . .
`
`A Brief Guide
`to Anti-Aging Supplements
`and Growth-Hormone-Releasing
`Nutrients for the Skin . . . . . . . . .
`
`. . . . . .
`Oral Antioxidant Nutrients
`1.12
`Vitamin C . . . . . . . . . . . . . . . .
`1.12.1
`1.12.1.1 Food Sources . . . . . . . . . . . . . .
`1.12.1.2 Risks with High Doses . . . . . . . . .
`1.12.2
`Vitamin E . . . . . . . . . . . . . . . .
`1.12.2.1 Role in the Body and Consequences
`of Deficiency . . . . . . . . . . . . . .
`1.12.2.2 Recommended Daily Allowance . . . .
`1.12.2.3 Food Sources . . . . . . . . . . . . . .
`1.12.2.4 Risks with High Doses . . . . . . . . .
`1.12.2.5 Interactions with Other Nutrients
`and Drugs . . . . . . . . . . . . . . . .
`Carotenoids . . . . . . . . . . . . . . .
`1.12.3
`1.12.3.1 Role in the Body and Consequences
`of Deficiency . . . . . . . . . . . . . .
`1.12.3.2 Recommended Daily Allowance . . . .
`1.12.3.3 Food Sources . . . . . . . . . . . . . .
`1.12.3.4 Risks with High Doses . . . . . . . . .
`1.12.4
`Selenium . . . . . . . . . . . . . . . . .
`1.12.4.1 Role in the Body and Consequences
`of Deficiency . . . . . . . . . . . . . .
`1.12.4.2 Recommended Daily Allowance . . . .
`1.12.4.3 Food Sources . . . . . . . . . . . . . .
`1.12.4.4 Risks with High Doses . . . . . . . . .
`1.12.4.5 Interactions with Other Nutrients . . .
`
`1.13
`
`1.14
`
`Glycemic Index . . . . . . . . . . . . .
`
`Final Remarks
`
`. . . . . . . . . . . . .
`
`References . . . . . . . . . . . . . . . .
`
`6
`
`6
`
`8
`8
`
`9
`
`10
`
`10
`10
`11
`11
`11
`
`11
`11
`12
`12
`
`12
`12
`
`12
`13
`13
`13
`13
`
`13
`13
`13
`14
`14
`
`14
`
`14
`
`14
`
`10
`
`

`

`2
`
`Rafaela M. Quiroga
`
`1 O ld age is the most unexpected of
`
`all things that happen to man.
`Leon Trotsky
`
`’’
`
`1.1 Introduction
`
`Changes in diet and increasing exercise, togeth-
`er with a regimen of antioxidants, nutritional
`supplements, and growth factors, can alter how
`the genes express themselves. Both factors can
`greatly enhance the healing capability of the
`skin and can improve the results of cosmetic
`surgeries.
`Beyond the obvious advantages of a bal-
`anced diet and exercise there are the physiolog-
`ical ones that help people feel more alive with
`renewed and vital well-being.
`
`1.2 The Clinical Science
`of Anti-Aging Medicine
`
`Anti-aging medicine is practiced by physicians,
`scientists, and researchers dedicated to the be-
`lief that the process of physical aging in hu-
`mans can be slowed, stopped, or even reversed
`through existing medical and scientific inter-
`ventions. This specialty of medicine is based on
`the very early detection and prevention of age-
`related diseases. Physicians practicing anti-ag-
`ing medicine seek to enhance the quality of life
`as well as its length, limiting the period of ill-
`ness and disability toward the end of one’s life.
`Anti-aging medicine encompasses
`lifestyle
`changes (diet and exercise); hormone replace-
`ment therapies, as needed, determined by a
`physician through blood testing (DHEA, melat-
`onin, thyroid, human growth hormone, estro-
`gen, testosterone); antioxidants and vitamin
`supplements; and testing protocols that can
`measure not only hormone levels and blood
`chemistry but every metabolic factor right
`down to the cellular level.
`
`1.3 The Aging Process
`
`Aging can be viewed as the accumulation of
`changes in cells and tissues resulting from a
`greater disorderliness of regulatory mecha-
`nisms that result in reduced robustness of the
`organism to encountered stress and disease.
`The notion of greater disorderliness in aging is
`illustrated by the erosion of the orderly neuro-
`endocrine feedback regulation of the secretion
`of luteinizing hormone (LH), follicle stimulat-
`ing hormone (FSH), adrenocorticotropic hor-
`mone (ACTH) and growth hormone (GH).
`These changes are manifested as menopause,
`andropause, adrenopause, and somatopause.
`Skin aging is part of the slow decline in ap-
`pearance and function that appears to be at-
`tributed in large part to the drastic decline of
`hormones in the body after adulthood. At the
`cellular level, several processes are involved in
`the physiology of aging and the development of
`some age-related diseases. The process of apop-
`tosis signifies the process of nontraumatic and
`noninflammatory cell death [1].
`Dysregulation of apoptosis has been impli-
`cated in the increased incidence of cutaneous
`malignancies that are more prevalent in older
`individuals, such as basal cell carcinoma, squa-
`mous cell carcinoma, and malignant melano-
`ma. Cell senescence limits cell divisions in nor-
`mal somatic cells and may play a central role in
`age-related diseases. Telomeres are thought to
`play a role in cellular aging and might contrib-
`ute to the genetic background of human aging
`and longevity. It has been speculated that the
`limited proliferation potential of human cells is
`a result of the telomere shortening that occurs
`during DNA synthesis at each cell division.
`Photoaging may accelerate the shortening of
`telomeres and push cells into senescence soon-
`er. That could be the reason why various growth
`factors may affect the speed and quality of
`wound healing [2]. Biochemical insults also
`arise within aging cells, in part from the action
`of reactive oxygen species generated and scav-
`enged incompletely throughout the cell cycle.
`Aging-associated changes also occur between
`and among cells via alterations in the intercel-
`lular matrix,
`the intercellular exchange of
`
`11
`
`

`

`Anti-Aging Medicine As It Relates to Dermatology
`
`Chapter 1
`
`3
`
`trophic factors, the release of inflammatory cy-
`tokine mediators, and the degree of infiltration
`by other associated cell types. In addition, the
`quantity and distribution of various growth
`factors may affect wound healing [2]. Decline of
`DNA repair in combination with loss of mela-
`nin increases the risk of photocarcinogenesis
`and can also cause the decline of enzymatically
`active melanocytes (10–20% each decade) that
`contributes to increased sensitivity to ultravio-
`let (UV) radiation.
`However, it is not known why free radical
`damage does not adversely affect all of the
`body’s cells (e.g., gonadal germ cells) [3].
`
`1.4 Free Radical Theory of Aging
`
`Antioxidizing nutrients are believed to play a
`role in the prevention and treatment of a varie-
`ty of chronic diseases. The proposed mecha-
`nism by which antioxidants protect cells from
`oxidative stress is by scavenging free radicals
`and halting lipid peroxidation chain reactions,
`which can cause DNA damage [4].
`
`1.4.1 Antioxidizing Processes
`
`Two forms of chemical reactions, oxidation and
`reduction, occur widely in nature. Oxidation is
`the loss of electrons, and reduction is the gain
`of electrons. Oxidation and reduction reactions
`always occur in pairs. Highly reactive mole-
`cules can oxidize molecules that were previous-
`ly stable and may cause them to become un-
`stable species, such as free radicals. A free radi-
`cal is a chemical with an unpaired electron that
`can be neutral, positively charged, or negatively
`charged. Thus, without termination by an agent
`such as an antioxidant, a single free radical can
`damage numerous molecules. A certain amount
`of oxidative function is necessary for proper
`health. For example, oxidation processes are
`used by the body’s immune systems to kill mi-
`croorganisms [5].
`Cells contain a number of antioxidants that
`have various roles in protecting against free
`radical reactions. The major water-soluble anti-
`
`oxidant metabolites are glutathione (GSH) and
`vitamin C (ascorbic acid), which reside primar-
`ily in the cytoplasm and mitochondria. Many
`water-soluble enzymes also catalyze these reac-
`tions. Glutathione peroxidase catalyzes the re-
`action between GSH and hydrogen peroxide to
`form water and oxidized GSH, which is stable
`[6].Vitamin E and the carotenoids are the prin-
`cipal lipid-soluble antioxidants. Vitamin E is
`the major lipid-soluble antioxidant in cell
`membranes that can break the chain of lipid
`peroxidation. Therefore, theoretically, it is the
`most important antioxidant in preventing oxi-
`dation of these fatty acids.Vitamin E is recycled
`by a reaction with vitamin C [7].
`Despite the actions of antioxidant nutrients,
`some oxidative damage will occur, and accu-
`mulation of this damage throughout life is be-
`lieved to be a major contributing factor to aging
`and disease [6].
`
`1.5 Diet and Nutrition
`
`A good diet slows aging and can improve over-
`all success of surgical procedures and wound
`healing. Among other benefits, a good diet:
`
`쐽 Provides the food, water, and oxygen that
`cells need to reproduce, transmit infor-
`mation, and repair damage
`쐽 Assures the body of a continuous supply
`of usable energy, which improves emo-
`tional stability and energy levels
`쐽 Helps eliminate free radical damage,
`damage that can increase risk of cancer
`and other degenerative diseases
`쐽 Decreases the risk of cancer, arterioscle-
`rosis, hypertension, heart disease, osteo-
`porosis, senility, and depression
`쐽 Synchronizes the body, helping people
`function physically, mentally, and emo-
`tionally at peak efficiency
`쐽 Adds healthier years to life
`
`12
`
`

`

`4
`
`1
`
`Rafaela M. Quiroga
`
`The diet that will most support healthy longev-
`ity follows these principles: It’s nontoxic. That
`means it contains a minimum of preservatives,
`additives, pesticides, antibiotics, food coloring,
`and chemical flavoring. The diet should contain
`enough nutrients to satisfy daily needs. Since
`most fresh fruits and vegetables lose much of
`their nutritional value within hours after being
`picked, it is necessary to supplement with vita-
`mins and minerals.
`According to the American Journal of Public
`Health, studies show that less than one-third of
`Americans meet the U.S. government’s Healthy
`People 2000 goal of eating five or more servings
`of fruits and vegetables per day; people eat only
`1.2 servings of fruits and 3.1 servings of vegeta-
`bles daily.
`Another element of the healthy diet benefi-
`cial for women should be soy proteins due to
`the phytoestrogens that regulate endogenous
`estrogen production, which is helpful in easing
`hot flashes and hormonal acne associated with
`menopause. Topical estrogen induces an in-
`crease in skin thickness through proliferation,
`resulting in decreased rhytids. Scientists at the
`University of Pennsylvania School of Medicine
`found that soybeans contain a protease inhibi-
`tor called the Bowman-Birk inhibitor, which is
`so versatile against various cancers that it has
`been dubbed “the universal cancer preventive
`agent.”
`Natural fats provide a concentrated form of
`energy and create the environment in which fat
`soluble vitamins can be digested; they also pro-
`vide the essential fatty acids that the body uses
`to maintain its cellular structure. Examples of
`fat are “saturated,” from dairy, meat, and fish
`products; “unsaturated,” from vegetable and
`fish oils; “polyunsaturated,”, such as sunflower
`seed oil and sesame seed oil; and “hydrogenat-
`ed,” such as margarine and highly heated or re-
`heated fats.
`The American Heart Association and the
`National Cholesterol Education Project recom-
`mend that the “prudent” diet for everyone, re-
`gardless of gender, race, or age, should not ex-
`ceed 300 mg of cholesterol daily and 65 mg to-
`tal fat for the person who eats an average of
`2,000 daily, inclusive of 22 g of saturated fat.
`
`1.6 Hormonal Regulation of Aging
`
`Aging involves a decline of GH, which causes
`the immune system response to decline and the
`amount of oxygen and free radicals to increase.
`The skin suffers from the consequences of the
`decline in GH, which is reduced nourishment
`and repair of cells in the different tissues. The
`overall functions of the skin decrease with ag-
`ing. The decline is noted in cell replacement,
`sensory perception, thermal regulation, and
`chemical clearance. Also, there is a higher
`threshold for pain, predisposing to skin irrita-
`tions, ulcerations, and wounds [8].
`Additional changes of skin aging include
`flattening of the dermal–epidermal junction,
`which decreases the contact surface between
`the dermis and epidermis. This change may
`compromise communication and nutrient
`transfer between skin layers. There is a decrease
`in epidermal filaggrin, a protein required to
`bind keratin filaments into macrofibrils, that
`contributes to skin dryness and flaking. In ad-
`dition, there is an increased dermal separation
`that may cause increased blistering or tearing.
`The endocrine system regulates body com-
`position, fat deposition, skeletal mass, muscle
`strength, metabolism, body weight, and physi-
`cal well-being. Multiple endocrine changes
`evolve with aging in all species and, not surpris-
`ingly, some of the physiologic manifestations of
`aging are related to the effects of declining hor-
`mone levels. The central nervous system (CNS)
`regulates the pituitary gland, which secretes
`hormones to target tissues that, in turn, pro-
`duce substances that feed back on the hypotha-
`lamic–pituitary axis. This feedback-control
`network can be assessed via novel entropy sta-
`tistics.
`In humans, aging is associated with a de-
`crease in the gonadal production of estrogen in
`females (menopause) and testosterone in males
`(andropause), the adrenal production of dehy-
`droepiandrosterone (DHEA) and DHEA sulfate
`(DHEA-S) (adrenopause), and a decrease in the
`activity of the GH/insulin-like growth factor
`(IGF) axis (somatopause). Replacing hormones
`that decline with age had been shown to have a
`
`13
`
`

`

`Anti-Aging Medicine As It Relates to Dermatology
`
`Chapter 1
`
`5
`
`broad anti-aging and anti-disease effect on the
`skin and in the body. As a result, hormone re-
`placement regimens are being developed as a
`strategy to delay or prevent some of the conse-
`quences of aging.
`
`1.6.1 Adrenopause
`
`The enzymatic machinery of the adrenal zona
`reticularis fails in aging men and women. How-
`ever, the ability of the zona fasciculata to pro-
`duce cortisol is preserved (based on ACTH in-
`fusion, insulin tolerance, and metyrapone test-
`ing). Mineralocorticoid and glucocorticoid re-
`ceptors in the hippocampus are variably down
`regulated in aging humans. Excessive lifelong
`adrenal cortisol feedback on the brain may ex-
`acerbate the aging-associated loss in neuronal
`synapses and plasticity. Potential implications
`of aging skin includes a decrease in vascular re-
`sponsiveness due to involution of the dermal
`vascular bed, which decreases thermoregula-
`tion and contributes to skin pallor; there is a
`decrease in subcutaneous fat and changes in
`distribution that may limit conductive heat loss
`that decreases the protective ability in bony ar-
`eas such as the ischial tuberosities; and there is
`a delayed recovery of the stratum corneum’s
`function as a barrier, which may increase the
`penetration of certain types of topical medica-
`tions leading to systemic absorption [9].
`
`1.6.2 Menopause
`
`There is still no known biochemical signal that
`reliably indicates the onset of menopause. How-
`ever, serum FSH levels tend to rise in regularly
`menstruating as well as premenopausal women
`(42–50 years of age). The pulsatility and order-
`liness of LH release also change before men-
`strual cyclicity falters [10]. Estrogen secretion
`in perimenopause is variable and includes
`intervals of increased production. A greater
`stimulation by FSH may increase follicular
`aromatase activity and induce estrogen excess
`while inhibin concentrations fall perimenopau-
`sally and contribute to heightened FSH release.
`
`Physical complaints such as breast tender-
`ness, irregular menstrual bleeding, dyspareu-
`nia, and hot flushes may precede the onset of
`anovulatory cycles in perimenopause in addi-
`tion to emotional concerns such as disrupted
`sleep, fatigue, tension, and irritability, which are
`equally represented among menopausal wom-
`en in North America [11]. Skin changes that
`may occur include hyperpigmentation as well
`as wrinkles, laxity, pallor, and pruritus. These
`changes are associated with estrogen depriva-
`tion, which leads to decreased skin elasticity
`and blood supply [12]. Histologically, although
`the stratum corneum is unaltered in thickness,
`there is apparently a slow replacement of neu-
`tral lipids adversely affecting the barrier func-
`tion [13, 14].
`
`1.6.3 Andropause
`
`In the hypogonadal male, reduced libido is of-
`ten accompanied by diminished well-being
`and/or depression that may be relieved by an-
`drogen replacement [15]. Cognitive decline, vis-
`ceral obesity, osteopenia, and relative sarcope-
`nia also accompany androgen deficiency in ag-
`ing [16]. These conditions respond favorably to
`androgen supplementation, especially in men
`with very low testosterone levels [17]. Enhanced
`physical performance has not been established
`in this context. Few studies have examined
`whether testosterone supplementation enhanc-
`es cognitive function in elderly men [18]. Al-
`though it appears that neoplastic transforma-
`tion of prostate tissue is not elicited by physio-
`logic testosterone repletion, proliferation of ex-
`isting androgen-responsive carcinomas may be
`stimulated. Thus, a normal prostate-specific
`antigen (PSA) and prostatic digital examina-
`tion should precede any androgen treatment in
`older individuals.
`Skin decreases in elasticity, extensibility, and
`turgor. Appendages, including hair follicles, ap-
`ocrine, and eccrine glands, are decreased in
`number. Pacinian and Meissner’s corpuscles,
`responsible for pressure and light touch sensa-
`tion, are similarly decreased. The epidermis
`may exhibit variable thickness, cell size, and
`shape with occasional nuclear atypia.
`
`14
`
`

`

`6
`
`1
`
`Rafaela M. Quiroga
`
`1.6.4 Somatopause
`
`1.7 Growth Hormone
`in the Aging Process
`
`Gender markedly influences GH secretion in
`young adults. Premenopausal women exhibit a
`two-fold less rapid decline than men in daily
`GH production with increasing age. Young
`women also manifest less vulnerability to the
`suppressive effects of increased total body fat
`and reduced physical fitness on GH secretion
`[19].An important ongoing clinical issue relates
`to the uncertain role of sex-hormone deficien-
`cy in the aging-related impoverishment of GH
`and IGF-I production in both women and men
`[20]. Preliminary data from clinical studies
`raise the possibility that combined GH and an-
`drogen repletion in older men can have an ad-
`ditive effect on increasing muscle mass [19].
`Levels of the nutritional signaling peptide
`leptin, mostly produced in white adipose tissue,
`conveys signals to the hypothalamus about fat
`stores and, in response, hypothalamic efferents
`regulate food intake and energy expenditure.
`Leptin inhibits the hypothalamic release of the
`orexigenic (appetite-inducing) peptide neuro-
`peptide Y (NPY) and activates the sympathetic
`nervous system. The latter stimulates lipolysis
`in adipose tissue via the beta-3 adrenergic re-
`ceptor, cAMP accumulation, and increased ac-
`tivity of mitochondrial uncoupling protein
`(UCP)-3, thus generating heat (which is dissi-
`pated) rather than ATP (whic