July 18, 2018

Phytoceramides - Skin Rejuvenation From The Inside Out


As you age, your skin progressively loses natural lipids called ceramides.1-4 The result is visible aging that includes wrinkles, age spots, and rough, uneven skin.5-8

Ceramides are major skin components that help form the “glue” that holds surface cells together.9,10 Depletion of these molecules not only causes skin to wrinkle, but also makes it more susceptible to moisture loss, environmental allergens, skin diseases such as atopic dermatitis, and possibly cancer.5,11-13

For these reasons, ceramides have long been a key ingredient in expensive skin creams. The problem is that topical application may not penetrate deeply enough into the skin to effectively block wrinkle formation and skin aging.

Fortunately, plant-derived ceramides—or phytoceramides—have been developed that can be taken orally, ensuring that these potent molecules are absorbed into the bloodstream.14 Once absorbed, they are carried to the cells of the inner layer of the skin and subsequently seep to the outermost layer.14,15 These rejuvenating molecules reach skin all over the body, not just where creams are applied.

Oral phytoceramides effectively work from the inside out to hydrate, smooth, and rejuvenate aging and wrinkled skin.14,15

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Your Skin’s Natural Regeneration Molecules

As the years pass, ceramide production declines dramatically. Without substantial replenishment of ceramides, the mortar that holds the skin-cell bricks together deteriorates, and the skin moisture barrier becomes greatly compromised.9,14,16

The result is a thinning of your skin—with noticeable wrinkles, dryness, roughness, and even infection.14,17-19

Although ceramides are present in many of the foods we eat, including rice and wheat, they do not naturally occur in sufficient quantities to optimally rejuvenate aging skin.14 This means that slowing and reversing skin aging requires effective supplementation.

The Phytoceramide Breakthrough

To help prevent skin infections, skin dryness, and wrinkling, researchers have investigated the effectiveness of topically applying ceramides to the skin surface. What they discovered is that adding lipids such as ceramides directly to the skin can improve the moisture barrier function—but only modestly.14,20,21 The problem is that a topical ceramide application is not the body’s natural route for infusing the skin’s outer layer with ceramide molecules—that occurs from the inside out.

That’s why creams and lotions, applied to the outer surface of the skin, simply can’t match the steady supply of ceramides that naturally comes from healthy, youthful skin.

To solve this problem, researchers turned their attention to oral ceramides. Initially, research focused on identifying potentially useful oral ceramides only from animal sources.14 Then scientists switched to using a number of different ceramides available in grains such as rice, corn, and wheat.14,21 These plant-based ceramides are called phytoceramides.

In an important breakthrough, scientists developed a proprietary wheat-derived phytoceramide extract. Taken orally, it can reach the skin’s outer layer through the natural route—delivery by the bloodstream to the deepest skin-cell layers, then gently nudged into the extracellular matrix.14 There, it restores the barrier function.14

This innovation was achieved by using natural, nongenetically modified wheat as the raw material and producing an extract containing only purified oils.14 This extract is so purified it is classified as gluten-free by current government standards. A number of studies now validate the effectiveness of this novel phytoceramide.14,15,22

In a laboratory cell study, this wheat-derived extract was shown to hydrate human skin and restore its youthful structure after the skin cells’ protective barrier function had been disrupted.22

This study also found that wheat phytoceramides reduced levels of free radicals in the skin and inhibited elastase enzymes, which would ordinarily destroy elastin and contribute to loss of skin flexibility and increased wrinkling.23

Ceramides have also been shown to inhibit melanogenesis, the process by which the skin produces the hyperpigmentation behind age spots and other discolorations of the skin. This suggests that by replacing ceramides from the inside out, oral wheat-derived phytoceramides may inhibit or reverse the uneven pigmentation of skin aging.7,8,24

Scientists realized that if clinical trials validated these effects in humans, it would at last be possible to rejuvenate aging skin—simply by swallowing a capsule.

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Rejuvenate Skin From The Inside Out 

  • Natural skin-based lipid molecules—called ceramides—have shown critical capacity to preserve youthful-looking skin and strong defenses against certain skin diseases and infections. 
  • They critically maintain the water-retaining properties of the skin by blocking water loss from aging or physical trauma. 
  • As we age, the skin content of ceramides substantially decreases, and topically applied ceramide-containing creams have shown limited effectiveness. 
  • Natural phytoceramides can be taken orally, allowing them to enter the bloodstream where they are naturally transported through all layers of the skin, working from the inside out. 
  • Placebo-controlled, clinical studies show that oral wheat-derived phytoceramides boost skin hydration, smoothness, suppleness, and other measures of youthful skin. Ceramides also defend against skin-based infections and diseases. 

Phytoceramides’ Effectiveness Validated In Clinical Trials

To demonstrate wheat-derived phytoceramides’ effectiveness, investigators conducted experiments of the scientifically most rigorous type: double-blind, placebo-controlled, clinical studies.

In the first study, women with dry to very dry skin were given 200 mg daily of either a placebo or a powdered phytoceramide extract for three months. Skin hydration was then evaluated using three distinct methods: a special testing machine, a dermatologist’s examination, and the subjects’ own subjective scores.15

The women taking the phytoceramide extract experienced significant improvement in skin hydration as assessed by all three of these testing methods. Additionally, in the ceramide group, participants experienced significantly reduced dry patches, roughness, and itching.15 These changes were not seen in the placebo arm of the study. This placebo-controlled human data provided scientists with a clear indication that the phytoceramides had made their way through the bloodstream to the skin cells, where they provided a powerful rehydrating and rejuvenating effect.15

To confirm these remarkable results, another clinical trial evaluated the wheat-derived phytoceramide extract in its oil form.14 For the study, women with dry to very dry skin took 350 mg daily of the wheat ceramide oil, or a placebo, in a double-blind trial. Results were assessed after just three months of supplementation.14

First, researchers objectively measured skin hydration using a special technique known as corneometry. The supplement, but not the placebo, was shown to significantly increase skin hydration of the arms, legs, and the body overall. On the arms, skin hydration increased by more than  35%, compared to less than 1% in the placebo group.14

Second, researchers asked participants to rate their own perceptions of the effects of the supplement or placebo treatments. At all points of measurement in the study, the wheat phytoceramide oil extract provided greater improvement in all factors—facial skin hydration, leg skin hydration, suppleness, roughness, uniformity of complexion, itchiness, and overall state of the skin—without any significant adverse effects and with a superior level of acceptability.14

These controlled clinical trials delivered clear confirmation that orally taken wheat-derived phytoceramides substantially boost skin hydration, smoothness, suppleness, and other levels—reflecting reversal of age-related skin wrinkling, drying, and decline.14


Ceramides are components of specialized lipid molecules called sphingolipids, an essential element of human skin.41

The presence of ceramides as a category within sphingolipids was first discovered in the human brain in 1884.42 The ceramides that are found in both plants and the human body are now known to be structurally similar.19

All four layers of the epidermis contain ceramides, and they play a critical role in skin health by creating a barrier that reduces infection and helps to retain the skin’s moisture and smoothness.19 

Over a period of four weeks, new cells created at the deepest epidermal layer migrate upwards to form the top layer of the skin (the stratum corneum) where extracellular matrix lipids inhibit loss of water.43 By the time skin cells reach the skin’s surface, they become cornified or horn-like, transforming into protein-rich bricks tightly bound together by a layer of mortar composed of various lipids, up to 50% of which are ceramides.44

The primary function of the epidermis is to generate a relatively impermeable layer to protect the skin from dehydration and environmental stress.44 Ceramides play a critical role in this barrier function and in the retention of water by the stratum corneum.44

The aging process reduces the content of ceramides in the epidermal skin layers. This contributes to dry skin and dermatitis, and is a major cause of skin wrinkling.1-6,9-12

Research has shown that optimal amounts of ceramides, in relation to other lipids, in the top layer of the skin are required to maintain youthful and healthy skin.12,44

Wrinkled, dry, irritated, and sensitive skin often lacks ceramides. Topical application of ceramides has shown limited benefit. However, orally taken wheat-derived phytoceramides—both in powdered and oil form—have been clinically demonstrated to hydrate skin and promote more youthful appearance and smoothness.14,15

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Why You Need To Replace Age-Diminished Ceramides

Because ceramides are bioactive lipids,25 they are involved in much more than the appearance of the skin—and their age-related decline represents more than a mere cosmetic problem. Full functionality of the skin—which requires adequate ceramides and intact barrier function—helps regulate body temperature, synthesize optimum amounts of vitamin D, and provide critical sensory input from the environment.26-28

By contrast, falling ceramide levels expose one to health risks due to greater susceptibility to contact dermatitis from environmental chemicals, infectious microorganisms, and altered permeability to topically administered drugs.4,18,29 As shown in research, the outer layer (  stratum corneum) in aging human skin has decreased moisture content17,30,31 with greater susceptibility to inflammation32 and infection.19

Scientists have also determined that as humans age, their skin’s diminished lipid content—mostly a decreased level of ceramides4—results in reduced structural integrity.10,17,33 This loss of structural integrity exposes the skin to a greater threat from environmental assaults, such as low humidity, solvents, and detergents, and a much lower capacity to recover from them.11

Research suggests that the decline in ceramide content in mature skin4 may stem from a decline in the enzyme activity that normally promotes the delivery of ceramides in a usable form to the skin.34

To inhibit the loss of skin ceramides—and the wrinkling, moisture loss, and multiple health risks that occur as a result—it is essential to boost ceramide levels not just on the surface where lotions sit, but deep inside the skin cells beneath the stratum corneum.

In addition, maintaining youthful levels of ceramides in all layers of the skin promotes more than better appearance and feel—it powerfully blocks skin infections18 and other skin diseases.4,11


The outer layer of your skin (epidermis) plays a key role in maintaining homeostasis,45 the internal process that automatically modulates internal conditions to keep them constant and stable throughout your body. The skin surface, or stratum corneum, serves as a barrier between the external environment and the internal body. This barrier prevents water loss due to evaporation and inhibits foreign insults.9,45

Scientists often describe the structure of the stratum corneum as “bricks and mortar.”45 About 90% of the stratum corneum surface is made up of cells called keratinocytes.46 These are the “bricks” of the skin barrier. 

Between those cells are intercellular lipids that are made up of ceramides, free fatty acids, and cholesterol, all of which constitute the “mortar” that holds the “bricks” of your stratum corneum together.9 Ceramides comprise up to 50% of this vital intercellular material.44

This brick-and-mortar structure effectively prevents transepidermal water loss,9 unless impaired by damage to the stratum corneum, a tragic effect of skin aging. 

Protection Against Skin Infections And Diseases

Lipids at the skin’s surface, including ceramides, comprise a major part of an antimicrobial barrier, the first line of defense against infection. Age-related deterioration of this barrier raises the risk of numerous health conditions.11

For example, atopic dermatitis is characterized by reduced ceramide concentrations in the stratum corneum.12,35 Scientists suggest a correlation between this reduction and higher concentrations and colonization of Staphylococcus aureus in atopic dermatitis.12,36,37 This can be especially concerning because when skin barrier function is disrupted—as it is with diminished ceramide content—S. aureus has an increased potential for causing infections.38 In addition, disruption of skin barrier function is a risk factor for infection with various microorganisms including Streptococcus pyogenes.39

A scientific investigation into the pathogenesis of allergic contact dermatitis and other inflammatory skin conditions found that repairing the breakdown in the ceramide barrier, while continuing topical medications, could greatly alleviate atopic dermatitis.40 This is especially significant, because the topical corticosteroids and other immunosuppressive agents of mainstream therapy involve toxicity risks.


Ceramides are natural skin-based lipid molecules that have shown critical importance in preserving skin’s youthful appearance and texture, as well as providing strong defenses against skin diseases.

Their essential role is in the maintenance of water-retaining properties of the skin, protecting against water loss of both physical trauma and aging.

With age, the presence of ceramides in the skin decreases. However, topical creams that contain ceramides have shown only modest effectiveness.

When taken orally, phytoceramides are transported deep into the cells of all layers of the skin and work from the inside out.

Rigorous clinical studies show that oral wheat-derived phytoceramides increase skin hydration, smoothness, suppleness, and other measures of youthful skin. Ceramides may also protect against skin-based infections and diseases.

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  1. Rogers J, Harding C, Mayo A, Banks J, Rawlings A. Stratum corneum lipids: the effect of ageing and the seasons. Arch Dermatol Res. 1996 Nov;288(12):765-70.
  2. Denda M, Koyama J, Hori J, et al. Age- and sex-dependent change in stratum corneum sphingolipids. Arch Dermatol Res. 1993;285(7):415-7.
  3. Boireau-Adamezyk E, Baillet-Guffroy A, Stamatas GN. Age-dependent changes in stratum corneum barrier function. Skin Res Technol. 2014 Feb 12.
  4. Imokawa G, Abe A, Jin K, Higaki Y, Kawashima M, Hidano A. Decreased level of ceramides in stratum corneum of atopic dermatitis: an etiologic factor in atopic dry skin? J Invest Dermatol. 1991 Apr;96(4):523-6.
  5. Yarosh DB, Both D, Brown D. Liposomal ursolic acid (Merotaine) increases ceramides and collagen in human skin. Horm Res. 2000;54:318-21.
  6. Motta S, Monti M, Sesana S, Caputo R, Carelli S, Ghidoni R. Ceramide composition of the psoriatic scale. Biochim Biophys Acta. 1993 Sep 8;1182(2):147-51.
  7. Kim DS, Kim SY, Chung JH, Kim KH, Eun HC, Park KC. Delayed ERK activation by ceramide reduces melanin synthesis in human melanocytes. Cell Signal. 2002 Sep;14(9):779-85.
  8. Jeong HS, Choi HR, Yun HY, et al. Ceramide PC102 inhibits melanin synthesis via proteasomal degradation of microphthalmia-associated transcription factor and tyrosinase. Mol Cell Biochem. 2013 Mar;375(1-2):81-7.
  9. Coderch L, López O, de la Maza A, Parra JL. Ceramides and skin function. Am J Clin Dermatol. 2003;4(2):107-29.
  10. Rabionet M , Gorgas K, Sandhoff R. Ceramide synthesis in the epidermis. Biochim Biophys Acta. 2014 Mar;1841(3):422-34.
  11. Proksch E, Brandner JM, Jensen JM. The skin: an indispensable barrier. Exp Dermatol. 2008 Dec;17(12):1063-72.
  12. Choi MJ, Maibach HI. Role of ceramides in barrier function of healthy and diseased skin.  Am J Clin Dermatol. 2005;6(4):215-23.
  13. Guenther GG, Edinger AL. A new take on ceramide: starving cells by cutting off the nutrient supply. Cell Cycle. 2009 Apr 15;8(8):1122-6.
  14. Guillou S, Ghabri S, Jannot C, Gaillard E, Lamour I, Boisnic S. The moisturizing effect of a wheat extract food supplement on women’s skin: a randomized, double-blind placebo-controlled trial. Int J Cosmet Sci. 2011 Apr;33(2):138-43.
  15. Boisnic S. Clinical evaluation of a hydrating food supplement: double blind randomized study versus placebo. HITEX. 2005.
  16. Takagi S, Tojo H, Tomita S, et al. Alteration of the 4-sphingenine scaffolds of ceramides in keratinocyte-specific Arnt-deficient mice affects skin barrier function. J Clin Invest. 2003 Nov;112(9):1372-82.
  17. Leveque JL, Corcuff P, de Rigal J, Agache P. In vivo studies of the evolution of physical properties of the human skin with age. Int J Dermatol. 1984 Jun;23(5):322-9.
  18. Jennemann R, Rabionet M, Gorgas K, et al. Loss of ceramide synthase 3 causes lethal skin barrier disruption. Hum Mol Genet. 2012 Feb 1;21(3):586-608.
  19. Available at: http://www.fda.gov/ohrms/dockets/dockets/95s0316/95s-0316-rpt0275-04-Udell-vol211.pdf. Accessed August 25, 2014. 
  20. Yilmaz E, Borchert HH. Effect of lipid-containing, positively charged nanoemulsions on skin hydration, elasticity and erythema—an in vivo study.  Int J Pharm. 2006 Jan 13;307(2):232-8.
  21. Asai S, Miyachi H. Evaluation of skin-moisturizing effects of oral or percutaneous use of plant ceramides. Rinsho Byori. 2007 Mar;55(3):209-15.
  22. Boisnic S, Beranger JY, Branchet MC. Cutaneous hydration evaluation after a vegetal ceramide-based cream application on normal human skin tissue model maintained alive, submitted to a dehydration model. HITEX;2003.
  23. Boisnic S, Beranger JY, Branchet MC. Anti-elastase and anti-radicalar effect of ceramides. Product Research Report. HITEX;2005.
  24. Kim DS, Kim SY, Moon SJ, Chung JH, Kim KH, Cho KH, et al. Ceramide inhibits cell proliferation through Akt/PKB inactivation and decreases melanin synthesis in Mel-Ab cells. Pigment Cell Res. 2001 Apr;14(2):110-5.
  25. Bielawski J, Pierce JS, Snider J, Rembiesa B, Szulc ZM, Bielawska A. Comprehensive quantitative analysis of bioactive sphingolipids by high-performance liquid chromatography-tandem mass spectrometry. Methods Mol Biol. 2009;579:443-67.
  26. Charkoudian N. Skin blood flow in adult human thermoregulation: how it works, when it does not, and why. Mayo Clin Proc. 2003 May;78(5):603-12.
  27. Webb AR . Who, what, where and when-influences on cutaneous vitamin D synthesis.  Prog Biophys Mol Biol. 2006 Sep;92(1):17-25.
  28. Yu YD, Zhang YZ, Bi WD, Wu T. Functional sensory function recovery of random-pattern abdominal skin flap in the repair of fingertip skin defects. Exp Ther Med . 2013 Mar;5(3):830-4.
  29. Perry AD, Trafeli JP. Hand dermatitis: review of etiology, diagnosis, and treatment. J Am Board Fam Med 2009;22:325-30.
  30. Man MQ, Xin SJ, Song SP, Cho SY, Zhang XJ, Tu CX, et al. Variation of skin surface pH, sebum content and stratum corneum hydration with age and gender in a large Chinese population. Skin Pharmacol Physiol. 2009;22(4):190-9.
  31. Potts RO, Buras EM, Chrisman DA Jr. Changes with age in the moisture content of human skin. J Invest Dermatol. 1984 Jan;82(1):97-100.
  32. Available at: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0003734/. Accessed August 25, 2014. 
  33. Del Rosso JQ, Levin J. The clinical relevance of maintaining the functional integrity of the stratum corneum in both healthy and disease-affected skin.  J Clin Aesthet Dermatol. 2011 Sep;4(9):22-42.
  34. Yamamura T, Tezuka T. Change in sphingomyelinase activity in human epidermis during aging. J Dermatol Sci. 1990 Mar;1(2):79-83.
  35. Imokawa G. Lipid abnormalities in atopic dermatitis. J Am Acad Dermatol. 2001 Jul;45(1 Suppl):S29-32.
  36. Abeck D, Mempel M. Staphylococcus aureus colonization in atopic dermatitis and its therapeutic implications. Br J Dermatol. 1998 Dec;139 Suppl 53:13-6.
  37. Arikawa J, Ishibashi M, Kawashima M, Takagi Y, Ichikawa Y, Imokawa G. Decreased levels of sphingosine, a natural antimicrobial agent, may be associated with vulnerability of the stratum corneum from patients with atopic dermatitis to colonization by Staphylococcus aureus. J Invest Dermatol. 2002 Aug;119(2):433-9.
  38. Fritz SA, Hogan PG, Hayek G, et al. Staphylococcus aureus colonization in children with community-associated Staphylococcus aureus skin infections and their household contacts. Arch Pediatr Adolesc Med. 2012 Jun 1;166(6):551-7.
  39. Lamagni TL, Neal S, Keshishian C, et al. Severe Streptococcus pyogenes infections, United Kingdom, 2003-2004. Emerg Infect Dis. 2008 Feb;14(2):202-9.
  40. Chamlin SL, Kao J, Frieden IJ, et al. Ceramide-dominant barrier repair lipids alleviate childhood atopic dermatitis: changes in barrier function provide a sensitive indicator of disease activity. J Am Acad Dermatol. 2002 Aug;47(2):198-208.
  41. Novotny J, Hrabalek A, Vavrova K. Synthesis and structure-activity relationships of skin ceramides. Curr Med Chem. 2010;17(21):2301-24.
  42. Available at: http://www.oryza.co.jp/html/english/pdf/ceramide_clinical.pdf. Accessed August 25, 2014 
  43. Goldstein AM, Abramovits W. Ceramides and the stratum corneum: structure, function, and new methods to promote repair. Int J Dermatol. 2003 Apr;42(4):256-9.
  44. Feingold KR, Elias PM. Role of lipids in the formation and maintenance of the cutaneous permeability barrier. Biochim Biophys Acta. 2014 Mar;1841(3):280-94.
  45. Harding CR. The stratum corneum: structure and function in health and disease. Dermatol Ther. 2004;17(Suppl):6-15.
  46. Wong DJ, Chang H. Stem Book; 2009: Cambridge, MA. HY Skin tissue engineering.

March 21, 2018

Tretinoin (Retin-A), a Vitamin A Derivative, Reverses Signs of Skin Aging - Still

Retin-A (tretinoin) has been around for about 35 years now. And you know what? It works better than anything else! On Sale Now

Skin cells contain retinoid receptors that help regulate how the cell functions. As people age, their cells behave more erratically. “But consistent use of Retin-A helps normalize the cells,” said Dr. Min-Wei Christine Lee, a dermatologist in Walnut Creek, Calif.

Retin-A can improve skin texture and fade dark spots and freckles because it causes skin cells to turn over more rapidly. It shrinks dilated pores and improves cell turnover within the pores so they are less likely to clog and become blackheads and whiteheads. But what has earned Retin-A its long-held reputation is its ability to affect the retention of collagen.

Collagen is what gives skin its structure, firmness and elasticity. Repeated sun exposure breaks down collagen and, with age, cells produce less and less collagen to repair the damage. Skin wrinkles, sags and loses fullness.

Retin-A does double duty in helping to boost collagen. According to research at Michigan, it has the potential to stop photoaging before it starts. “The retinoids prevent the rise of collagenase after UV exposure,” Dr. Voorhees said. Collagenase is what breaks down collagen.

But regular use of a retinoid product also increases the amount of new collagen formed, research has found, and that new collagen will last for years.

Susan Hobbs, 56, of Royal Palm Beach, Fla., a retired firefighter, said she spends a lot of time outdoors, and has been using Retin-A for about 15 years. “And I really don’t have a lot of wrinkles, compared to other people my age," she said.

“I think that using Retin-A has made a big difference,” Ms. Hobbs said. “I think if I didn’t use it, the sun damage would have really taken its toll.”

The results are not just cosmetic. Dr. Voorhees said that retinoids have been used to treat precancerous skin cells. Studies show that after two years of use, those abnormal cells returned to normal.

So if Retin-A is so effective and so well studied, why isn’t everyone using it? Many dermatologists blame a lack of patient education. “It’s one of the most misunderstood drugs,” said Dr. Kenneth Beer, a dermatologist in Palm Beach, Fla., and a clinical investigator for Allergan, the maker of prescription Avage and Tazorac. He is also an Allergan shareholder. People use Retin-A too much, use it too often, experience negative side effects and then give up on it too soon, doctors say.

The problem with Retin-A is that it may actually make skin look worse — with redness, flakiness and peeling — for up to eight weeks. “But by 24 weeks, patients will see dramatic, marked improvements,” Dr. Lee said.

Ms. Hobbs said when she first started using Retin A, she broke out with severe acne. “I remember I called the doctor and told him I was going to stop using it because my face had never looked worse,” she said. But her doctor advised her not to give up. “And he was right,” Ms. Hobbs said. “In another couple of weeks, my skin cleared up.”

Manufacturers have come up with ways to make it more tolerable, less irritating and more effective. Brand-name prescription versions contain emollient moisturizers and have more-advanced delivery systems for getting the active ingredient into the skin. These additions are the main difference between generic Retin-A and the pricier name-brand versions (a large tube of a name brand will run about $150 versus about $80 for a generic).

But in every case, patience and common sense are required. “You need to take six weeks to ramp up very slowly, but people will glob it on every night from the start and then call their doctor in a panic that their skin is red and peeling,” Dr. Beer said.

Doctors generally recommend using no more than a pea-size dab for the entire face. They advise using the product once every three nights (or once a week if skin feels irritated) for a couple of weeks, then every other night, eventually working up to every night if the skin can handle it.

Dr. Cohen cautions that Retin-A is not recommended for pregnant women or people with rosacea (a condition that causes skin redness). He said it is wise to limit its use with other potential irritants, like glycolic acids and vitamin C. Many doctors recommend applying a moisturizer over Retin-A (especially the generic versions) to help soothe skin, but suggest first waiting at least 20 minutes for the product to be absorbed.

Doctors also warn that newly irritated skin requires vigilant sun protection, and there are some concerns that waxing while using Retin-A may tear the skin.

“I can’t say there’s anything on the horizon that will rival Retin-A,” Dr. Cohen said. “It’s exciting to see all the research going into this area, but kind of funny that the thing we’re still recommending most is something that’s 30 years old.”

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January 12, 2018

Novel Strategy To Restore Youthful Facial Contour

Over time, the skin’s underlying support structure of collagen and elastin degenerates from repeated sun exposure. Combined with the effects of gravity, these factors rob facial skin of its youthful firmness and resilience.1-3

Medical interventions to improve loose and sagging skin such as surgical face lifts are costly and associated with side effects.4,5 This leaves many people without a viable option.

You may not have to be one of them. Scientists have uncovered several new compounds that can turn the tide in your favor—providing a safe and effective alternative to current treatments.

This article will describe how an innovative peptide and three plant stem cell extracts work together to stimulate new production of collagen and elastin in aging skin, while protecting existing collagen and elastin against damaging ultraviolet radiation (UV). This novel strategy results in visibly firmer, more defined, younger-looking facial skin.

Collagen And Elastin: The Dynamic Duo
The physical appearance of your skin largely depends on the condition of the extracellular matrix that lies between cells in the dermis. In younger skin, the extracellular matrix is a highly organized structure rich in collagen and elastin proteins that work in tandem to maintain firmness and resilience.6,7

Collagen types I and III comprise most of the extracellular matrix, forming rope-like fibers that supply high-tensile strength and resist stretching.8 A different type of collagen—type IV—is a major component of the basement membrane that connects the dermis to the epidermis, where it self-assembles into a scaffolding network to provide mechanical stability.1

Elastin, on the other hand, accounts for the impressive ability of skin to stretch and recoil, allowing it to return to its original shape after facial expressions such as smiling, laughing, and squinting. Although elastin makes up only a small percentage of the total dry weight of the dermis, it is equally as important as collagen in supporting the appearance of youthful skin.9,10

As we age, however, elastin and collagen fibers decrease as a result of reduced synthesis,11,12 as well as increased degradation from UV-induced matrix metalloproteinases which are enzymes that destroy our skin’s support structure.13,14 Combined with the force of gravity, these age-related changes translate into loose and saggy facial skin with fine lines and wrinkles.15

Since surgical face lifts, injections, and laser treatments are expensive, uncomfortable, and often accompanied by side effects,14,15 researchers have been investigating compounds that could lift and tighten loose skin without these notable drawbacks.

Let’s take a look at how a unique peptide regenerates collagen and elastin to deliver remarkable skin tightening effects.

Acetyl Tetrapeptide-2 Creates New Collagen And Elastin
Aware of the fact that collagen and elastin molecules are too large in molecular weight to significantly penetrate the skin,16 scientists designed a low-molecular weight peptide called acetyl tetrapeptide-2 to overcome this problem.17

When scientists treated dermal fibroblasts with acetyl tetrapeptide-2, they observed a 47% increase in type I collagen synthesis.17 In addition, it was shown to favorably modulate gene expression of collagen types I and IV to improve skin cohesion and resistance. 17

Elastin is made from its precursor molecule tropoelastin, which forms elastic fibers after key steps involving the enzyme lysyl oxidase-like 1 (LOXL1) and glycoprotein fibulin-5 (FBLN5).18-20 Both of these compounds decline with advancing age and consequently interfere with the proper formation of elastic fibers that give skin its elasticity.212,22

Acetyl tetrapeptide-2 has not only been shown to increase the synthesis of elastin by 22%, but also encouraged its formation into functional fibers by raising LOXL1 and FBLN5 1.7 fold and 2.3 fold, respectively.17

Additional research shows that acetyl tetrapeptide-2 further supports skin firmness and elasticity by producing adhesion molecules that strengthen the attachment of cells to the extracellular matrix.17

To determine its effectiveness in humans, researchers conducted a clinical trial involving a group of mature women suffering from saggy facial skin. After eight weeks of twice daily applications of acetyl tetrapeptide-2 to the targeted region, participants had average reductions of 9.5% in indentation and 23.2% in a skin flaccidity area parameter—leaving them with noticeably tighter and smoother facial skin.17

Next, we’ll examine plant secondary metabolites and their protective role against sun damage that damages elastin and collagen in the first place.

Targeting Plant Secondary Metabolites
Have you ever wondered why some plants have astonishing life spans? The answer lies in the remarkable regenerative capacity of meristematic cells located in the tips of plant roots and shoots.23,24 These plant stem cells, like human stem cells, can self-renew or differentiate into any other type of cell with a specific function based on the surrounding environment.25

For instance, meristematic cells give rise to secondary metabolites as part of the plant’s survival strategy under stress conditions imposed by living microorganisms (biotic stress) or the physical environment (abiotic stress).26,27 Although once believed to be useless waste products, secondary metabolites have now been shown to demonstrate potent, anti-inflammatory and anti-microbial properties—all of which shield the skin against its external enemies.28,29

Scientists quickly turned to plant cell culture as a means to access secondary metabolites, but early research was unsuccessful.30 After going back to the drawing board, scientists soon discovered a novel way to target secondary metabolites. By co-culturing plant stem cells with microorganisms (like bacteria), biotic stress is created that promotes the formation of secondary metabolites.31-33 More importantly, this approach yields sufficient quantities of these high-value compounds.

As we age, the skin’s underlying structural support of collagen and elastin breaks down from repeated sun exposure, and combined with the effects of gravity, make loose and sagging facial skin almost an inevitable part of aging.

Researchers have identified several new compounds that provide a safe and effective alternative to current treatments with high cost and substantial side effects.
Acetyl tetrapeptide-2 enhances skin cohesion and firmness in humans by triggering new production of collagen and elastin in aging skin.

Three plant stem cell extracts and their secondary metabolites reduce damage to existing collagen and elastin fibers from UV rays through multiple mechanisms including decreasing interleukin-6 synthesis and boosting ATP production.

Human studies show their ability to increase water content in aging cells, with Euterpe oleracea fruit extract improving moisture by 51% within 24 hours of topical application.
Taken together, these four compounds create visibly firmer, more defined, younger-looking skin.

Plant Stem Cell Extracts And Their Secondary Metabolites
Researchers have identified three plants around the world—Açaí palm, Quercus alba, and Perilla frutescens—shown to adapt and resist harsh environmental conditions, from droughts to intense UV radiation.31-33 To stimulate production of the compounds responsible for this longevity, cells of each plant were extracted and then co-cultured with bacteria. This resulted in the following plant stem cell extracts, each of which provide a specific secondary metabolite:

Euterpe oleracea fruit extract (Cabbage Palm Fruit of the açaí palm family)—ferulic acid31
Perilla frutescens extract—rosmarinic acid32
Quercus alba bark extract—tannic acid33

The skin’s loss of firmness and flexibility can be traced back to unprotected sun exposure. Plant stem cell extracts and their respective secondary metabolites have been demonstrated in laboratory studies to reduce damage to existing collagen and elastin fibers from ultraviolet radiation in several ways:

Plant stem cell extracts modulate pro-inflammatory cytokine production following exposure to ultraviolet radiation. For instance, these stem cell extracts decrease the synthesis of a damaging cytokine called interleukin-6 (IL-6).31-33 As people age, IL-6 levels increase, which triggers the release of matrix metalloproteinase ezymes that degrade collagen and elastin.34,35

They suppress UV-induced free radicals—evident by their high oxygen radical absorbance capacity (ORAC) scores 31-33 that contribute to oxidative stress involved in the destructive cross-linking of healthy collagen and elastin fibers.36 This process renders both proteins dysfunctional, leading to loose and inflexible skin.

By inhibiting free radical generation, plant stem cell extracts protect vulnerable DNA and preserve the natural order for regenerating new collagen and elastin.31,37

Ultraviolet radiation alters mitochondrial energy production in dermal fibroblasts, resulting in less energy in the form of adenosine triphosphate (ATP).38 This slows down cellular activities that maintain firm and smooth skin. By ramping up ATP production, plant stem cell extracts replenish energy levels to improve cellular metabolism, promote new collagen and elastin, and boost DNA repair. 31-33

Human studies using the same three plant extracts confirm their ability to increase water content in aging cells, keeping them plump to give the appearance of firmer and smoother skin.31-33 In one of these human studies, Euterpe oleracea fruit extract improved moisture by 51% within 24 hours and 102% after four weeks compared to a control, thereby demonstrating its immediate and long-lasting hydrating effects. 31

While wrinkles and fine lines have been treated successfully with topical solutions, improving loose and sagging skin so far has been a losing battle. One primary reason is that medical interventions are costly, uncomfortable, and often accompanied by side effects.

Fortunately, scientists have identified new compounds that provide a safe and effective alternative to current treatments.

Acetyl tetrapeptide-2 enhances skin cohesion and firmness by triggering new production of collagen and elastin, while three plant stem cell extracts and their respective secondary metabolites work to protect existing collagen and elastin fibers from damaging UV rays.

This novel strategy results in visibly firmer, more defined, younger-looking facial skin. Review this new product here ->

Bernstein EF, Chen YQ, Kopp JB, et al. Long-term sun exposure alters the collagen of the papillary dermis. Comparison of sun-protected and photoaged skin by northern analysis, immunohistochemical staining, and confocal laser scanning microscopy. J Am Acad Dermatol. 1996 Feb;34(2 Pt 1):209-18.
Suwabe H, Serizawa A, Kajiwara H, et al. Degenerative processes of elastic fibers in sun-protected and sun-exposed skin: immunoelectron microscopic observation of elastin, fibrillin-1, amyloid P component, lysozyme and alpha1-antitrypsin. Pathol Int. 1999 May;49(5):391-402.
Ohshima H, Tada A, Kanamaru A, et al. Relevance of the directionality of skin elasticity to aging and sagging of the face. Skin Res Technol. 2011 Feb;17(1):101-7.
Moyer JS, Baker SR. Complications of rhytidectomy. Facial Plast Surg Clin North Am. 2005 Aug;13(3):469-78.
Haedersdal M. Cutaneous side effects from laser treatment of the skin: skin cancer, scars, wounds, pigmentary changes, and purpura—use of pulsed dye laser, copper vapor laser, and argon laser. Acta Derm Venereol Suppl. 1999;207:1-32.
Krieg T, Aumailley M. The extracellular matrix of the dermis: flexible structures with dynamic functions. Exp Dermatol. 2011 Aug;20(8):689-95.
Frantz C, Stewart KM, Weaver VM. The extracellular matrix at a glance. J Cell Sci. 2010 Dec;123:4195-200.
Lovell CR, Smolenski KA, Duance VC, et al. Type I and III collagen content and fibre distribution in normal human skin during ageing. Br J Dermatol. 1987;117(4):419-28.
Uitto J, Li Q, Urban Z. The complexity of elastic fiber biogenesis in the skin—a perspective to the clinical heterogeneity of cutis laxa. Exp Dermatol. 2013 Feb;22(2):88-92.
Oikarinen A. Aging of the skin connective tissue: how to measure the biochemical and mechanical properties of aging dermis. Photodermatol Photoimmunol Photomed. 1994 Apr;10(2):47-52.
Uitto J. The role of elastin and collagen in cutaneous aging: intrinsic aging versus photoexposure. J Drugs Dermatol. 2008 Feb;7(2 Suppl):s12-6.
Rossetti D, Kielmanowicz MG, Vigodman S, et al. A novel anti-ageing mechanism for retinol: induction of dermal elastin synthesis and elastin fibre formation. Int J Cosmet Sci. Feb 2011;33(1):62-9.
Fisher GJ, Datta SC, Talwar HS, et al. Molecular basis of sun-induced premature skin ageing and retinoid antagonism. Nature. Jan 1996;379:335-9.
Brennan M, Bhatti H, Nerusu K, et al. Matrix metalloproteinase-1 is the collagenolytic enzyme responsible for collagen damage in UV-irradiated human skin. Photochem Photobiol. 2003;78:43-8.
Ganceviciene R, Liakou AI, Theodoridis A, et al. Skin anti-aging strategies. Dermatolendocrinol. 2012 Jul 1;4(3):308-19.
Posner R. Liposomes. J Drugs Dermatol. 2002 Sep;1(2):161-4.
Product monograph: UplevityTM. Lipotec. June 2013.
Wagenseil JE, Mecham RP. New insights into elastic fiber assembly. Birth Defects Res. 2007 Dec;81(4):229-40.
Thomassin L, Werneck CC, Broekelmann TJ, et al. The Pro-regions of lysyl oxidase and lysyl oxidase-like 1 are required for deposition onto elastic fibers. J Biol Chem. 2005 Dec 30;280(52):42848-55.
Kadoya K, Sasaki T, Kostka G, et al. Fibulin-5 deposition in human skin: decrease with ageing and ultraviolet B exposure and increase in solar elastosis. Br J Dermatol. 2005 Sep;153(3):607-12.
Langton AK, Sherratt MJ, Griffiths CE, Watson RE. Differential expression of elastic fibre components in intrinsically aged skin. Biogerontology. 2012 Feb;13(1):37-48.
Hirai M, Ohbayashi T, Horiguchi M, et al. Fibulin-5/DANCE has an elastogenic organizer activity that is abrogated by proteolytic cleavage in vivo. J Cell Biol. 2007 Mar 26;176(7):1061-71.
Stahl Y, Simon R. Plant stem cell niches. Int J Dev Biol. 2005;49(5-6):479-89.
Sablowski R. The dynamic plant stem cell niches. Curr Opin Plant Biol. 2007 Dec;10(6):639-44.
Heidstra R, Sabatini S. Plant and animal stem cells: similar yet different. Nat Rev Mol Cell Biol. 2014 May;15(5):301-12.
Nascimento NC, Fett-Neto AG. Plant secondary metabolism and challenges in modifying its operation: an overview. Methods Mol Biol. 2010;643:1-13.
Hussain MS, Fareed S, Ansari S, et al. Current approaches toward production of secondary plant metabolites. J Pharm Bioallied Sci. 2012 Jan;4(1):10-20.
Hartmann T. From waste products to ecochemicals: fifty years of research of plant secondary metabolism. Phytochemistry. 2007 Nov-Dec;68(22-24):2831-46.
Dickson RA, Ekuadzi E, Annan K, Komlaga G. Antibacterial, anti-inflammatory, and antioxidant effects of the leaves and stem bark of Glyphaea brevis (Spreng) Monachino (Tiliaceae): A comparative study. Pharmacognosy Res. Jul 2011;3(3):166-72.
Hussain MS, Fareed S, Ansari S, et al. Current approaches toward production of secondary plant metabolites. J Pharm Bioallied Sci. 2013 Jan-Mar;4(1):10-20.
Product monograph: Phyto-Biotics AcaiTM. Active Concepts. 2009.
Product monograph: Phyto-Biotics PecillaTM. Active Concepts. 2009.
Product monograph: Phyto-Biotics QuercusTM. Active Concepts. 2009.
Urbanski A, Schwarz T, Neuner P, et al. Ultraviolet light induces increased circulating interleukin-6 in humans. J Invest Dermatol. 1990 Jun;94(6):808-11.
Sundararaj KP, Samuvel DJ, Li Y, et al. Interleukin-6 released from fibroblasts is essential for up-regulation of matrix metalloproteinase-1 expression by U937 macrophages in coculture: cross-talking between fibroblasts and U937 macrophages exposed to high glucose. J Biol Chem. 2009 May 15;284(20):13714-24.
Monnier VM, Mustata GT, Biemel KL, et al. Cross-linking of the extracellular matrix by the maillard reaction in aging and diabetes: an update on “a puzzle nearing resolution.” Ann N Y Acad Sci. 2005;1043:533-4.
Dizdaroglu M, Jaruga P, Birinciolglu M, Rodriguez H. Free radical-induced damage to DNA: mechanisms and measurement. Free Rad Biol Med. 2002 Jun;32(11):1102-15.
Krutmann J, Schroeder P. Role of mitochondria in photoaging of human skin: the defective powerhouse model. J Invest Dermatol. 2009;14:44-9.

November 11, 2016

Higher vitamin D levels linked with improved breast cancer survival

November 11 2016. On November 10, 2016 in JAMA Oncology reported the outcome of a study conducted by researchers from Kaiser Permanente and Roswell Park Cancer Institute which found improved overall survival in breast cancer patients whose serum vitamin D levels were highest.

The study included 1,666 women with invasive breast cancer who enrolled in the Pathways Study of breast cancer survivors beginning in 2006. Blood samples collected after diagnosis were analyzed for serum 25-hydroxyvitamin D. Follow-ups conducted at 12, 24, 48, 72 and 96 months provided information on health outcomes.

"With the extremely rich data sources from a large sample size, we were able to prospectively analyze three major breast cancer outcomes -- recurrence, second primary cancer and death," noted lead author Song Yao, PhD, of the Roswell Park Cancer Institute. "We were also able to adjust for multiple possible contributing factors that could influence vitamin D levels, such as age, obesity, race and ethnicity, socioeconomic status, and several tumor characteristics that are known to influence breast cancer outcomes -- to ensure that the effects we observed were independent of these factors.”

"We found that women with the highest levels of vitamin D levels had about a 30 percent better likelihood of survival than women with the lowest levels of vitamin D," reported lead investigator Lawrence H. Kushi, ScD, of the Kaiser Permanente Northern California Division of Research." The effect was even stronger among premenopausal women.

"The more we know about vitamin D, the more we understand that it may play a key role in cancer prevention and prognosis," Dr. Kushi added. “This study adds to the evidence that vitamin D is an important nutrient."

© 2016 Life Extension Foundation

August 01, 2016

Support Healthy Hair Regeneration - By Caring For the Scalp

A hallmark outward sign of aging is thinning hair. Commercial products focus on the symptoms of thinning hair, rather than the cause.

Recent discoveries have uncovered compounds that, when combined, offer a diverse approach for improving the condition and appearance of the scalp —laying the foundation for healthier hair.

The scalp remains one of the most neglected parts of the body until the signs of dryness and itching appear—or, even worse, thinning hair and hair loss occur.

This article describes how a novel plant extract derived from the Argan tree gets to the root of thinning hair and hair loss by stimulating the activity of self-renewing dermal stem cells to alleviate a dry scalp and induce hair growth.

To purchase this innovative new formula, GO HERE ->

Discovery Of A Dermal Stem Cell Role 

In 2009, a research team at the University of Toronto discovered a therapeutic application for restoring hair growth in those suffering from hair loss (alopecia)—and in those combatting the underlying causes that lead to the telltale signs of a damaged scalp. Their research was in the area of adult stem cells.

Adult stem cells have the ability to differentiate into tissue cell types with a specific function.1 The skin relies on a reservoir of active stem cells in both the epidermis(upper layer) and dermis (middle layer) to renew and repair itself, and also to enable proper wound healing.1-3

The location of dermal stem cells was only recently discovered by the Toronto-based research team.4

After conducting a series of studies, the researchers reported that cells localized at the base of the hair follicle (dermal papilla) expressed the stem cell marker Sox2and exhibited the property to grow in colonies in the form of spheres, both characteristics of dermal stem cells. In addition to differentiating into fibroblasts that support dermal rejuvenation, these cells (referred to as  skin-derived precursors, or SKPs) were also shown to generate hair follicle formation and stimulate hair growth in experimental mice. This evidence led the research team to conclude that skin-derived precursors are in fact “dermal stem cells that serve to induce hair morphogenesis and maintain the dermis.”4

Once scientists made this important discovery, the next step entailed identifying compounds that can improve the regenerative capacity of aging dermal stem cells. They soon discovered the answer in a rare plant: the Argan tree.


  • Procyanidin B-2 stimulates hair growth in balding men, leading one research team to recognize it “as a promising cure for male pattern baldness.” 
  • Biotin combats thinning hair. 
  • Copper supports hair follicles. 
  • Antioxidant-rich tea extracts quench excess free radicals that result in skin damage. 

Activate And Vitalize Aging Dermal Stem Cells

Belonging to one of the oldest tree species in the world, the Argan tree grows in southwest Morocco where it adapts to extreme droughts and high temperatures. The plant’s survival under these diverse conditions speaks to the remarkable regenerative capacity of its stem cells.5 This prompted researchers to investigate whether these stem cells can activate our own aging dermal stem cells. Multiple preliminary studies indicate that they do.

For example, in an advanced cell culture technique, the presence of 0.1% Argan stem cell extract had beneficial effects on two important characteristics of dermal stem cells: It significantly enhanced the expression of the stem cell marker Sox2, and it increased the number of secondary spheres by 89% compared to untreated controls in aging dermal skin cells, thus improving their activity.6 This indicates that these newly activated dermal stem cells could then stimulate the formation of hair follicles and hair growth in humans.

In a clinical trial, human skin treated with Argan stem cell extract increased dermal density by nearly 13% compared to a placebo after eight weeks.6 This is important because aging is associated with a decreased number of fibroblasts that provide structural integrity to the dermis.7,8 The resulting reduction in dermal thickness gives way to a dry and damaged scalp.9 Thus, by increasing dermal density, Argan stem cell extract can help support a healthy scalp.


Dermal Stem Cells Stimulate Hair Growth

  • In 2009, a University of Toronto-based research team discovered a role for dermal stem cells in the dermal papilla (base of the hair follicle). 
  • Dermal stem cells induce hair follicle formation and hair growth in mice, which in turn raises their therapeutic potential to treat hair loss (alopecia) in humans. 
  • Scientists identified stem cells from the Argan tree that have been shown to activate dermal stem cells. This could stimulate the formation of hair follicles and hair growth in humans. 
  • Argan stem cells increase dermal density to support a healthy scalp. 
  • In addition, procyanidin B-2 and biotin support hair growth; copper supports hair follicles; and tea extracts protect the skin by fighting free-radical damage. 
  • When combined, these nutrients offer a multi-faceted approach for improving the health and appearance of the scalp—laying the foundation for healthy hair. 

Four Additional Compounds That Support Healthy Hair

Two other nutrients, procyanidin B-2 and biotin, further encourage hair growth via different mechanisms than Argan stem cells. Additionaly, copper and tea extractscomplement procyanidin B-2 and biotin’s hair-growing action by rejuvenating the scalp and hair from the inside out. Copper helps solidify the hair’s structure. Tea extracts quench excess free radicals that result in dryness, itchiness, and dullness of the scalp.

1. Procyanidins

Procyanidins are a subclass of flavonoids found at high concentrations in chocolate, apples, and grapes.10 Scientists have discovered that a particular form of procyanidin known as procyanidin B-2 favorably affects the natural hair growth cycle by reverting hair follicles from the telogen (resting) phase to the anagen (growth) phase.11 Procyanidin B-2 stimulates natural hair growth and has been found to increase hair density and average hair diameter in men.12,13

In a human study, researchers observed that 43 men with male pattern baldness who applied procyanidin B-2 twice daily to their scalp area for one year exhibited a significantly greater total number of hairs in a targeted scalp area than those who applied a placebo.12

In another double-blind, controlled clinical trial, balding men ranging in age from 30 to 57 applied either a topical application of procyanidin B-2 or a placebo twice daily to the scalp area for four months. At the study’s end, 78.9% of patients in the treatment group experienced increases in average hair diameter versus only 30% for the placebo group.13 Equally noteworthy, the procyanidin B-2 group also had a significantly higher ratio of hairs measuring 40 microns or more in diameter than the placebo group, demonstrating an improvement in hair thickness.13

These substantial hair-increasing effects led the team of researchers to recognize procyanidin B-2 as a promising treatment for male pattern baldness.13

2. Biotin

Biotin is a water-soluble vitamin whose deficiency has been shown to manifest itself as hair loss, suggesting that the micronutrient plays a vital role in supporting healthy hair.14

Oral supplementation of 1 mg per day of biotin for just a week led to the disappearance of biotin-deficiency symptoms, including alopecia.15

3. Copper

Dermal papilla (the base of the hair follicle) is the source of adult stem cells. Researchers observed that tripeptide-copper complex, a growth factor for various types of cells, stimulated the elongation of human hair follicles and of dermal papilla cells.16

4. Tea Extracts

The scalp is bombarded with free radicals on a daily basis, especially from UV exposure.17 As antioxidants produced within the body are depleted, excess free radicals begin to modify the scalp’s structure. This process causes a dry, damaged scalp.9

Green, black, white, and red tea extracts are brimming with potent antioxidants and anti-inflammatory compounds that protect the skin against the damaging effects of free radicals.16,18,19


The scalp is often the most neglected body part, yet it forms the foundation for healthy, beautiful hair.

A novel plant extract derived from the rare Argan tree enhances the regenerative capacity of aging dermal stem cells to induce hair follicle formation and stimulate hair growth, as well as improve dermal density to alleviate signs of a damaged scalp.

This extract has been formulated into a serum which, along with additional compounds, supports the health and appearance of the hair and scalp.

To purchase this innovative new formula, GO HERE ->


  1. Cerqueira MT, Marques AP, Reis RL. Using stem cells in skin regeneration: possibilities and reality. Stem Cells Dev. 2012 May;21(8):1201-14.
  2. Available at: http://www.ncbi.nlm.hin.gov/pubmed/22057442. Accessed March 21, 2014. 
  3. Available at: http://www.ncbi.nlm.nih.gov/books/MBK26865. Accessed March 21, 2014. 
  4. Biernaske J, Oaris M, Morozova O, et al. SKPs derive from hair follicle precursors and exhibit properties of adult dermal stem cells.  Cell Stem Cell. 2009 Dec;5(6):610-23.
  5. Abassi A, Khalid N, et al. Physicochemical characteristics, nutritional properties and health benefits of argan oil: a review.  Crit Rev Food Sci Nutr. 2014; 54(11):1401-14.
  6. Available at: http://www.protectingredia.com/downloads/Dermal stem cells are the target of the latest treatments for deep-seated skin regeneration. CosmeticsDesign Feb 2012.pdf. Accessed March 21, 2014. 
  7. Guin AG, Kornilova NK, Vasilieva OV, Petrov VV. Age-related changes in proliferation, the numbers of mast cells, eosinophils, and cd45-positive cells in human dermis. J Gerontol A Biol Sci Med Sci. 2011 Apr;66(4):385-92.
  8. Varani J, Dame MD, Rittie L, Fligiel SE, Kang S, Fisher GJ, Voorhees JJ. Decreased collagen production in chronologically aged skin: roles of age-dependent alteration in fibroblast function and defective mechanical stimulation. Am J Pathol. 2006 Jun:168(6):1861-8.
  9. Gan D, Sinclair R. Aging of the scalp and age-related disorders of the scalp. In:Trube RM, ed. Aging hair. Apringer Heidelberg Dordrecht Londa New York; 2010:167-171.
  10. Hammerstone JF, Lazarus SA, Schmitz HH. Procyanidin content and variation in some commonly consumed foods. J Nutr. 2000 Aug;130:2086S-92S.
  11. Takahashi T, Kamiya T, Hasegawa A, Yokoo Y. Procyanidin oligomers selectively and intensively promote proliferation of mouse hair epithelial cells in vitro and activate hair follicle growth in vivo. J Invest Dermatol. 1999 Mar;112(3):310-6.
  12. Takahashi T, Kamimura A, Kagoura M, et al. Investigation of the topical application of procyanidin oligomers from apples to identify their potential use as hair-growing agent. J Cosmet Dermatol. 2005 Dec;4(4):245-9.
  13. Takahashi T, Kamimura A, Kagoura M, et al. The first clinical trial of topical application of procyanidin B-2 to investigate its potential as a hair grrowing agent. Phytother Res. 2001 Jun;15(4):331-6.
  14. Tosti A, Piraccini BM, Sisti A, Duqu-Estrada B. Hair loss in women. Minerva Ginecol. 2009 Oct;61(5):445-52.
  15. Higuchi R, Noda E, et al. Biotin deficiency in an infant fed with amino acid formula and hypoallergenic rice. Acta Paediatr. 1996 Jul;85(7):872-4.
  16. Pyo HK, Yoo HG, et al. The effect of tripeptide-copper complex on human hair growth in vitro. Arch Pharm Res. 2007 Jul;30(7):834-9.
  17. Trüeb RM . Oxidative stress in ageing of hair.  Int J Trichology. 2009 Jan;1(1):6-14. 
  18. Camouse MM, Domingo DS, et al. Topical application of green and white tea extracts provides protection from solar-simulated ultraviolet light in human skin. Exp Dermatol. 2009 Jun;18(6):522-6.
  19. Reni ML. Free radical scavenging properties of antioxidants like Beta-carotene, Lutein, Lucopene, Catachins, Cryptoxanthings, Zoochemicals and various indoles and flavonoids. JMPAS. 2013; 4:52-62.

July 05, 2016

Turning To Stone: The Life-Saving Mechanism of Vitamin K

by Willam Faloon

As we age, our soft tissues harden as a result of calcium infiltration. This calcification process is a major contributor to degenerative disease. Vitamin K functions to keep calcium out of soft tissues. New findings reveal that a vitamin K deficit creates more vascular calcification than initially thought.

A recent study showed when women were given a drug that blocks vitamin K, there was a 50% greater prevalence of  arterial calcification compared to women not taking this drug (warfarin). This pathological effect occurred in as little as one month.1 This study showed that longer term use of warfarin was associated with even greater arterial calcification prevalence.

Kidney dialysis patients suffer severe arterial calcification with cardiovascular disease accounting for almost half of all their deaths.2 A clinical study examined vitamin K levels in dialysis patients. The results showed that 93% of the patients were at risk for arterial calcification. This risk was shown to be reduced with  vitamin K2 supplementation.3

The quotation on the right side of this page comes from a report published by the American Heart Association.4 Despite this indisputable data, doctors today typically do nothing to protect their aging patients from the devastating impact of  vascular calcification.

This article briefly describes how proper use of vitamin K can markedly protect our soft tissues against  calcification. Purchase our finest Vitamin K supplement here.->


“Most individuals aged over 60 years have progressively enlarging deposits of calcium mineral in their major arteries.5 This vascular calcification reduces aortic and arterial elastance, which impairs cardiovascular hemodynamics, resulting in substantial morbidity and mortality6-8 in the form of hypertension, aortic stenosis, cardiac hypertrophy, myocardial and lower-limb ischemia, congestive heart failure, and compromised structural integrity.9-11 The severity and extent of mineralization reflect atherosclerotic plaque burden12 and strongly and independently predict cardiovascular morbidity and mortality.13

Source: American Heart Association

A search of the National Library of Medicine data base using the term “vascular calcification at the time of this writing turns up the following numbers of published scientific articles:

Year | New Articles 

1982 | 16

1994 | 53

2004 | 214

2008 | 373

2014 | 700+

The total number of articles that discuss arterial calcification in the National Library of Medicine as of April, 2015, is over 6,400.

The surge from a mere 16 articles in 1982 to over 6,400 today is a reflection of the exponential increase in knowledge about this widespread pathological process.

The problem is that this lifesaving data is not being translated into clinical medical practice where it is urgently needed to protect aging humans against a host of cardio-vascular disorders.


Calcification And Hypertension

When arteries are soft and elastic, they readily expand and contract with each heartbeat. As arteries harden (calcify) and lose youthful elasticity, there is a progressive elevation in blood pressure.14

This happens because the heart is forced to beat stronger to force blood into the increasingly rigid arterial system. Calcification of the large artery exiting the heart (the aorta) helps explain why blood pressure elevates as people age.

A hallmark sign of long-term hypertension is enlargement of the heart’s left ventricle,15 which is the chamber of the heart that pushes blood into the aorta from where it is then distributed throughout the body.

The increase in cardiac workload caused by aortic rigidity (calcification) contributes to heart failure that afflicts over 5 million Americans.16,17

Aortic Valve Stenosis

A dilemma faced by elderly persons is progressive dysfunction of the valve between their heart and aorta that opens and closes with each heartbeat.

When the aortic valve fails to completely close, blood regurgitates back into the left ventricle of the heart.18,19 Without surgical replacement/repair of the aortic valve, death from congestive heart failure often occurs.20

Elderly persons are challenged to fully recover from aortic valve replacement, though newer intra-arterial techniques are becoming available whereby an artificial valve is threaded through the aorta and sewn into place.21Those with successful mechanical valve replacements usually require anticoagulant drug therapy for life, which poses its own complicated set of side effects.22

It used to be thought that aortic stenosis was caused by a lifetime of “wear and tear.”23 It is now clear that  calcification of the aortic valve leaflets is a cause of aortic valve failure, along with chronic inflammation, elevated glucose, high homocysteine, and low magnesium.24-31

Coronary Artery Calcification

Blockage of the coronary arteries that feed the heart muscle necessitates enormous amounts of hospital expenditures each year in the form of open heart coronary bypass surgeries and intra-arterial “stenting” procedures.

Interestingly, when open heart surgery is performed to replace a calcified aortic valve, the surgeon will often also bypass blocked coronary arteries in the same patient.32 This is not surprising since coronary atherosclerosis and aortic valve stenosis have similar underlying causes such as elevated homocysteine, chronic inflammation, and  calcification.33-36

Calcification plays a significant role in accelerating the formation of the atherosclerotic plaque that narrows the coronary arteries of aging humans. In patients with  coronary artery disease, calcification is present in 90% of cases.37,38

Clinically, vascular calcification is now accepted as a valuable predictor of coronary heart disease.39 Yet most cardiologists use it only as a diagnostic marker (the coronary calcium score test) as opposed to directly treating the underlying calcification pathology.40

What Causes Arteries To Calcify?


Many of the known risk factors that underlie atherosclerosis have been shown to promote arterial calcification. These include elevated LDL cholesterol, elevated homocysteine, diabetes, kidney failure, chronic inflammation, and oxidative stress.33,41-55

Additional calcification contributors include low magnesium (a natural calcium channel blocker), hormone imbalance, and excess blood calcium (caused by hyperparathyroidism).56-66

An underappreciated, major reason our vascular system turns to stone (calcifies) as we age, however, is inadequate intake of  vitamin K.

As you’ll read next, a low blood level of vitamin K2 causes a protein in the vascular wall to bind calcium to arteries, heart valves, and other soft tissues.

A Calcium Inhibitor In Need Of Vitamin K

Matrix Gla-protein is a vitamin K-dependent protein, and it must be carboxylated to function properly. Poor vitamin K status leads to inactive uncarboxylated matrix Gla, which enables calcium to accumulate in soft tissues.67-69

Failure to optimally carboxylate matrix Gla-protein is a risk factor for atherosclerosis, coronary heart attack, and kidney disease.70-74 The title of a 2008 study that examined the impact of cardiovascular calcification is: “Matrix Gla-Protein: The Calcification Inhibitor In Need Of Vitamin K.”75,76

Matrix Gla-protein lines our vascular system and its function is governed by the quantity of vitamin K in our bloodstream.

When vitamin K levels are less than optimal, matrix Gla-protein allows calcium to infiltrate into our soft tissues similar to the way calcium absorbs into bone. When you hear the term “hardening of the arteries,” this can literally mean one’s previously flexible blood vessels are turning into rigid (calcified) bony structures.

With optimal levels of vitamin K, matrix Gla-protein becomes activated to shield calcium from entering arteries, heart valves, and other soft tissues.

Said differently, vitamin K functions as a control switch. When matrix Gla-protein is turned “on” by vitamin K, itblocks calcium from entering soft tissues. In the absence of adequate vitamin K, the  matrix Gla-proteinswitch is turned “off” and calcium quickly infiltrates into soft tissues.

So the title of the 2008 study is quite revealing in that matrix Gla-protein is clearly a “  calcification inhibitor in need of vitamin K.”


Early forms of life emanated from calcium-rich oceans, which required primitive organisms to develop mechanisms to prevent widespread calcium crystallization of living soft tissues.77

A prominent calcium-blocking mechanism is through activation of a protein called matrix gamma-carboxyglutamic acid, more commonly referred to as matrix Gla-protein or matrix Gla.78

The key to how matrix Gla-protein functions lies with its “carboxyl” group. Matrix Gla must be carboxylated to function properly.74

In the presence of vitamin K2, matrix Gla-protein becomes “carboxylated,” which means it’s being turned “ on” to repel calcium infiltration.74

Insufficient vitamin K2 results in matrix Gla being inadequately carboxylated or turned “off,” which means it’s unable to inhibit calcium infiltration into soft tissues. 

To keep our natural calcium inhibitor matrix Gla continuously carboxylated, we need to provide it with a steady supply of vitamin K2. This is easy to do with one-per-day dosing of the proper forms of vitamin K

What Happens When Vitamin K Is Acutely Withdrawn?

A recent study provided real-world evidence of what happens to aging humans who are deprived of vitamin K.

Warfarin is an anticoagulant drug that functions by antagonizing the effects of vitamin K in the body.79 This drug has been sold under the trade name Coumadin® for many decades.

Scientists were long ago aware that warfarin users suffered accelerated arterial calcification, but until recently, there was no alternative to protect high-risk patients from a thrombotic (arterial clotting) event, such as an ischemic stroke.

A study published in 2015 evaluated 451 women using mammograms to measure arterialcalcification. After just one month or more of warfarin drug therapy, the prevalence of arterial calcification increased by an astounding50% compared to that in untreated women. When these women were evaluated again after five years, the prevalence of  arterial calcification increased almost 3-fold.1

This new human trial provides stark evidence of rapid calcification occurring in response to vitamin K withdrawal caused by  warfarin (a vitamin K antagonist drug.)

We discuss the pros and cons of anticoagulant drugs that may be used in place of warfarin in this month’s issue of  Life Extension® magazine.

What Happens When Vitamin K Is Introduced To Deficient Patients?

Kidney failure patients are kept alive by thrice weekly dialysis treatments. While the advent of hemodialysis has added countless human life years, it produces devastating side effects over the longer term. Over 50% of hemodialysis patients have  vascular calcification, a major cause of cardiovascular disease. Cardiovascular disease accounts for about 50% of all deaths in these patients.80-82

A study was done to evaluate the effects of varying doses of the MK-7 form of vitamin K2 on markers of arterial calcification including  carboxylation (activation) of matrix Gla-proteins.83

MK-7 (menaquinone-7) is a unique form of vitamin K2 because it remains active in the body for 24 hours and longer.84

At baseline, hemodialysis patients had a 4.5-fold higher level of uncarboxylated matrix Gla compared to controls.83 Daily doses of MK-7 of 45 mcg135 mcg, and  360 mcg were then administered over a six-week period.

Results were measured by the reduction of uncarboxylated matrix Gla and other measures of systemic calcification. Recall that when matrix Gla is under-carboxylated, it enables calcification of its surrounding tissue.

Supplementation with the MK-7 form of vitamin K2 reduced uncarboxylated matrix Gla by 36.7% in the 135 mcg dose group and 61.1% in the 360 mcg dose group. In the group given  360 mcg per day of MK-7, the favorable response rate was a remarkable 93%.83

When vitamin K2 supplementation was ceased in these dialysis patients, plasma levels of uncarboxylated matrix Gla-protein increased significantly, which indicated these high-risk individuals were once again vulnerable to severe  vascular calcification.


Based on the totality of evidence and low cost, it is prudent to take a supplement that contains multiple forms of vitamin K. The three forms of vitamin K most applicable to human health are: 

  • Vitamin K1 . Vitamin K1, also known as phylloquinone, is found in plants and some of it converts to vitamin K2 in the body.85 This form is considered the least effective because it depends on conversion into activated K2 to confer significant protection against calcification. There are nonetheless published studies showing disease risk reduction in response to ingestion of vitamin K1.86-90
  • Vitamin K2 (MK-4) . MK-4 is found in meat, eggs, and dairy products.91 It is the most studied form of vitamin K to preserve bone health. It is rapidly absorbed and rapidly metabolized by the body.92-96
  • Vitamin K2 (MK-7) . MK-7 is found in fermented soybeans and fermented cheeses.97,98 What makes this form so special is that it remains active in the body for more than 24 hours.84 This is critical when protecting against calcification since matrix Gla-proteins quickly inactivate in the absence of vitamin K2.99

The federal government says that adults only need 90 to 120 mcg per day of vitamin K.100-102 While this is enough to enable proper blood clotting, current research suggests it falls below levels needed to protect against vascular calcification.99,103-106

Importance Of Adequate Calcium Intake

Calcium serves numerous life-sustaining processes, the most important of which is to maintain the electrolyte balance needed for proper rhythmic heart beats.107 If one were to deplete their bloodstream of calcium, they could die from a heart attack caused by an acute arrhythmic disorder.

In a healthy body, 99% of all calcium is stored in bone where it provides structural support.108 The amount of calcium that is allowed in the bloodstream is tightly controlled by the parathyroid glands.109

In bone, vitamin K2 activates proteins that bind calcium.110 Populations with high dietary intake of vitamin K2 have lower rates of osteoporosis.111-114

People need around 1,200 mg per day of calcium from diet and supplements to maintain bone density. We suggest around  700 mg per day of supplemental calcium for women and around 500 mg per day for men. Most people can rely on their diet for the balance of their calcium needs.115

Supplementing with moderate daily doses of calcium will not accelerate arterial calcification.116,117 One reason is that calcium blood levels are tightly regulated in the body and most ingested calcium will be stored in one’s bones. Your bloodstream has top priority when it comes to getting the calcium it needs, which means that if you intentionally deprive yourself of calcium from food and supplements, your parathyroid glands will rob calcium from your bones to maintain a constant calcium blood level to ensure electrolyte balance.118

Vitamin K is a calcium-regulating nutrient. When properly supplemented, vitamin K2 activates matrix Gla-proteins in soft tissues to keep calcium out. On the flip side, vitamin K2 activates calcium binding proteins in bone to maintain skeletal density.

In the absence of vitamin K, bony structures form in soft tissues. Early pathologists were perplexed to find arteries that were supposed to be soft and pliable instead had literally turned to stone. In 1863, Rudolf Virchow, known as the “father of pathology,” described vascular changes he observed as “ossification, not mere calcification, occurring by the same mechanism by which an osteophyte forms on the surface of bone.”  119

These observations confirmed by modern findings clearly demonstrate the power of vitamin K, or lack thereof, to control whether we maintain strong bone density and soft pliable tissues, or develop osteoporosis together with vascular calcification.

Can Calcification Be Reversed?

Most adults probably suffer some degree of calcification, as intake of vitamin K in Western societies remains at epidemic low levels.

Some of us are severely calcified because of medical disorders requiring dialysis or the drug warfarin, or we allowed blood levels of homocysteine, LDL, or glucose to remain too high for too long.

So the question begs is there anything we can do now to reverse the accumulation of calcium in our arteries, heart valves, glands, and other soft tissues? We found one animal study published in 2007 suggesting that high-dose vitamin K might work. The authors of the study wrote:  99

“Given that arterial calcifications are predictive of cardiovascular events, regression of arterial calcification may help to reduce the risk of death in people with chronic kidney disease and coronary artery disease.”

The study involved four groups of rats who were all initially fed a six-week diet that contained warfarin to induce calcium buildup in the blood vessels. This diet also included a low-dose (normal) vitamin K1 to ensure the animals were not vitamin K deficient. The rats were divided into several groups, of which the following four groups comprised the main part of the experiment:


Group 1: Continue the warfarin plus normal K1 diet;

Group 2: Stop warfarin, but continue with normal dose of vitamin K1;

Group 3: Stop warfarin, but use a high-dose of vitamin K1;

Group 4: Stop warfarin, but add high-dose of MK-4 formof vitamin K2.

During the initial six weeks of warfarin plus normal K1, all animals showed a significant increase in arterial calcification.

In the groups receiving high-dose vitamin K1 or K2 (MK-4), not only was there no further arterial calcium accumulation, but there was a greater than 37% reduction of previously accumulated arterial calcification after six weeks. After 12 weeks, there was a 53% reduction in accumulated arterial calcium deposits.

The groups receiving the high-dose vitamin K1 and K2 also showed a reversal in carotid artery stiffness.99

This study provides intriguing evidence that warfarin-induced calcification may be reversible by high vitamin K intake.

An estimate of the human equivalent dose given to the rats whose arterial calcification was reversed is difficult to precisely calculate because of many variables involved. Our calculations based on estimates of food consumption and animal body weight suggest that the human equivalent dose of the vitamin K2 (MK-4) used in this study is in the range of approximately  52,000 mcg to 97,000 mcg per day (i.e. 52 mg to 97 mg per day).

Since the RDA for vitamin K is only 90 to 120 mcg, the dose of vitamin K used in this rat study may seem extremely high. Yet in Japan, the MK-4 form of vitamin K2 is approved as a drug to treat osteoporosis in humans, and the daily dose is  45,000 mcg (45 mg), which has not been reported to have any toxic effects.120-123

Most Life Extension® members take a combination supplement that provides 1,000 mcg of vitamin K1, 1,000 mcg of vitamin K2 (MK-4), and 200 mcg of vitamin K2 (MK-7).

These are high doses compared to dietary supplement industry standards, and one could postulate that taking these daily doses over an extended time period might induce a regression of arterial calcification, but more human research is needed to establish this. Some members are taking higher doses of vitamin K now with the objective of reversing accumulated soft tissue calcification.

Systemic Calcification 

Cardiovascular tissues are particularly prone to calcium infiltration

The calcification process, however, is also commonly observed in the skin, kidney, tendons, glands, and other soft tissues as a result of disease, and/or aging.124-132


How To Properly Supplement With Vitamin K

A review of the published scientific literature provides a rationale for aging people to supplement with all three vitamin K forms, i.e.  vitamin K1vitamin K2 (MK-4), and vitamin K2 (MK-7).

Since vitamin K is fat-soluble, taking it with the fattiest meal of the day will greatly augment absorption into one’s bloodstream.

A lot of members ask why they cannot take just the MK-7 form of vitamin K2 since this has long-acting effects in the body and has demonstrated powerful calcium blocking properties. Our response is that vitamin K1 and MK-4 have demonstrated impressive results in other studies, so it is best to take a formula that contains all three forms of vitamin K. As mentioned already, the MK-4 form of vitamin K2 has been used in high doses as a prescription drug in Japan to treat osteoporosis.

Since vitamin K1 and MK-4 are inexpensive, it makes sense to include them with the long-acting MK-7 form of vitamin K2 to inhibit and possibly reverse as much vascular calcification as possible, while providing support for strong bones.

Why Doctors Are Apprehensive About Vitamin K

In 1999, one of our scientific advisors recommended to me that aging people supplement with vitamin K.

Vitamin K is known as the “coagulation vitamin” because of the critical role in plays in essential blood clotting.

I was initially apprehensive because abnormal clotting inside blood vessels (thrombosis) is a leading cause of death in the elderly.  133,134 Thrombosis is a frequent underlying cause of coronary occlusion heart attacks and ischemic strokes.135,136

One might think that taking higher amounts of vitamin K would increase thrombotic risk. This concern, however, has no basis in reality. The reason is that only small amounts of vitamin K are required to fully saturatecoagulation 

Once coagulation proteins are fully saturated by vitamin K, then there is no increased thrombotic risk in response to additional vitamin K intake.

The misconception about the role vitamin K plays in coagulation is contributing to the epidemic of diseases caused by  vascular calcification. A plethora of published studies indicate that the most common degenerative diseases afflicting aging humans could be prevented by taking the proper doses of vitamin K.

What mainstream doctors still don’t understand is vitamin K’s critical role of blocking the calcification of heart valves, arterial linings, and other soft tissues, while helping to keep calcium in bone where it is needed.

Eye-opening recent studies shed light on the importance for people to optimize their intake of vitamin K to protect against soft tissue  calcification.

An urgent need exists to convey this information to the medical community. This may not happen any time soon because vitamin K is sold as a low-cost  dietary supplement and not an expensive prescription drug.

 Purchase our finest Vitamin K supplement here.->


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July 02, 2016

NAD+ Shown to Reverse Aging Biomarkers

By Edward R. Rosick, DO, MPH, DABIHM

As we age, our vitality declines as cells can no longer produce the energy of youth.

An essential co-factor required for cellular energy transfer is NAD+, which plays a critical role in regulating the rate at which we biologically age.

NAD+ is used by every cell in the body. Harvard researchers have shown that increasing NAD+ levels in mammals can reverse several biochemical parameters associated with the aging process.1

In a recent study,2 researchers have shown that NAD+ works in two distinct ways to mitigate aging. First, it increases mitochondrial activity and secondly, it activates specific sirtuins shown to regulate life span.3-6

The good news is that higher levels of NAD+ can be restored via a unique form of vitamin B3 called nicotinamide riboside. With this advance, it is possible for aging individuals to boost their NAD+ cellular levels.

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NAD+: An Essential Component of Life 

Nicotinamide adenine dinucleotide (NAD+) is found in every cell in the body and is critical for regulating genes that accelerate aging.7

NAD+ also plays an important part in the transfer of energy released from fatty acids and glucose to the mitochondria to be converted into cellular energy.8,9

When NAD+ levels decline, energy transfer in cells breaks down, leading to mitochondrial dysfunction that results in many of the physical symptoms of aging.1,10,11 Fortunately, by increasing intracellular levels of NAD+, age-related mitochondrial dysfunction can be reversed.1

NAD+ battles aging by activating key anti-aging enzymes called sirtuins, specifically SIRT1 and  SIRT3. Sirtuins contribute to longevity by favorably controlling gene expression.8,11-15

SIRT1 and SIRT3 modulate multiple biological processes summarized in the table at the end of this article.3

Sirtuins can be activated at any age through caloric restriction. In response to undereating, cellular levels of  NAD+ increase.8

Studies in yeast have shown that increasing NAD+ levels positively affects the function of sirtuins and significantly extends yeast life span.18 A study done in worms (C. elegans) showed that older worms had lower levels of NAD+ when compared to younger worms. When NAD+ levels were decreased even further, the worms aged faster. When worms had their NAD+ levels restored, it prevented metabolic changes of aging and increased their life span.5

Of course, it is a large step—evolutionarily and biologically—from yeast and worms to mammals. However, studies done in mammals have also shown that NAD+ levels are critical for not only healthy cellular and mitochondrial functioning, but aging itself.

A study done at Harvard has shown that increasing NAD+ levels in mammals can reverse the aging process.1 This study was done on mice that were bred to have a defect in SIRT1. These mice exhibited multiple signs of accelerated aging, including mitochondrial dysfunction. However, when the levels of NAD+ were increased in these 22-month-old mice, the results were nothing short of amazing: Key markers of aging, including insulin resistance, inflammation, and muscle wasting—all processes commonly associated as a “normal” part of aging—were lowered to that of mice aged 6 months.

Knowing that NAD+ is vital to cellular functioning and that NAD+ levels decrease as we age, many scientists believe a key process in slowing, stopping, or even reversing the aging process is to maintain healthy, youthful NAD+ levels. The interest in finding ways to maintain youthful NAD+ levels has given rise to a form of vitamin B3, nicotinamide riboside, which converts to NAD+ in the body.19,20

By increasing NAD+ levels, nicotinamide riboside has been shown in multiple studies to positively affect mitochondria. In addition, a recently released study2 has shown that nicotinamide riboside can both increase healthy mitochondrial activity and activate specific sirtuins shown to regulate life span.3-6

Let’s now examine some of the well-studied mammalian sirtuins to better understand the importance of maintaining healthy NAD+ levels in preventing premature aging.

The Importance of Optimal NAD+ 

  • Nicotinamide adenine dinucleotide, or NAD+, is a co-factor that plays a crucial role in many biochemical reactions. 
  • Optimal levels of NAD+ are essential for the proper functioning of mitochondria, the producer of energy for the body, and sirtuins, which are enzymes known to be an integral part of the aging process. 
  • While NAD+ levels decrease with age, the use of the natural compound nicotinamide riboside can restore NAD+ to healthy, youthful levels. 
  • Raising levels of NAD+ has been shown to reverse key indicators of aging. 

SIRT1 and Longevity

SIRT1 is the most extensively studied mammalian sirtuin. It plays an important part in multiple biological functions, including tumor suppression, apoptosis, metabolic regulation, and the aging process. Several mouse studies have demonstrated the influence of SIRT1 activity on extending life span.34,35 Delayed bone loss, reductions in the incidence of sarcomas and carcinomas, and improved glucose control and wound healing have been shown in a model of SIRT1 transgenic mice.34 In another transgenic mouse model, increased activity of brain-specific SIRT1 resulted in an approximate  11% increase in median life span.35

An array of research has shown the connection of SIRT1 with premature cellular senescence, a process that contributes to accelerated aging.36,37 By interacting with biological molecules like p53, SIRT1 regulates cellular senescence, apoptosis, metabolism, and cell cycle.36 A study examining the effects of SIRT1 inhibition in human umbilical vein endothelial cells suggested the role of this enzyme in protecting against endothelial dysfunction, one of the consequences of cellular senescence.36

SIRT1 is emerging as an outstanding housekeeper for the maintenance of stem cells by fighting cellular senescence. This was seen in a study involving human mesenchymal stem cells in which the reduction of SIRT1 activity resulted in accelerated cellular senescence. However, when SIRT1 activity was increased in bone marrow-derived stem cells, it showed that senescence was delayed, leading the authors to conclude that SIRT1 may contribute to the prevention of human mesenchymal stem cell senescence.38

A more recent study discussed the importance of SIRT1 in the maintenance of hematopoietic stem cells’ homeostasis and that loss of SIRT1 in hematopoietic stem cells resulted in DNA damage.39

It is well established that genomic instability and impaired DNA damage repair are some of the contributing factors that result in accelerated aging and cellular senescence.40 Exciting findings show that SIRT1 fosters DNA damage repair41and that it protects vascular smooth muscle cells against DNA damage and atherosclerosis.42 Neurodegenerative disorders and age-related cognitive decline have been linked with defects in DNA repair.

Researchers at MIT determined that SIRT1 activation reduces DNA damage and provides an important therapeutic path in neurodegenerative diseases.43 Together, these findings confirm the protective roles that SIRT1 has not only in maintaining genomic integrity but also against neurodegeneration.

A study in mice found that an increase of SIRT1 activity in the brain increased longevity by an approximate 11%, while at the same time reducing the incidence of cancer.45 Yet a more recent study on age-related muscle loss or sarcopenia determined that activation of SIRT1 can improve muscle performance, one of the hallmarks of sarcopenia.44 This is clear evidence that SIRT1 can fight premature aging and promote longevity.


The defects in both gene- and energy-related functions caused by the age-related decrease in NAD+ characterize the disorders that we identify as aging.11 The consequences of a decline in NAD+ levels and subsequent reduction in sirtuins are: 

  • Neurodegeneration in the brain,11,21,22
  • Vascular inflammation, producing damage to blood vessels that can result in stroke or heart attack,21,23,24
  • Increased fat storage in the liver, which can lead to non-alcoholic fatty liver disease (NAFLD),25-27
  • Increased fat production and deposition in white adipose tissue, the primary fat storage form found in dangerousbelly fat,28,29
  • Insulin resistance, preventing cells from appropriately removing glucose from blood, producing higher blood sugar levels and leading directly to metabolic syndrome, 23,30,31
  • Fatigueloss of muscle strengthand fatty infiltration of muscles, resulting in reduced fatty acid oxidation (“burning”), thereby depriving muscles of their normal sources of energy.32,33

SIRT3: A Key Mitochondrial Sirtuin

Primarily located in the mitochondria, SIRT3 plays an important role in the regulation of several mitochondrial processes.45 It has been associated with fatty liver, obesity, hyperlipidemia, and insulin resistance in mice lacking SIRT3 and fed high-fat diets.46

A recent report found that increased SIRT3 activity improved the regenerative capacity of hematopoietic stem cells.47 It is also recognized that this sirtuin is important in neurodegenerative disorders like Huntington’s disease.48 Clearly, the impact that SIRT3 has on metabolic regulation, neurodegenerative disorders, and stem cell regeneration plays a crucial role in premature aging when impaired.


Sirtuins and Their Impact on Pathways That Contribute to Premature Aging When Dysregulated3,16,17

Pathways that contribute to premature aging



Cellular senescence

Genomic integrity maintenance



Metabolic regulation


Stem cells maintenance

Tumor regulation

✔: Confirmed roles ?: Possible roles 


Nicotinamide adenine dinucleotide, or NAD+, is a critically important molecule for multiple biochemical processes in the body.

Numerous studies show that maintaining optimal levels of NAD+ through the use of natural compounds such as nicotinamide riboside are necessary for the health of mitochondria.

Sirtuins, which are enzymes that play a crucial role in the aging process, are dependent upon NAD+ to perform their life-giving functions.

New and groundbreaking studies are showing that maintaining optimal NAD+ levels can positively impact indicators of aging such as insulin resistance, muscle wasting, and inflammation. This gives credence to the hypothesis that aging itself is not only preventable, but reversible.

HENDRIKS SCIENTIFIC and the Life Extension Foundation offer two products that have demonstrated efficacy in raising NAD+. Learn more->


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  44. Mohamed JS, Wilson JC, Myers MJ, et al. Dysregulation of SIRT-1 in aging mice increases skeletal muscle fatigue by a PARP-1-dependent mechanism.  Aging (Albany NY). 2014;6(10):820-34.
  45. Giblin W, Skinner ME, Lombard DB. Sirtuins: guardians of mammalian healthspan. Trends Genet. 2014;30(7):271-86.
  46. Hirschey MD, Shimazu T, Jing E, et al. SIRT3 deficiency and mitochondrial protein hyperacetylation accelerate the development of the metabolic syndrome.  Mol Cell. 2011;44(2):177-90.
  47. Brown K, Xie S, Qiu X, et al. SIRT3 Reverses aging-associated degeneration. Cell reports. 2013;3(2):319-27.
  48. Fu J, Jin J, Cichewicz RH, et al. trans-(-)-epsilon-Viniferin increases mitochondrial sirtuin 3 (SIRT3), activates AMP-activated protein kinase (AMPK), and protects cells in models of Huntington Disease. J Biol Chem. 2012;287(29):24460-72.

June 07, 2016

Impede Unwanted Hair Growth

A cosmetic nuisance endured by women and men is the need to constantly remove body hair. 

Few people realize how inefficient the shaving process is. Daily shaving chops off only a fraction of the hair shaft, leaving most unwanted hair impacted beneath the skin’s surface, ready to re-emerge within 24 hours.

Those who shave daily can spend 100 hours a year running a razor over their delicate skin. An 80-year old who shaves daily from age 15 will spend nine months of their life removing hair using this primitive method. 

Those who pluck hair squander even more time. Modern methods of hair removal also leave a lot to be desired, as you will soon read. 

Recognizing that people are removing hair from more parts of their body than ever before, European scientists have developed a topical compound that produced the following results in human clinical trials.1-3

  • Reduced frequency of shaving or depilation in female legs up to 82%
  • Reduced frequency of shaving or depilation in female groin up to 70%
  • Reduced frequency of shaving or depilation in female armpit up to 50%
  • Delayed the growth of stubborn beard hair in men by 30%
  • Reduced beard hair density in men by 16%

This compound is now available in a soothing topical formula designed to inhibit unwanted hair growth and reduce the time one spends shaving, waxing, plucking, and engaging in other unpleasant forms of hair removal. Order it Now ->

Unwanted Hair in Today’s World 

Whether you’re a man or a woman, your entire body is covered with hair—all except for your lips, the palms of your hands, and the soles of your feet.

For many aging women unwanted facial hair is the main problem. The social stigma attached to hirsutism (excess facial or body hair in women) probably reached its height during the Middle Ages when the Malleus Maleficarum or “Hammer of Witches” claimed that facial hair was one of the ways to recognize a witch. But facial hair is quite natural. 

Every woman has lots of hair follicles hiding below the skin surface of her face. In many cases, these follicles can become over-stimulated by the simple process of aging. Every woman also has a certain amount of male hormones or “androgens” in her body. As some women age, their body produces more of these androgens. This often causes the hair on their chin, upper lip, or neck area to grow. The color and thickness of this hair is largely determined by heredity. So if the women in their family typically have dense, dark, facial hair, they probably will, too. 

Excess body weight, either alone or accompanied by polycystic ovary syndrome, is another reason women may produce excess androgens. Fat retains androgen, so the heavier a women is, the more androgen she keeps in her body.4,5 In many women, this can also cause a spurt of male-patterned hair growth.

What You Need To Know

  • Throughout history, men and women have endured unpleasant hair removal techniques to uphold aesthetic ideals and maintain good hygiene.
  • Today, removing unwanted body hair through shaving or depilation remains a time-consuming ordeal. Even the newest hair-removal techniques leave much to be desired.
  • Now, cosmetic scientists have developed a new topical formula that inhibits the growth of unwanted hair, reducing the amount of time one spends shaving, waxing, plucking, or engaged in other types of hair removal.
  • A novel topical compound called Decelerine™ inhibits actively growing hair follicles, decreasing the length and density of unwanted hair. 
  • After 60 days of use, Decelerine™ delayed the growth of men’s beard hair by 30% and decreased its density by 16%. 
  • In women, Decelerine™ decreased the frequency of shaving or depilation by up to 82% on the legs, 70% in the groin, and 50% in the armpits.
  • Topical ingredients such as Pseudoalteromonas ferment extract, allantoin, and aloe vera soothe, moisturize, and protect the skin. 
  • A topical formula containing Decelerine™ is an ideal after-shaving treatment that slows future hair growth while soothing and calming the skin.

Order it Now ->

But whatever the reason, if you suffer from this problem—you’re definitely not alone. Unwanted facial hair is more common than you might think: 41 million women in the United States remove unwanted facial hair at least once every six months.6 Twenty percent of these women remove it weekly, and 4% of them remove it every single day. And of course, American women also have to deal with the hair on their legs and underarms. 

According to one account, the practice of shaving underarms first started in 1915 when sleeveless dresses became popular, and opened up a whole new field of female vulnerability for marketers to exploit. Gillette’s “Great Underarm Campaign” began in May 1915 with an ad in Harper’s Bazaar that was so successful, McCall’s followed suit in 1917. Women’s razors and depilatories started appearing in Sears & Roebuck’scatalog as early as 1922, and America’s obsession with hairless armpits was officially in full swing.

Hairless legs didn’t catch on until some years later, however. This was mainly because there wasn’t much practical need for them. After rising in the 1920s, hemlines dropped again in the 1930s and most women were content to just leave their leg hair alone. In the 1940s, however, Betty Grable’s famous WWII pinup plus the rise of shorter skirts and silk stockings (that looked unattractive with leg hair underneath) finally put the issue in the forefront. And that’s how American women got persuaded into shaving their legs and underarms. 

But What About Men?

Most historical accounts credit Alexander the Great as being the one who originally made shaving popular. Alexander obsessed about having a clean-shaven face and would never go into battle with a five o’clock shadow. Julius Caesar also set a mighty example by insisting on having his facial hairs plucked out daily with tweezers. 

Today 90% of all American males over the age of 15 shave their face. Seventy-five percent of them shave every day. That means the average man will shave his face about 20,000 times between the ages of 15 and 75.7 That’s a lot of time invested in hair removal.

Women and men can take now advantage of a recent discovery in the age-old fight against unwanted hair growth. A formulation has evolved to inhibit the time-consuming, boring, and often painful process of eliminating body hair that hasn’t evolved much for mankind in over 6,000 years. Before we reveal this new formulation, let’s explore some facts about hair growth. 

Getting to the Root of Hair Growth

The first stage of your hair growth is known as anagen. This growing phase lasts an average of almost three years, but it can range anywhere from two years to six years depending on the individual. During this time, your hair is actively growing at a rate of approximately one centimeter a month (a centimeter is 0.39 inches, or almost one-half of an inch).8 Melanin pigment is also being produced in the hair bulb throughout this entire stage.

The next step is a short transition or resting stage called catagen that lasts around two to three weeks. During this time, your hair stops growing. Also at this point, your hair follicle shrinks and part of it begins to die. Only about 4% of your hairs are in this intermediate stage at any given time. 

In the final or shedding stage (telogen), your hair follicle becomes active once more and starts the cycle of hair growth again. (Each single follicle will produce an average of 20 hairs in its lifetime.) This fresh growth pushes the dead hair up the follicle and expels it to make room for the new hair. It takes roughly three to four months for this particular stage of the process to occur. Only one in ten hair follicles on your head is in this shedding phase at any particular moment. It should be noted that the length of these cycles will vary with the sex of the individual, the person themselves, and the part of the body on which the hair is growing.

But one thing is absolutely certain: the key to slowing hair growth lies exclusively in the anagen phase, because only anagen hairs are vulnerable to physical damage or stimuli.

Topically applied compounds can now painlessly slow down hair growth—and even decrease hair densityso it’s less noticeable. That means you don’t have to shave, wax, or tweeze as often. You can spend the time you save doing something you enjoy instead—all thanks to an exciting new topical formulation. Order it Now ->

How Topical Ingredients Suppress Hair Growth 

After removing your hair (either by mechanical means such as shaving and tweezing or with chemical agents like depilatories), a compound named Decelerine™ penetrates the remaining hair shaft and weakens the hair in the follicle. This causes the new hair to be thinner and of lesser color intensity. 

Unlike many other ingredients that work in a highly abrasive way (destroying skin cells and hair cells alike), Decelerine™ bases its action on the selective destruction of germinating hair follicle cells during the anagenstage. This tactic effectively inhibits hair growth. The Decelerine™ mixture has been clinically proven to delay the growth of stubborn beard hair by 30% and reduce its density by 16% in just two months.1,2

The results for women are even more impressive. Human clinical studies show Decelerine™ can reduce the frequency of shaving or depilation by up to 82% on the legs, 70% in the groin area, and 50% in the armpits.3

These studies reveal that Decelerine’s mechanism of action in men and women is to target and disrupt the anagen phase of the hair growth cycle.

Pseudoalteromonas ferment extract was discovered in the summer of 1988 when a scientific expedition collecting mud samples from an inlet in Antarctica found a new bacterial strain. They named it Pseudoalteromonas antarctica. The scientists found this particular strain of bacteria produced an extracellular material that helped it retain water, adhere to surfaces, and withstand the extreme cold.9-11 This biological adaptation protected the growing bacteria from the extremely harsh environmental conditions they had to endure. When applied to human skin, the natural bio-protective properties of Pseudoalteromonas ferment extract help promote keratinocyte growth and fibroblast adhesion. This unique exopolymer is included in the new hair suppress formula because of its ability to regenerate tissues and protect the skin by enabling faster healing of microscopic irritations, breaks in the skin, and inflammation—all of which can occur during most hair removal techniques (e.g., shaving, waxing, plucking, etc.). Order it Now ->

An additional ingredient included in this hair suppress formula is allantoin, which helps moisturize, protect, and soothe your skin. The moisturizing effect of allantoin increases the water content of your skin’s extracellular matrix and also enhances the exfoliation of your dead skin cells, increasing the smoothness of your skin. Allantoin is also a valuable healing agent that stimulates healthy tissue formation. It provides a soothing, anti-irritating, and skin-protecting effect by forming complexes with irritants and sensitizing agents.12

The last ingredient in this new hair-decelerating system is aloe vera. Oddly enough, this cactus-like plant is actually a member of the lily family.13 There are over 300 varieties of aloe, but Aloe barbadensis has the greatest medicinal power. 

More than 70 active ingredients, including essential oils, amino acids, minerals, vitamins, enzymes, and glycoproteins offer valuable antibiotic, astringent, pain-reducing, growth-supporting, and scar-inhibiting properties14-17 to make aloe vera one of the most important ingredients in the cosmetics industry today. In fact, 95% of the dermatological extracts manufactured around the world feature aloe vera.18

Treasured even before biblical times for its soothing and healing effects on burns and other wounds, aloe vera increases the closure rate of nicks and cuts and improves the tensile strength of wounds by encouraging the proliferation of new cells.14-18

Another reason for aloe vera’s popularity is its incredible moisturizing ability. Aloe vera improves your skin’s hydration, removes dead skin cells, and also acts as a biological vehicle to aid the penetration and absorption of other bioactive ingredients deep into your tissue.14-18

And finally, aloe vera can help improve the look of aging skin and lessen the visual impact of lines, creases, and age spots by stimulating new collagen and elastin synthesis.14-18

The Solution to Unwanted Hair Growth

A new topical formula features active ingredients that inhibit hair growth and decrease the length and density of unwanted hair. Applying this lotion reduces the frequency of shaving, waxing, plucking, or depilation. It also helps your skin recover rapidly with its powerful moisturizing, soothing, and anti-inflammatory effects. 

This innovative formulation offers a complete post-hair-removal treatment by not only impeding hair growth, but also moisturizing and protecting parts of the skin that are revealed to the world.

What Is Decelerine™? 

Decelerine™ is the trade name for a unique mixture of active ingredients that has been proven to inhibit hair growth and decrease the length and density of unwanted hair.2 The action of this mixture allows for the reduction in the frequency of shaving and other types of hair removal techniques. It specifically targets a certain stage of the hair growth cycle that occurs in hair follicle cells. This specific targeting in the growth cycle causes a decreasing, thinning, and weakening of new hair formation, allowing for less frequent hair removal techniques. It also has a soothing, moisturizing, and anti-inflammatory effect on the skin, providing an excellent after-hair removal regimen.

The primary hair-suppressing ingredient in Decelerine™ is a plant derivative of lauric acid. Lauric acid is found in high levels in nature. Natural sources of lauric acid include coconut oil and palm kernel oil. Decelerine™ is one of three active ingredients in the new hair suppress formula. Order it Now ->


1. www.lipotec.com/ficha.php?producto=41. 

2. www.dermoday.com/dosyalar/1234888016.pdf. 

3. Lipotec. Data on file.

4. J Clin Endocrinol Metab. 2009 Feb 17.

5. Climacteric. 2008;11(6):509-17.

6. www.medscape.com/viewarticle/412063. 

7. www.quikshave.com/statfact.htm.

8. www.pg.com/science/haircare/hair_twh_22.htm.

9. J Colloid Interface Sci. 1997 Aug 15;192(2):286-93.

10. Int J Pharm. 2000 Oct 10;207(1-2):39-47.

11. Environ Microbiol. 2006 Sep;8(9):1523-33.

12. www.thesage.com/catalog/products/Allantoin.html. 

13. www.nccam.nih.gov/health/aloevera/. 

14. Mol Cell Biochem. 1998 Apr;181(1-2):71-6.

15. Ceska Slov Farm. 2005 Jan;54(1):43-6.

16. J Wound Care. 2004 Apr;13(4):157-8.

17. Clin Hemorheol Microcirc. 2003;29(3-4):239-46.

18. www.healthandaloe.com/Ingles/ingles.htm. 

19. www.depilatory.com/core/twentieth.html.

May 13, 2016

Fight Skin Aging with Coffee Extracts

Purchase this product now ->

While various factors influence skin aging (including stress and environmental pollutants), long-term sunlight exposure is a primary environmental accelerator.1

As you grow older, your face is the first area to exhibit the visible effects of ultraviolet (UV) radiation, also known as photoaging,with the manifestation of fine lines, wrinkles, loose and dry skin, and discoloration.2

These unsightly changes reflect the deteriorating condition of the components that make up the inner layer of the skin, the dermis.This extracellular matrix is a combination of the fibrous proteins collagen and elastin, along with water-binding glycosaminoglycans.4 Together, these substances form a strong and resilient framework of connective tissue that gives the skin elasticity, strength, and compressibility—ultimately supporting the appearance of youthful and vibrant skin.3

Ultraviolet rays from sunlight wreak havoc on the skin by generating the production of free radicals that break down the vital components of the extracellular matrix.5 Over time, this contributes to the tell-tale signs of photoaging.

International teams of researchers stretching from Brazil to Japan have discovered that ingredients extracted from coffee beans have been scientifically shown to rejuvenate aging skin.6-9 In one study, treated subjects experienced significantimprovements in the appearance of wrinkles, firmness, redness, and texture of facial skin.9

Coffea Arabica Seed Oil 

Americans consume more than 580 million cups of coffee each day as part of their daily ritual.10 Research is emerging that green, unroasted coffee beans provide numerous skin-related benefits when applied topically.6 This is especially true of one of the most commonly grown species of the coffee plant, Coffea arabica.6,11

Coffea arabica seed oil is extracted by cold pressing green coffee beans.6,12 Its high concentration of essential fatty acids, sterols, and vitamin E make it a potent antioxidant that can offer protection against skin damage such as sunburn cell formation and DNA degradation. It can also assist in the prevention of the development of photoaging and inflammatory skin disorders.6

In a placebo-controlled clinical study of 40 female participants, a topical mixture containing Coffea arabica was applied twice daily as a facial wash and once per day as a lotion and night cream. After 12 weeks, treated subjects experienced significant improvements in the appearance of wrinkles,firmness, redness, and texture, compared to the control group.9

These impressive results were due to Coffea arabica’s ability to increase production of collagen and elastin and to protect against the loss of moisture.6

When Brazilian scientists tested Coffea arabica seed oil on human skin, they found a 1.5-fold increase in elastin production and a nearly 2-fold increase in collagen production compared to the controls.6 These two proteins are essential for smoothing wrinkles and preserving the firmness and flexibility of facial skin. 

In addition, treated skin cells had nearly 7-fold higher expression of aquaglycerolporins-3 (AQP-3) and a 2-fold increase in the amount of glycosaminoglycans.6 These proteins act as a tag-team to halt moisture loss and improve skin hydration. First, glycosaminoglycans behave like a sponge to bind and trap water molecules in a water reservoir, then AQP-3 transports them to the upper layers of the skin where they reduce excessive facial dryness and fine lines.


Coffea Robusta Seed Extract 

Robusta coffee is native to western Africa and contains a greater quantity of caffeine and active constituents than Arabica coffee due to its processing method.13 These compounds possess strong antioxidant properties that minimize the adverse effects of cumulative UV exposure.7-9

In an in vitro study conducted by Japanese researchers, topical chlorogenic acid reduced redness induced by excess ultraviolet exposure.7

And in another study, scientists tested topical caffeine’s ability to protect against photoaging.8 For the study, researchers exposed hairless mice to ultraviolet B (UVB) and then applied topical caffeine three times per week for 11 weeks. The results revealed that caffeine administration limited photodamage.

This protection could be related to caffeine’s ability to increase apoptosis (programmed cell death) of UVB damaged keratinocytes, which remove damaged skin cells before they cause photoaging and skin cancer.8

Caffeine also effectively targets and diminishes the appearance of crow’s feet.14 In a study involving 35 women between 30 and 70 years old, a cream containing caffeine was applied to the skin surrounding the eye on one half of the face twice daily while the other half of the face received no treatment. After four weeks, researchers observed a significant improvement in overall skin smoothness and the depth of wrinkles in the skin around the treated area, as measured with a three dimensional optical imaging technique.14


Coffee Rejuvenates Aging Facial Skin 

  • Your face is the first area to exhibit the visible effects of ultraviolet (UV) radiation, also known as photoaging, with the manifestation of fine lines, wrinkles, discoloration, and loose, dry skin. 
  • Extracts from the two most common species of coffee plant directly combat UV damage to improve the strength, resilience, and elasticity of your facial skin. 
  • Coffea arabica seed oil significantly improves collagen and elastin production. 
  • Coffea robusta has a high concentration of chlorgenic acid (which reduces redness associated with excessive sunlight exposure) and caffeine (which limits photodamage, decreases skin roughness and wrinkle formation, and reduces the appearance of crow’s feet). 


Researchers have designed an innovative facial cream that includes ingredients that have been documented to improve the appearance of wrinkles, firmness, redness, and texture.9,14  Purchase Now ->

Coffea arabica seed oil and Coffea robusta seed extract (which contains chlorogenic acid and caffeine) defend against photoaging and support the skin’s structure to restore moisture and hydration for the appearance of brighter and firmer youthful-looking facial skin.6


  1. Fisher GJ, Kang S, Varani J, et al. Mechanisms of photoaging and chronological skin aging. Arch Dermatol. 2002 Nov;138(11):1462-70. 
  2. Sjerobabski Masnec I, Poduje S. Photoaging. Coll Antropol. 2008 Oct;32 Suppl 2:177-80. 
  3. Rinaldi A. Healing beauty? More technology cosmetic products that claim drug-like properties reach the market. EMBO Rep. 2008 Nov;9(11):1073-7. 
  4. Available at: http://www.worldwidewounds.com/2005/august/Schultz/Extrace-Matric-Acute-Chronic-Wounds.html. Accessed August 1, 2013.
  5. Pattison DI, Davies MJ. Actions of ultraviolet light on cellular structures. EXS. 2006;(96):131-57.
  6. Velazquez PMC, Dieamant GC, Eberlin S, et al. Effect of green Coffea arabica L. seed oil on extracellular matrix components and water-channelexpression in vitro and ex vivo human skin models. J Cosmet Dermatol. 2009 Mar;8(1):56-62.
  7. Kitagawa S, Yoshii K, Morita SY, Teraoka R. Efficient topical delivery of chlorogenic acid by an oil-in-water microemulsion to protect skin againstUV-induced damage. Chem Pharm Bull (Tokyo). 2011;59(6):793-6.
  8. Koo SW, Hirakawa S, Fujii S, Kawasumi M, Nghiem P. Protection from photodamage by topical application of caffeine after ultraviolet irradiation. Br J Dermatol. 2007 May;156(5):957-64.
  9. Palmer DM, Kitchin JS. A double-blind, randomized, controlled clinical trial evaluating the efficacy and tolerance of a novel phenolic antioxidant skincare system containing Coffea arabica and concentrated fruit and vegetable extracts. J Drugs Dermatol. 2010 Dec; 9(12):1480-7.
  10. Available at: http://www.usatoday.com/story/money/business/2013/04/09/coffee-mania/2069335/. Accessed August 2, 2013.
  11. Available at: http://www.ico.org/botanical.asp. Accessed August 2, 2013.
  12. Product monograph: Lipactive Green Coffee. Green TechNaturally. January 2008.
  13. Product monograph: Crodarom Green Coffee. Crodarom.
  14. Kaczvinsky JR, Griffiths CE, Schnicker MS, Li J. Efficacy of anti-aging products for perioribtal wrinkles as measured by 3-D imaging. J Cosmet Dermatol. 2009 Sep;8(3):228-33.

January 16, 2016

Shield Yourself from Environmental Cancer Risks

By Steve Frankel

Shampoos, pesticides, drinking water, plastics, and vehicle emissions contain cancer-causing toxins that we are exposed to on a daily basis. 

These chemicals can ultimately lead to cancer by damaging our DNA and impeding our detoxification pathways.1-4  In a cruel twist, some of these toxins even activate cancer-causing genes that could otherwise have remained dormant.5,6

Today, it is impossible to avoid the constant onslaught of environmental toxins. But what is possible is to equip your body with the tools it needs to identify toxins and remove them from your system before they can cause any damage. 

Cruciferous vegetables do just that. They optimize your body’s detoxification system in order to neutralize many of these chemical threats—and maintain the integrity of your DNA in the process.7-9

Decades of research have shown that ingesting cruciferous vegetables can slash risk of cancer by up to 54%.10-18 These findings show reduced risk of virtually every major type of cancer.19-29

In this article, you’ll learn about the specific components of cruciferous vegetables that fight cancer—and, more importantly, you’ll discover how to harness the powers of cruciferous vegetables to maximize their cancer-fighting benefits. 

Reducing the Effect of Environmental Toxins

Cruciferous vegetables (cabbage family, broccoli, cauliflower, mustard greens, and Brussels sprouts) are some of the most powerful cancer-fighters nature has to offer. Numerous studies have shown that consuming cruciferous vegetables can sharply reduce your risk of cancer.10-18

They’ve been found to be effective against a vast array of cancers including breast, prostate, colon, lung, bladder, ovarian, kidney, and more. Compounds in cruciferous vegetables also have been found to provide long-term anticancer protection even after they’ve been cleared from the body!30,31

No other food group can boast such powerful, broad-reaching anti-cancer benefits. We’ve known for years that people with the highest overall intake of cruciferous vegetables experience a substantial reduction in the risk of many kinds of cancer—now we’re starting to understand why. 

Research has shown that the compounds in cruciferous vegetables have the ability to control cancer’s on/off switch.32-35  Essentially, they help fight against cancer either by activating genes that prevent cancer, or by suppressing genes that cause cancer.36,37 

Environmental toxins affect the growth and spread of cancer. Pollutants found in air, water, soil, and a large number of industrial products (especially plastics) contain toxins with cancer-causing potential.1-4

Our bodies are equipped with enzyme systems to fight off toxic threats.3,38 Unfortunately, if your enzyme systems aren’t functioning properly, they can have the opposite effect: They can activate those toxins, causing them to become even more lethally carcinogenic. Making matters worse, some toxins suppress protective enzymes, impairing their ability to protect us from cancer.2,7,38-41

That’s where cruciferous compounds come in. Cruciferous compounds help support the key enzyme systems that are so vital for detoxifying your body of harmful, cancer-causing environmental toxins.9,42,43 The result is unprecedented protection from many of the unavoidable cancer-causing toxins we face on a daily basis. 


  • Arugula
  • Black and brown mustard
  • Bok choy
  • Broccoli
  • Brussels sprouts
  • Cabbage
  • Cauliflower
  • Collard greens
  • Horseradish
  • Japanese radishes
  • Kale
  • Kohlrabi
  • Parsnips
  • Radishes
  • Rape
  • Rutabaga
  • Turnips
  • Watercress
  • Wasabi

Glucosinolates: Powerful Chemoprevention 

Among cruciferous vegetables’ many powerful components, one group stands out. They’re called glucosinolates, which are found in broccoli and broccoli sprouts. They are converted within the body to a number of active constituents that fight cancer through multi-targeted mechanisms.44-47

For example:

  • Glucosinolates reduce the carcinogenicity of many environmental toxins by boosting the genetic expression of important detoxifying enzymes.8,48
  • They protect DNA from oxidative damage caused by toxins (up to 28% reduction in human research), thereby preventing the initial changes that can lead to cancer.49
  • Glucosinolate derivatives encourage cancer cells to commit suicide, and they suppress genes that create the new blood vessels that support rapid growth of tumors.50
  • Finally, there’s evidence that glucosinolate derivatives can turn off genes that promote the spread of cancer.50

Because glucosinolates directly affect the function and expression of genes (the epigenetic effect), experts point out that their protective effects are both wide-ranging and long-lasting.50

Human research reveals that higher dietary intakes of glucosinolates are associated with a reduction in prostate cancer risk by 32%.45 Derivatives of the glucosinolates abundant in broccoli sprouts help prevent stomach cancer by killing the H. pylori bacterium. They also reduce symptoms and biomarkers of inflammation in infected individuals.51

It’s important to note that cooking cruciferous vegetables reduces the rate of glucosinolate conversion to active molecules by about 300%, which is one good reason why supplementation may offer a better alternative.52-54


Slash Your Cancer Risk with Cruciferous Vegetables

  • Environmental toxins are a growing problem, threatening to raise already high rates of preventable cancers. 
  • While our bodies contain systems capable of detoxifying harmful chemicals, some enzyme systems in fact activate potential carcinogens, making them more, not less, likely to produce malignancy. 
  • Toxins, radiation, and other forces exert negative epigenetic effects on our chromosomes, potentially revealing cancer-causing genes for activation. 
  • Phytochemicals from cruciferous vegetables can attack these natural cancer-promoting processes at their root. 
  • Cruciferous components work together to inhibit toxin-activating enzymes, boost detoxifying enzymes, and reverse negative epigenetic changes in our chromosomes. 
  • Because many such compounds are inactivated by cooking, consider using a concentrated supplement containing extracts from multiple types of beneficial cruciferous plants. 

Indole-3 Carbinol (I3C)

Indole-3-carbinol (I3C) is one of the most widely-studied components of cruciferous vegetables. Studies have shown that it helps fight cancers of the breast, prostate, and reproductive tract, as well as colon and blood cancers.55 

In cancers of the reproductive tract, I3C helps prevent the development of tumors by benefitting important ratios of estrogen metabolites such as the 2-hydroxyestrone:16a-hydroxyestrone ratio and 2-hydroxyestrone:estriol ratios.56-58 Note that 2-hydroxyestrone is an estrogen metabolite that seems to protect against cancer, whereas 16-hydroxyestrone may promote cancer. 

Treatment with I3C has also been shown to have a positive effect on recurrent respiratory papillomatosis, a precancerous condition that produces growths in the throat and voice-box. Studies show that treatment with I3C completely stops the growth of papilloma in about 33% of patients and reduces the growth rate and need for surgery in another 33% of patients.59,60

I3C is also beneficial in early cervical cancers known as carcinoma in situ. In one study, 50% of the patients receiving 200 mg/day of  I3C had complete regression of carcinoma in situ, while none of the patients in the placebo group were found to be free of carcinoma in situ after 12 weeks.61 And in women with a potentially pre-cancerous condition known as vulvar intraepithelial neoplasia, treatment with 200 or 400 mg/day of I3C reduced the size and severity of lesions on the vaginal labia.62

Animal studies of I3C show a reduction in tumor number and size in experimental models of cancers of the breast, lung, and prostate.63-65


Many cancers, especially those of the reproductive tissues, depend on the presence of sex hormones (primarily estrogen and testosterone) to sustain their growth. Therefore, many treatment approaches rely on blocking or reducing levels of sex hormones in cancer victims. The problem is, conventional drugs can cause side effects and may harm reproductive potential. That’s where cruciferous vegetables come in.

Some components of cruciferous vegetables act more gently and by multiple mechanisms to impede the growth of such hormone-dependent cancers, making them an important part of chemoprevention strategies. 

Phenethyl isothiocyanate (PEITC), a natural metabolite of glucosinolates from watercress, has been found, for example, to down-regulate androgen receptors, minimizing stimulation of prostate cancer by testosterone.94 3,3’-Diindolylmethane (DIM), another glucosinolate metabolic product, prevents stimulation of prostate cancer cells by both androgens and estrogen.69,95,96

Breast cancers are commonly estrogen-dependent; sulforaphane and indole-3-carbinol (I3C), still other glucosinolate products, decrease the amounts of cancer-stimulating estrogen receptor-alpha molecules present on cells, inhibiting their proliferation.97,98 This effect has been shown to be active in thyroid cancers as well, which are much more common in women than in men.66,99 DIM has a complementary effect, stimulating cancer-suppressing estrogen receptor-beta molecules.100

Finally, a late 2012 study revealed that I3C also induces degradation of the pro-cancer estrogen receptor alpha, and at the same time reduces expression of tumor-promoting insulin-like growth factor receptor-1 in breast cancer cells.101

Thus, a single serving of a complete cruciferous vegetable supplement can protect reproductive tissues from a whole array of harmful hormonal influences, potentially making you much less likely to develop these devastating malignancies.

Di-indolyl-methane (DIM)


The compound DIM is produced in the body following ingestion of glucosinolates derived from cruciferous vegetables. Animal models, basic lab studies, and limited phase 1 clinical trials show that DIM prevents tumors of the prostate, ovary, cervix, and thyroid, as well as several types of leukemia.66-73 DIM also appears to suppress cancer stem cells, the lingering, super-potent cells that can cause a cancer to recur even years after apparently successful treatment.74,75

Like the other components of cruciferous vegetables, DIM induces cancer cell death by apoptosis, inhibits cancer cell growth, slows or stops new blood vessel development in tumors, and can inhibit factors allowing cancer cells to invade healthy tissue.69

Like I3C, DIM helps prevent the growth of estrogen-dependent tumors, such as those of the female breast and reproductive tract, by boosting the ratio of 2-hydroxyestrone:16a-hydroxyestrone.66,76

Studies in mice demonstrate that DIM can completely prevent the progression of pre-cancerous lesions of the cervix, caused by human papilloma virus (HPV), to full-blown cancer.77 In fact, researchers now theorize that DIM could possibly make the human papilloma virus vaccine more effective, so that it could be given to women already infected with the virus. (Currently it is only effective prior to infection.)77 DIM also increases levels of protective interferon gamma in mouse models of cervical cancer.68

Watercress Extract

One particular cruciferous vegetable, watercress, brings together the very best actions of the other cruciferous vegetables and their components we’ve discussed so far. Studies have shown that watercress has a positive effect on lung, colorectal, and prostate cancers.

Watercress is especially rich in another glucosinolate derivative, called phenethyl-isothiocyanate (PEITC).78 PEITC inhibits carcinogen-activating enzymes, induces cancer detoxification enzymes, and protects against DNA damage.78,79 PEITC is also a remarkably specific epigenetic modulator that turns on genes that suppress cancer.80,81

These effects make watercress extracts particularly appealing in the case of some of our most potent environmental carcinogens, such as those found in tobacco smoke.82-84 Watercress and PEITC are also showing promise in other malignancies caused by activated carcinogens, such as colorectal and prostate cancers.85-87

Look for supplements that contain watercress extract, rather than purified PEITC, because the watercress extracts also contain small amounts of other detoxifying enzyme inducers with even greater potency.78 These substances help prevent cancer growth by reducing inflammatory stimuli such as nitric oxide.88


Cancer Type

Risk Reduction



Melanoma Skin Cancer 


















Mouth and Throat 


This table shows the reduction in risk for various cancer types, for those consuming the highest versus the lowest amounts of cruciferous vegetables.

How to Get the Most Benefit from Cruciferous Vegetables

In order to get the maximum health benefits from cruciferous vegetables, make sure you’re consuming a variety of them. Every member of the cruciferous family contains a different set of the glucosinolates that help fight cancer. 

For example, broccoliBrussels sprouts, and cabbage are good sources of a glucosinolate called glucoraphanin, the precursor of sulforaphane. Watercress is an excellent source of the glucosinolate gluconasturtiin, the precursor of PEITC. And garden cresscabbage, and Indian cress are top sources of a glucosinolate known as glucotropaeolin, the precursor of benzyl isothiocyanate (BITC).

Next, make sure they’re not overcooked. Boiling, steaming, and microwaving at high power substantially decreases the bioavailability of cruciferous vegetables’ cancer-fighting compounds.89-92As beneficial for you as cruciferous vegetables are, there are some things you need to be aware of: The glucosinolate content varies greatly even among individual plants of the same type—and even among parts of the same plant. Even these relative concentrations change during the course of a single plant’s growth cycle.93

That’s why, in addition to eating a variety of cruciferous vegetables, it’s important to take a standardized cruciferous compound supplement. A good cruciferous vegetable supplement should contain I3C, DIM, and PEITC—and for even greater impact, should also include extracts of raw broccoli, cabbage, watercress, and other plant compounds such as apigenin. 


Several plant extracts complement the detoxifying and epigenetic effects of cruciferous vegetables, making them valuable additions to a comprehensive cancer-prevention supplement. The three most potent ones include apigenin, cat’s claw, and rosemary.

  1. Apigenin is a bioflavonoid found in celery, parsley, and some other plants that has known chemopreventive effects. These include stopping the cell reproductive cycle, inducing cancer cell death by apoptosis, preventing metastasis, and slowing new blood vessel formation.102-105 Clinical studies show that 20 mg/day of apigenin, in combination with 20 mg/day of the green tea extract EGCG, drastically reduced the rate of colon cancer recurrence following surgical treatment (only 7% of treated patients had recurrences, while 47% of the control patients had recurrences).106 Apigenin shows promise in laboratory and animal studies of cancers of the mouth, skin, and pancreas, as well as in leukemia.102,104,107-109
  2. The second extract that can be used to complement cruciferous compounds is called Cat’s Claw (Uncaria tomentosa). Lab studies have shown that Uncaria extracts are effective against tumor cells from breast, cervical, lung, thyroid, and colon cancers as well as leukemia.110-112 Uncaria extracts contain powerful antioxidants that protect—and can even repair—DNA from environmental damage.113,114 The result is protection from cancer, especially in organs with a rapid rate of cell turnover, such as skin, colon, and lung, where a small amount of DNA damage can have a rapidly accumulating pro-cancer effect. Uncaria extracts reduced reductions in immune function after chemotherapy while inducing programmed cell death (apoptosis) in malignant cells.110,111,115-117
  3. Rosemary extracts have shown effectiveness in lab studies of colon, skin, and ovarian cancers, and leukemia.118-124 Rosemary is capable of enhancing the ability of the body to rid itself of potential carcinogens.125,126 In addition, rosemary offers remarkable protection against radiation, shielding cells of the blood and gastrointestinal tract in particular from radiation’s ionizing and oxidizing effects.127-130 Rosemary slows or stops DNA damage and tumor cell proliferation, induces apoptosis of tumor cells, and markedly suppresses genes that enable tissue invasion and metastatic spread.118,131-133 Currently, oncologists are giving special attention to the combination of rosemary extracts plus vitamin D3—and for good reason. Together, these supplements promote normal cell differentiation into mature, non-cancerous white blood cells, helping prevent conversion into leukemia cells.124,134


Environmental toxins are major causes of cancer. They cause damage to our DNA and can activate cancer-causing genes that would otherwise have remained dormant. Although it’s impossible to avoid these toxins, you can arm your body with the tools it needs to identify the toxins and remove them from your system before they can cause any damage. 

Cruciferous vegetables neutralize chemical threats by optimizing your body’s detoxification system, by maintaining the integrity of your DNA, and by activating the genes necessary to fight cancer. The result is unprecedented cancer protection from the unavoidable assaults of daily living.

Many of the cruciferous vegetables’ constituents hold up poorly under cooking and processing conditions. That’s why the best way to consistently gain the benefits of cruciferous compounds is to lightly steam the vegetables and/or obtain them in standardized dietary supplements. 

Purchase Life Extension Foundation's Cruciferous Vegetable Extract ->



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